Week 13 Flashcards
(159 cards)
1
Q
What is the body plan of a Nematode?
A
Stylised body plan eg ‘a tube within a tube’ - alimentary canal extends from mouth to anterior (head) to anus at posterior (tail)
2
Q
Parasitic nematodes exhibit a high degree of preadaptation which contributes to their success. What is preadaptation?
A
An adaptation that serves a different purpose from the one for which it evolved
3
Q
How is Nematode biochemistry/physiology highly adapted?
A
survive wide range of conditions e.g. osmotic pressure, temperature and pH
survive under both aerobic and anaerobic conditions
utilise wide range of food sources
tough outer cuticle can withstand environmental insults – e.g. host immune responses
4
Q
What is polyparasitism?
A
People harbouring many different species of parasites
5
Q
What % of people harbour at least one species of gastrointestinal nematode?
A
20%
6
Q
WHO definition of health
A
The state of complete physical, mental and social well-being and not merely the absence of disease or infirmity
7
Q
Give two examples of parasitic nematodes?
A
Ascaris lumbricoides - direct life cycle
Wuchereria bancrofti - vector transmitted
7
Q
A
8
Q
What disease is caused by infection with Ascaris lumbricoides parasite?
A
Ascariasis
9
Q
Reasons for the high prevalence of Soil Transmitted Helminths (STHs)
A
Widespread distribution of nematodes
Resilience of eggs to harsh environmental conditions
High number of eggs produced per parasite
Poor socioeconomic conditions
Lack of education
10
Q
In what three ways do Ascariasis cause pathology?
A
Associated with the ingestion and migration of larvae
Associated with adult parasites in the intestine
Due to “wandering” adults outside of the intestine
11
Q
What disease is caused by Wuchereria bancrofti?
A
A type of Filariasis known as Elephantiasis
(Vector transmitted by female mosquito feeding; but other types of Filariasis can be caused by the black fly)
12
Q
What are the stages of a nematodes life cycle?
A
4 Laval and 4 moulting stages.
At L3 larvae stage, the larvae infects the host where the cycle continues.
These life cycles are complex and don’t represent an evolutionary sequence
13
Q
How many separate occasions has parasitism developed in nematodes?
A
at least 9 times
14
Q
If intestinal nematodes do not multiply within an individual host, the number of adult worms in a host is to due what?
A
The number of infection events (L3 larvae) and degree of exposure.
15
Q
In endemic populations number of worms in individuals is over dispersed, what does this mean?
A
Some individuals have many more adult worms than others.
For example >70% of worms found in <15% of hosts
16
Q
Does overdispersed distribution of nematodes have a biological basis?
A
There may be an underlying physiological defect to explain this overdispersion; meaning that you can treat the highly infected individuals but they may be more susceptible to reinfection
17
Q
Where is a major ancestral site for parasites?
A
Vertebrate intestine (gastrointestinal tract) - helminths that have co-evolved with their hosts over Millenia suggesting that mammals have developed mechanisms to tolerate this infectious disease
18
Q
Features of Soil Transmitted Helminths (STHs)?
A
Access to host is easily achieved through ingestion
Parasite survival favoured by availability of nutrients in gut
Transmission ensured by the ease of exit to outside world
Gastro-intestinal nematode species - commonest but not most pathogenic
19
Q
Ascaris lumbricoides (Ascariasis) stage 1 life cycle?
A
Adult worms live in the small intestine.
A female may produce ~200,000 eggs per day with are passed with faeces.
Unfertilised eggs may be ingested but are not infective.
20
Q
Ascaris lumbricoides (Ascariasis) stage 2 life cycle?
A
Larvae develop to infectivity within fertile eggs are 18 days to several weeks, depending on the environmental conditions (optimum: moist, warm, shaded soil)
21
Q
Ascaris lumbricoides (Ascariasis) stage 3 life cycle?
A
After infective eggs are swallowed the larvae hatch, invade the intestinal mucosa and are carried via the portal, then systemic circulation to the lungs.
22
Q
Ascaris lumbricoides (Ascariasis) stage 4 life cycle?
A
The larvae mature in the lungs (10-14d), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed
23
Q
Ascaris lumbricoides (Ascariasis) stage 5 life cycle?
A
Upon reaching the small intestine, develop into adult worms. Between 2-3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1-2 years.
24
Where does Ascaris lumbricoides have the highest prevalence?
Tropical and subtropical regions and areas with inadequate sanitation
25
What occurs upon ingestion and migration of larvae: Symptoms/Pathology? (Ascariasis)
Severe symptoms associated with the larvae migrating through the lungs - severe haemorrhagic pneumonia – can lead to life-threatening respiratory failure.
More commonly, haemorrhages are smaller in scale – but this may still lead to breathing difficulties, pneumonia and/or fever
Many parasite proteins highly allergenic – causes eosinophilia and can cause allergic hypersensitivity reactions such as asthma
26
Pathology: Adult worms in the intestine may cause? (Ascariasis)
Generalised digestive disorders such as nausea,
Symptoms depend on parasite burden,
Heavy infections - contribute to malnutrition in the host
More serious and potentially fatal condition:
- Mass of worms physically blocking the intestine (surgery)
27
How can adult worms "wander" outside of the intestine? What might this cause?
(Ascariasis)
Bile duct - Becomes blocked causing jaundice and general interference in fat metabolism
Break through appendix or intestinal wall - may case fatal peritonitis
Up intestinal tract - vomited up or emerge through nose (may cause suffocation)
28
How is Ascariasis diagnosed?
Clinical and lab examinations:
- Coprological (detection of eggs in faeces)
- Serological (detection of antibodies or antigens)
- Molecular (PCR detection of parasite DNA from eggs passed in faeces)
- Image-based
29
How can molecular examinations be used to diagnose Ascariasis?
PCR detection of parasite DNA from eggs passed in faeces.
- Multiplex PCR can detect multiple parasite species in single reaction
- qPCR enables quantification of infection intensity (very heavy infections treated by surgery rather than chemotherapy in children)
30
What are the three types of Filariasis?
Lymphatic Filariasis
Subcutaneous Filariasis
Serous Cavity Filariasis
31
In summary What is Lymphatic Filariasis?
Worms occupy the lymphatic system (eg Wuchereria bancrofti - responsible for 90% of cases)
32
In summary, what is Subcutaneous Filariasis?
Worms occupy subcutaneous layer of skin (eg Loa loa and Onchocera volvulus - river blindness)
33
In summary, what is Serous cavity Filariasis?
Worms occupy peritoneal, pleural or pericardial cavity (eg Mansonella perstands and Dirofilaria immitis (dog heart worm))
34
Wuchereria bancrofti transmitted by mosquito bite causes a type of Filariasis called what?
Elephantiasis
35
Stage 1 of the Wuchereria bancrofti?
During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound
36
Stage 2 of the Wuchereria bancrofti?
They develop into adults that commonly reside in the lymphatics
37
Stage 3 of the Wuchereria bancrofti?
Adults produce microfilariae measuring 244-296um by 7.5-10um, which are sheathed and have nocturnal periodicity, except the South Specific microfilariae which have the absence of marked periodicity.
The microfilariae migrate into lymph and blood channels moving actively through lymph and blood.
38
What is the length/diameter of female and male Wuchereria bancrofti?
Females are 80-100mm long and 0.24-0.30mm diameter.
Males are 40mm by .1mm
39
Stage 4 of the Wuchereria bancrofti?
A mosquito ingests the microfilariae during a blood meal.
40
Stage 5 of the Wuchereria bancrofti?
After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles.
41
Stage 6 of the Wuchereria bancrofti?
There the microfilariae develop into first-stage larvae and subsequently into third stage infective larvae
42
Stage 7 of the Wuchereria bancrofti?
The third stage infective larvae migrate through the hemocoel to the mosquito's prosbocis and can infect another human when the mosquito takes a blood meal
43
What are the clinical presentations of Lymphatic filariasis?
Most infected people are asymptomatic, however some show:
Lymphoedema - improper functioning of lymph system
- results in swelling caused by fluid collection
- difficult to fight infection (bacterial infections cause hardening and thickening of skin - elephantiasis)
Tropical pulmonary eosinophilia syndrome (coughing, shortness of breath, wheezing, ect)
44
Body deformities caused by lymphatic elephantiasis have consequences. These include?
- Social stigma and sub-optimal mental health
- Loss of income-earning opportunities
- Increased medical expenses for patients
- Socioeconomic burdens of isolation and poverty
45
How can morbidity be managed for individuals with filariasis?
Surgery can alleviate most cases of hydrocele
Clinical severity and disease progression can be reduced with simple hygiene measures, skin care, exercises and elevation of affected limbs
People with lymphoedema should access continuing care throughout their lives, to manage and prevent the disease
46
How can filariasis be prevented and controlled?
Avoid mosquito bites:
- Sleep under a mosquito net,
- Wear long sleeves and trousers,
- Use mosquito repellent on exposed skin
Or, annual mass drug treatment of entire communities and control mosquitoes
47
How does Mebendazole act as a treatment for Ascaris?
Binds to β-tubulin and inhibits microtubule assembly . Therefore, impaired uptake of glucose by larval and adult stages causes reduced energy production and immobilises the parasite; eventually killing it.
48
Why is Mebendazole good for treating GI nematode infections?
Poorly absorbed (5-10%) from gut – good for treating GI nematode infections as drug concentration remains high - but treating tissue dwelling nematodes is more difficult
49
How can infection of nematodes be prevented?
Periodic administration of anti-helminthic drugs to eliminate infecting worms,
Health and hygiene education to prevent re-infection by encouraging 'healthy' behaviour
Improved sanitation to reduce soil contamination with infective eggs
50
How is Ivermectin used to treat nematode infections?
Ivermectin binds with high affinity to glutamate-gated chloride channels in invertebrate nerve and muscle cells causing increased permeability of cell membrane to chloride ions and hyperpolarization of nerve or muscle cell resulting in paralysis and death - either directly or by causing the worms to starve
51
How can preventative chemotherapy for lymphatic filariasis be used?
Mass drug administration - treat entire at-risk population with drug combinations.
Drugs - limit effect on adult worms but reduce microfilariae in bloodstream and prevent spread of parasite to mosquito
Drug schedule varies depending on whether there is co-occurrence of lymphatic filariasis with other filarial diseases
52
How many preventive chemotherapy for lymphatic filariasis treatments have been given?
6.7 billion treatments delivered to >850 million people in 66 countries (2000-2016) - population requiring drug treatment declined by 36% - estimated to have prevented economic losses of ~US$100 Billion
53
How many countries have achieved elimination of lymphatic filariasis due to preventive chemotherapy?
14 countries have achieved elimination of lymphatic filariasis as a public health problem, but preventive chemotherapy still required in 52 countries
54
Characteristic features of the tapeworm?
Dorso-ventrally flattened, ribbon-like bodies (can be very long).
Scolex body plan and stobila,
Degeneration of non-essential systems (sensory, muscles, locomotory reduced as no gut)
Body wall (tegument) is metabolically active layer where nutrients are absorbed and secretions and waste materials exported
55
What occurs during and after fertilisation of tapeworm in the proglottids?
- Each is monoecious
- Fertilisation can occur between proglottids of same/different tapeworm
- After fertilisation, proglottids fill with eggs and gravid proglottids break off the chain and pass out in faeces or crawl through the anal sphincter
56
What is the protonephridium in a tapeworm?
the functional unit of the excretory system
Also called flame cells (due to beating cilia looking like a flickering flame) – these extend into a fine tubule
57
How does excretion in the protonephridium of tapeworm occur?
Cilia generate current – excess water containing nitrogenous waste forced into tubule and eventually out of tapeworm body via excretory pores
Allows tapeworm to conserve water and eliminate salts - essential for survival in the host intestine
58
What organism is the only definitive host for T. saginata and T. solium?
Humans
(A definitive host is an organism which supports the adult or sexually reproductive form of a parasite)
59
When cooking beef/pork, what is ensured to prevent transmission of the tapeworm?
Meat carefully inspected for the presence of cysticerci (If only a few, infected parts condemned and meat is frozen for 21 days at <7degrees C)
Freezing lethal to cysticerci - but can withstand 70 days at 0°C
Extensive infection - entire carcass is destroyed
Meat must be thoroughly cooked to at least 56°C (133°F)
60
What are the symptoms of tapeworm in humans?
- Rarely cause intestinal blockage or penetrate gut all but pathology is usually inconsequential
- May have psychological distress at passing motile segments
- Infected with T. saginata may have more symptoms than T. solium as its larger.
- Mild symptoms include digestive disturbances, abdominal pain, nausea and weight loss
- Taeniasis
61
What is Taeniasis treated with, when tapeworms infect humans?
Praziquantel
62
What is Cysticercosis caused by?
Taenia solium (pork tapeworm)
63
How is Cysticercosis acquired? Where do cysts form?
By ingesting T.solium eggs excreted in human faeces
Cysts can form in brain, muscle and other tissues - major cause of adult onset seizures in low-income contries
64
Pathogenesis of pork tapeworm depends upon location of cysticerci?
Muscles - generally no symptoms, may feel lumps under skin
Eyes - Rare but cause disturbed vision or detached retina
65
Pathogenesis of pork tapeworm: neurocysticercosis? (brain spinal cord)
seizures and headaches but also confusion, difficulty with balance, swelling of the brain. Death can occur suddenly with heavy infections.
Leading cause of acquired epilepsy in developing world - also accounts for 10% of ‘emergency room’ visits for seizures in southwestern United States.
66
When does symptoms usually occur when an individual is infected with pork tape worm due to cysticerci?
Symptoms - occur months to years after infection – inflammation around dying cysts causes brain to swell – cause of most symptoms
67
What are the three cestode parasites?
Taenia solium
Taenia saginata
Echinococcus granulosus
68
What is a definitive host and an intermediate host?
Definitive host: An organism which supports the adult of sexually reproductive form of a parasite
Intermediate host: an organism that supports the immature or non-reproductive forms of a parasite
69
What is the scolex (tapeworm morphology)?
Small attachment organ that possesses either hooks + suckers or only suckers attach to host tissue
70
What is the strobila (tapeworm morphology)?
Chain of proglottids
- can grow 15-30cm a day
- proglottids bud sequentially from the neck behind the scolex
71
What is the proglottids (tapeworm morphology)?
Grow continuously from neck, new proglottids replace old: immature - mature - gravid
72
What is the scolex difference between human tapeworm species?
T solium (pork tapeworm) - 4 large suckers and rostellum containing double row of hooks
T. saginata (beef tapeworm) - 4 large suckers - NO rostellum and rostellar hooks
73
What allows identification of differing species of tapeworm?
Visualisation of primary lateral branches (by carmine staining) of the uterus allows differentiation between species and can be used for diagnosis
74
How do cestodes absorb nutrients from the hosts intestine?
Directly through the tegument (not a passive process, specialised membrane transport systems exist within the tegument - microvillous increase SA)
(Act in a similar manner to brush border on mammalian mucosal cells but may serve attachment function.)
75
Stage 1 of the life cycle of pork and beef tapeworms?
Eggs or gravid proglottids in faeces are passed into the environment
Cattle and pigs become infected by ingesting vegetation contaminated by eggs or gravid proglottids
76
Stage 2 of the life cycle of pork and beef tapeworms?
Oncospheres hatch, penetrate intestinal wall, and circulate to musculature.
Oncospheres develop into cysticerci in muscle
77
Stage 3 of the life cycle of pork and beef tapeworms?
Humans infected by ingesting raw or undercooked infected meat
78
Transmission of tapeworm to the intermediate host? (cow/pig)
millions of eggs produced/day – immediately viable and can remain in the environment for several weeks = enormous reproductive potential
eggs ingested by intermediate host contain a larval stage called the oncosphere.
79
When eggs of the tapeworm are ingested by the intermediate host, what occurs? (transmission to intermediate host)
The oncosphere penetrates through the gut wall through the mucosa of duodenum - passes into blood and encysts within tissues.
A thick membrane or wall (embryophore) - forms a highly protective structure around the oncosphere.(this is known as a cysticercus )
80
How is tapeworm passed from the intermediate host to the definitive host?
Cysticeri are infective within 7-10 weeks
Upon ingestion of infected meat – the cysticerci excyst within the human intestine –scolex evaginates (activated by bile) and attaches to intestinal wall and develops into adult tapeworm
81
What is the geographical distribution of Taenia saginata?
Worldwide distribution - common in Africa, some parts of Eastern Europe, Philippines and Latin America - very rare in India as Hindus do not eat beef
Partially cooked, smoked or pickled beef can be infective, although raw beef is commonest cause of infection
82
What is the geographical distribution of Taenia solium?
Worldwide distribution
More prevalent in regions where humans live in close contact with pigs and eat undercooked pork - very rare in Muslim countries as they do not eat pork
83
Taeniasis in the UK? (Tapeworm infection)
DEFRA (2006) states:
89 infections - overseas travel mentioned in only 2 cases (Sudan).
No reports of T. solium cysts in pigs for many years in UK but occasional reports of sporadic occurrence of T. saginata in cattle
T. saginata more difficult to eradicate due to:
- Greater difficulty in detecting animals that are lightly infected
- Global tendency to consume raw or semi-cooked beef
84
How can humans act as the intermediate host for Taenia solium?
Humans infected with eggs either by ingestion of food contaminated with faeces, or by autoinfection.
Autoinfection - humans infected with adult T. solium can ingest eggs through faecal contamination or, possibly, from proglottids being carried back into the stomach by reverse peristalsis.
85
Stage 1 of human becoming intermediate host of T. Solium instead of definitive host?
Embryonated eggs ingested by human host
86
Stage 2 of human becoming intermediate host of T. Solium instead of definitive host?
Oncospheres hatch, penetrate intestinal wall and circulate to musculature
87
Stage 3 of human becoming intermediate host of T. Solium instead of definitive host?
Cysticerci may develop in any organ, being more common in subcutaneous tissues as well as in the brain and eyes
88
What is the geographical distribution of Cysticercosis?
WHO estimates ~50million people worldwide are affected
Can occur in unexpected places, in populations that may not consume pork! Eg outbreak in Orthodox Jewish community in NY blamed on domestic employees from Latin America
89
How is cysticercosis diagnosed?
Definitive diagnosis: involves demonstration of cysticerci in tissue
90
What is the treatment for neurocysticercosis?
Treatment for neurocysticercosis depends on the location, number and stage of cysticerci and clinical manifestations.
Usually the focus is on the management of symptoms – seizure control with anti-epilepsy drugs and treatment of increased intracranial pressure
Drug treatment – praziquantel
91
How does Praziquantel treat cysticercosis?
As praziquantel kills viable cysts it can provoke an inflammatory response and so can actually make symptoms worse – co-administration with corticosteroids to manage inflammation
92
What causes Hydatid cyst?
Echinococcus granulosus
93
What is the definitive host of Echinococcus granulosus?
Dogs!
Sheep are the intermediate host
But humans can also become intermediate hosts leading to severe and life threatening complications
94
Stage 1 of Life cycle of dog tapeworm?
Adult in small intestine, lays eggs that are embryonated in faeces.
(If ingested by human at this stage, then the human becomes the intermediate host)
95
Stage 2 of Life cycle of dog tapeworm?
Oncosphere hatches, penetrates intestinal wall
Hydatid cyst in liver, lungs, etc
96
Stage 3 of Life cycle of dog tapeworm?
Dog ingests Hydatid cysts from the sheep, and protoscolex forms from the cyst.
Scolex attaches t intestine and matures into an adult.
97
If humans act as the intermediate host instead of the sheep for dog tapeworm (Echinococcus granulosus) then hydatid cysts form. What are these?
Cysts can be 1-20cm, containing fluid.
Germinal layer is a living syncytial tissue, within which developing and mature brood capsules form; producing protoscoleces.
Laminated layer is a thick non-living, carbohydrate-rich matrix, secreted by the germinal layer
98
When hydatid cysts form, they produce protoscoleces. How are these retained??
In brood capsules or burst out into cyst fluid - each protoscolex has potential to differentiate into another hydatid cyst
99
What occurs as Hydatid cysts enlarge?
They exert pressure on surrounding organs and can cause pathology
100
Where has increased incidence of Cystic Hydatid disease?
People living near Lake Turkana in Kenya
101
Where do Hydatid cysts usually develop?
95% develop in lungs or liver but some can form in the brain
102
Hydatid disease in the UK?
In 2015, there were 16 confirmed cases of hydatid disease in humans – 13 in England and Wales (all imported) and 3 in Scotland (travel histories unknown).
103
Where are hotspots for Hydatid disease infection in the UK?
Rural areas with close contact between humans and dogs and there are occupations at risk f occupationally acquired hydatid disease:
- Sheep farmers - contact with sheep dogs
- Dog breeders and dog handlers
- Street cleaners and waste disposal workers
- Veterinary surgeons
104
How is hydatid disease diagnosed?
Usually by ultrasound through computer tomography or magnetic resonance imaging, but as infection is often asymptomatic and only discovered at autopsy, during surgery or when imaging is being used for other reasons
105
How is Hydatid Disease treated in humans?
Echinococcosis is often expensive and complicated to treat, the 4 options are:
1) PAIR (puncture, aspiration, injection, re-absorption) technique
2) Surgery - if the lesion is confined, radical surgery can be curative
3) Drug treatment - albendazole (inhibitory effect on tubulin polymerization)
4) 'Watch and wait'
106
How is treatment for Hydatid disease decided?
Based on loction of hydatid cysts and both the medical infrastructure and human resources available - but frequent relapses often occur due to late diagnosis
107
108
109
109
Where is the majority of cases of schistosomiasis?
~85% occur in Africa
110
What are the three major factors responsible for maintaining schistosome transmission?
Pollution of water with excreta containing eggs
Presence of suitable snail hosts
Human contact with water infected with cercariae
111
By what % does basic sanitation reduce schistosome?
77%
112
Briefly outline the Termatode (Cercariae) life cycle within the human host?
Break the barrier
Migrate in circulation
Mature
Pair up
Find a home
Reproduce (lay eggs)
113
After breaking the skin barrier where do Schistosomula migrate to in order to mature?
From the skin to the liver via the lungs in the vasculature. Where they mature in the liver
114
What 3 developmental stages do Schistosomula go through during migration through the human host?
Skin schistosomula
Lung schistosomula
Liver schistosomula
Mature into adult worms in the liver
Only 30-50% of cercariae that penetrate host reach maturity
115
What do Cercariae mature into?
Schistosomes
116
Reproduction of Schistosomes?
Paired female worms release eggs throughout adult life
Daily egg production: 300-3,000 eggs per day
The eggs of most species have a characteristic spine – this is important for species identification and diagnosis
117
What is the period of time between infection of human host to beginning of egg laying by adult schistosomes?
Period of time between infection of human host to beginning of egg laying by adult worms ~ 25 to 30 days
118
Briefly outline the life cycle of the Cercariae free-living and within the snail host?
Hatch to become motile
Infect a snail
Transform so non-motile
Make copies
Release cercariae
Infect human host
119
What is the first clinical phase of untreated human schistosomiasis?
Cercarial dermatitis
- Swimmers itch - caused by cercariae burrowing into the skin and causing allergic reaction
120
Symptoms of cercarial dermatitis?
Occurs on secondary exposure to infection
Present <15 minutes after exposure
Continues to develop for 2-3 days
Resolves within 5 days
(may occur when species that cannot survive in human penetrates human skin)
121
What is the second clinical phase of untreated human schistosomiasis?
Parastite maturation
Known as acute schistosomiasis or Katayama syndrome.
Begins 2-8 weeks post infection - resolves after several days/weeks
Usually mild and transient but can be severe/life threatening
122
What are clinical features of parasite maturation of Schistosomia?
Dry cough
Mild to moderate hepatosplenomegaly
Pyrexia (fever)
Weight loss
Giant urticaria (hives) – transient, slightly elevated patches of skin redder or paler than surrounding skin - often accompanied by intense itching – caused by release of vasoactive mediators, predominantly histamine, from mast cells
123
What is the third clinical phase of untreated human schistosomiasis?
Established infection - After resolution of acute symptoms patient may become asymptomatic, otherwise symptoms depend on species:
S. haematobium:
Haematuria – blood in urine
Dysuria - painful or difficult urination
Abdominal pain
Bladder inflammation
Other species (S. mansoni etc.)
Abdominal pain
Diarrhoea – may be bloody
Hepatomegaly – with or without splenomegaly
124
What is the fourth clinical phase of untreated human schistosomiasis?
Late stage infection - Final stage occurs many years after primary infection and presents as one of several discrete syndromes:
S. japonicum - Intestinal schistosomiasis
S. mansoni - Hepatosplenic schistosomiasis, Pulmonary schistosomiasis, CNS schistosomiasis
S. haematobium Urogenital schistosomiasis,
Abundant bladder granulomas - ureteric obstruction and renal failure, bladder cancer, genital lesions, infertility, ectopic pregnancies (female genital schistosomiasis)
125
What causes as a result of pathogenesis of chronic schistosomiasis?
Egg deposition
Inflammation
Granuloma formation
Obstruction of urinary tract or portal circulation
Fibrosis
126
Human schistosomiasis is an immunopathological disease; caused by what?
host immune response against eggs which are trapped in the body
Over 50% of eggs remain trapped in host body
127
What is granuloma?
concentric layers of cells forming a distinct lesion
128
Epidemiology of schistosomiasis?
Infection rises rapidly through childhood,
Peaks in older children/younger adults at low transmission rates
Declines into older age
129
What does epidemiology of schistosomiasis suggest?
(Suggesting this age range is more susceptible to do spending more time around/in the fresh water. Peaks occur when people work in the water. Decline suggests we develop some sort of immune respone)
130
How is schistosomiasis diagnosed?
Presence of eggs in either stool or urine samples
Presence of worm antigen CCA in urine
Ultrasound - also evaluates the disease severity and complications in target organs
Bladder or rectal biopsy – eggs passing across intestinal or bladder wall
Serological testing – antibodies against adult worms
131
What is the therapeutic agent used as Chemotherapy to treat schistosomiasis? Why?
Praziquantel:
Effective against trematodes (and cestodes);
Single oral dose;
Well absorbed from gastrointestinal tract - but serum half-life of only 0.8-1.5 hours;
Few side effects and few contra-indications;
Distributed primarily to school age children (highest infection burden)
132
Why is elimination of schistosomiasis a challenge?
Re-infection is very common (presence of snail host)
Praziquantel is much less active against immature worms
Chemotherapy does not always kill adult worms but may just suppress egg production
Limited availability of praziquantel – in 2021 only 29.9% of people requiring treatment received it.
Disease control via preventative chemotherapy unlikely to interrupt transmission
133
Schistosomes are parasitic flukes; they are the second most devastating parasitic disease in terms of what?
Socio-economic importance and public health impact.
- Endemic > 70 tropical and sub-tropical countries
- 200 million people infected - 600 million people at risk
- Also known as Bilharzia or Snail Fever
134
Due to the distribution of schistosomiasis worldwide, it is classified as a?
Neglected tropical disease
135
What are the three major species causing schistosomiasis?
Schistosoma mansoni (Africa)
S. haematobium (Africa and Middle East)
S. japonicum (S.E. Asia and China)
136
What are the two minor species (localised distribution) causing schistosomiasis?
S. intercalatum (parts of Central and W. Africa)
S. mekongi (Cambodia and Laos)
137
Stage one of the schistosome life cycle?
Eggs released from human, into the water via urine and faeces.
Eggs hatch, releasing miracidia
138
Stage two of the schistosome life cycle?
Miracidia penetrate snail tissue and mature,
Sporocysts in snail (successive generations) and develop into cercariae
139
Stage three of the schistosome life cycle?
Cercariae released by snail into water and free-swimming, move towards water surface to penetrate the skin of a human nearby
140
Stage four of the schistosome life cycle?
Once penetrating through the skin, cercariae lose their tails and become schistosomula, moving through the circulation to desired organ for maturation
141
Stage five of the schistosome life cycle?
They migrate through circulation to portal blood in liver and mature into adults.
Paired adult worms migrate to: mesenteric venules of bowl/rectum (laying eggs that circulate to the liver and shed in stools), venous plexus of bladder and are released from the body via faeces and urine
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What is the advantage of secondary hosts for trematodes?
Increased reproductive potential - asexual reproduction can take place in the alternative host
Increases the range of the parasite in space and time - infecting more than one host species allows parasites to survive periods when one host is scarce
An intermediate host can ‘channel’ the parasite towards its definitive host - intermediate host releases parasites into host environment or is part of the definitive host's food chain
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How do cercaria break the skin barrier?
S. mansoni cercariae are photo-tropic
Shed by Intermediate Snail host
Free living, survive 12-48h
Very motile, use forked tail to swim
Use water turbulence and skin derived fatty acids to locate human host
Cercariae attach to skin and use proteases to break through the epidermis
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How long does it take cercariae to break past the skin barrier?
Cercariae can make it through the first layer of skin within 10 minutes !
Shed their glycocalyx (to avoid complement)
Shed tail to become Schistosomula
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How do Adult trematodes migrate to the final egg laying site?
Pair up and migrate to the final egg laying site; locating at the The venous system
They are dioecious and sexually dimorphic - Female lives within male’s gynaecophoric canal
Other Schistosome species located themselves in veins of the mesenteric plexus surrounding small and large intestines
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Features of Miracidia (trematodes)?
Eggs which reach suitable freshwater conditions hatch to release miracidia
This is a ciliated larval stage which is free living and motile
Remain infective for snails for ~6-8 hours after hatching
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How are Miracidia able to locate suitable snail hosts?
Using external stimuli such as light and snail derived chemicals
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Features of sporocysts in trematodes?
Inside snail tissue miracidium transforms into a non-motile primary sporocyst
Primary sporocysts produce generations of secondary sporocysts - produce numerous cercariae
Cercariae released from snail can infect human host
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Granuloma formation of schistosomes?
Immune cells accumulate around egg - Trapped eggs can develop into miracidia
Antigens are released by egg/miracidium
Miracidia die and the granuloma protects the host from effects of toxins released by dying miracidia
- T-cell deficient mice cannot form granulomas resulting in necrosis around egg
But egg-induced granulomas result in pathological change in liver – leading to disease
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What is fibrosis of schistosomiasis?
Egg-induced granulomas transformed into permanent fibrous lesions by deposits of fibrous tissue around egg
Pipe-stem fibrosis causes portal vein branches to resemble sections of clay pipe stems
Blockage of portal vein branches and development of anastomoses
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What are the clinical symptoms of Hepatosplenic disease caused by Trematodes?
Hepatosplenomegaly (enlarged liver and spleen)
Portal hypertension i.e. a build-up of pressure in the vein connecting intestines and liver due to:
- cirrhosis of liver (scarring of the liver)
- ascites (fluid within the abdominal cavity)
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Precise mode of action against trematodes by praziquantel isn't well understood, but observed effects of treatment include:
- Increased cell membrane permeability
- An imbalance in ion transport
- Loss of intracellular calcium
- Massive contraction and paralysis of musculature
- Disintegration of the schistosome tegument
The tegument covering trematodes and cestodes - metabolically active surface
Damage to the tegument exposes the worm to immune mediated damage
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How is schistosomiasis prevented when there are no drugs or vaccines to prevent infection?
Elimination will require integrated strategy:
- Chemotherapy (including – pre-school age children, adults with occupational exposure to infested water
- Snail control
- Improved sanitation
- Provision of safe water
- Health education
- Avoid swimming in freshwater in disease endemic countries
- Drink ‘safe water’ - filter, heat to 50oC for 5 minutes or allow to stand for 24 hours - can eliminate risk of infection
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Distinct morphological forms are produced during the schistosome life cycle. Starting with the life cycle stage released from the snail intermediate host, place the different stages in the correct chronological order:
Cercariae
Adult worms
Schistosomula
Miracidium
Eggs
1 = Cercariae
2 = Schistosomula
3 = Adults worms
4 = Eggs
5 = Miracidium
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In endemic populations the number of worms in an individual host is described as being
Overdispersed
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The pathogenesis of chronic schistosomiasis progresses through the 5 stages shown below. Place the different stages in the correct chronological order:
Fibrosis
Granuloma formation
Obstruction of urinary tract or portal circulation
Inflammation
Egg deposition
1 = Egg deposition
2 = Inflammation
3 = Granuloma formation
4 = Obstruction of urinary tract or portal circulation
5 = Fibrosis
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Which of the following statements concerning the nematode parasites are true?
a. Some nematodes undergo asexual reproduction during their life cycle
b. Ascaris lumbricoides is transmitted by an insect vector
c. For nematode parasites intensity of infection is important not prevalence
d. Wuchereria bancrofti is transmitted by a mosquito
C and D
