Intestinal Parasites Flashcards
1
Q
Protozoa
A
single celled animals – eukaryotes
2-100nm in length
Many species free-living, some are important parasites of humans.
2
Q
Classification of Protozoa
A
Classified according to their means of locomotion
Amoebae, Flagellates, Cilliates, Sporozoa (coccidia)
3
Q
Three species of particular importance
A
Cryptosporidium parvum / hominis
Entamoeba histolytica
Giardia intestinalis (aka lamblia/duodenalis)
4
Q
reproduction in protozoa
A
Reproduction in the human host is usually asexual, by division of growing stages (trophozoites)
In certain species, sexual reproduction may occur in insect vector phase of life cycle (eg malaria)
5
Q
Cryptosporidium
A
Domestic animals can be reservoirs
Organism arranges itself along microvilli of intestinal tract
Becomes intracellular – covered by host cell membrane
6
Q
Cryptosporidium life cycle
A
7
Q
oocysts
A
containing 4 sporozoites, are excreted by the infected host through feces and possibly other routes such as respiratory secretions.
Oocysts are infective upon excretion, thus permitting direct and immediate fecal-oral transmission.
Two different types of oocysts are produced
the thick-walled, which is commonly excreted from the host
the thin-walled oocyst, which is primarily involved in autoinfection.
8
Q
excystation
A
Following ingestion or inhalation of oocytsts…
sporozoites are released and parasitize epithelial cells of the gastrointestinal tract or other tissues such as the respiratory tract.
9
Q
sexual and asexual reproduction
A
Within host cells, the parasites undergo asexual multiplication (schizogony or merogony) and then sexual multiplication (gametogony) producing microgamonts (male)and macrogamonts (female).
Upon fertilization of the macrogamonts by the microgametes, oocysts develop that sporulate in the infected host.
10
Q
Cryptosporidium organisms
A
11
Q
Transmission ofCryptosporidium
A
parvumandC. hominisoccurs mainly through contact with contaminated water (e.g., drinking or recreational water).
Many outbreaks in the United States have occurred in waterparks, community swimming pools, and day care centres.
Zoonotic and anthroponotic transmission ofC. parvumand anthroponotic transmission ofC. hominisoccur through exposure to infected animals or exposure to water contaminated by feces of infected animals.
12
Q
Cryptosporidium diagnosis
A
Microscopy with an acid fast stained stool smear – stains oocysts bright red
Enzyme immunoassay EIA
Fluorescent microscopy using monoclonal antibody to oocyst wall
PCR commonly used for confirmation, epidemiological tracking
13
Q
Cryptosporidium symptoms In immunocompetent individuals
A
Begin 2-10 days after infection
Frequent watery diarrhoea (1-2 weeks, self-limiting)
Less commonly - Nausea, vomiting, abdominal cramps, fever
14
Q
Cryptosporidium symptoms in immunocompromised individuals
A
illness is more severe
Debilitating diarrhoea (up to 20l per day – electrolyte imbalance, dehydration) Severe abdominal cramps, fever, weight loss
15
Q
Cryptosporidium infection
A
no specific treatment
supportive treatment for symptoms that appear
16
Q
Protozoa as Intracellular parasites
A
can infect all the major tissues and organs of the body
in a wide variety of cells (red blood cells, macrophages, epithelial cells, brain, muscle) and take up nutrients from cytoplasm.
17
Q
Protozoa as extracellular parasites
A
Extracellular parasites in the blood, intestine or genito-urinary system and take up nutrients directly from environment, or by ingesting host cells.
18
Q
Helminths
A
refer to all groups of parasitic worms
Helminths are generally large multicellular organisms with complex body organisation
– although invading larval stages may only measure 100-200 μm, adult
worms may be centimetres or even metres long.
19
Q
Three main groups of Helminths important in humans
A
Tapeworms (Cestoda)
Flukes (Trematoda or Digenea)
Roundworms (Nematoda)
20
Q
Flatworms or platyhelminths
A
Tapeworms or flukes
Flatworms have flattened bodies with muscular suckers and/or hooks for attachment to the host.
21
Q
Roundworms
A
Roundworms have long cylindrical bodies and generally lack specialised attachment organs.
22
Q
Transmission of helminths x4
A
Swallowing infective eggs or larvae via the faecal-oral route
Swallowing infective larvae in the tissues of another host
Active penetration of the skin by larval stages
The bite of an infected blood-sucking insect vector
23
Q
Who gets these infections in the UK?
A
People who travel to the tropics/low income countries
Migrants
Protozoan species Cryptosporidium and Giardia can be acquired here, and in other high income countries.
24
Q
How do we diagnose them?
A
still depends largely on microscopic detection of the various parasite stages in faeces, duodenal fluid, or intestine biopsy specimens
25
Why use a wet mount identification technique.
Protozoan trophozoites, cysts, oocysts, and helminth eggs and larvae may be seen and identified
26
Stained smears used in identification x5
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Trichrome stain (Protozoa)
Modified trichrome stain (microsporidia)
Modified Fields stain
Giemsa
Modified Ziehl–Neelsen (ZN) stain, also known as acid-fast stain (coccidia)
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27
Why is it important for microscopist to be able to measure objects in the microscopic field?
Size might be a major diagnostic feature, when morphology very similar,
eg Trematode eggs
using a calibrated measuring scale in the eyepiece
28
Testing faecal samples
To improve sensitivity, concentration of faecal sample is recommended
Increases the chance of detecting parasitic ova, cysts and larvae
Eg by formalin-ether method, or commercially available concentrators
Multiple samples collected over several days often required – intermittent shedding
29
Detection of Parasite Antigens
Since faecal examination is very labour-intensive and requires a skilled microscopist,
antigen detection tests have been developed as alternatives
using direct fluorescent antibody (DFA), enzyme immunoassay (EIA), and rapid, dipstick-like tests.
30
Molecular methods of detection of parasite antigens
such as real time PCR, are becoming increasingly used as a front-line diagnostic tool (in developed countries).
DNA sequencing is useful, eg to investigate outbreaks
31
Pathogenic amoebae; Entamoeba histolytica
Obligate intracellular parasites
Invades intestinal mucosa (or occasionally blood, via the liver)
Trophozoites can feed on bacteria as well host tissue
32
Transmission of Entamoeba histolytica
Person-to-person spread, faecal oral route (eg contaminated water)
Both trophozoites and cysts can be passed in diarrhoea
33
Entamoeba histolytica symptoms
10% to 20% of people who are infected with E. histolytica become sick
Symptoms often quite mild - loose faeces, stomach pain, and stomach pain
Amoebic dysentery is a severe form of amoebiasis associated with stomach pain, bloody stools and fever
Released proteinases can cause tissue damage to colon – portal for other pathogens
Can form abscesses in liver, brain & other soft tissue sites (rare)
34
E. Histolytica life cycle
35
Entamoeba diagnosis using faecal samples
Fresh faecal sample: wet mounts and permanently stained preparations (e.g., trichrome).
Concentrates from faecal sample: wet mounts, with or without iodine stain, and permanently stained preparations (e.g., trichrome).
Concentration procedures not useful for demonstrating trophozoites.
36
Detecting E. histolytica trophozoites
E. histolytica trophozoites can also be identified in aspirates or biopsy samples obtained during colonoscopy or surgery.
37
Antigen detection
Antigen detection by EIA may be useful as an adjunct; can distinguish between pathogenic and nonpathogenic infections.
PCR for confirmation
38
E. Histolytica Stains
39
Giardia
the first intestinal parasite to be observed under a microscope -
Anton van Leeuwenhoek described it in 1681.
40
Giardia life cycle stages
1. Flagellate binucleate trophozoite
| 2. Resistant four nucleate cyst
41
Giardia Lifecycle
42
Cysts
Cysts are resistant forms and are responsible for transmission of giardiasis.
The cysts are hardy and can survive several months in cold water.
can be found in the feces (diagnostic stages) .
Infection occurs by the ingestion of cysts in contaminated water, food, or by the fecal-oral route (hands or fomites) .
Because the cysts are infectious when passed in the stool or shortly afterward, person-to-person transmission is possible.
43
trophozoites
can be found in the feces (diagnostic stages)
Trophozoites multiply by longitudinal binary fission, remaining in the lumen of the proximal small bowel where they can be free or attached to the mucosa by a ventral sucking disk .
44
excystation
In the small intestine, excystation releases trophozoites (each cyst produces two trophozoites) .
45
Encystation
occurs as the parasites transit toward the colon. The cyst is the stage found most commonly in nondiarrheal feces .
46
Giardia symptoms
spectrum varies from asymptomatic carriage to severe diarrhoea and malabsorption.
47
Acute giardiasis
develops after 1 to 14 days and usually lasts 1 to 3 weeks.
Symptoms include diarrhoea (explosive!), abdominal pain, bloating (sometimes large amounts of gas produced!), nausea, and vomiting.
48
chronic giardiasis
symptoms recurrent and malabsorption and debilitation may occur.
49
Giardia diagnosis
Identification of cysts or trophozoites in the faeces, using direct mounts as well as concentration procedures.
Repeated samplings may be necessary.
Antigen detection tests by EIA, and detection of parasites by immunofluorescence. Both available in commercial kits.
50
Identifying cysts
Cysts typically seen in wet mount preparations, while trophozoites are seen in permanent mounts (i.e. trichrome).
51
Identifying trophozoites
Samples of duodenal fluid or duodenal biopsy may demonstrate trophozoites.
52
Soil transmitted helminths: Nematodes species
Ascaris lumbricoides
Strongyloides stercoralis (threadworm)
Trichuris trichiura (whipworm) and
Necator americanus and Ancylostoma duodenale (hookworms)
53
Tapeworms (cestodes) species
Taenia saginata
Taenia solium
54
Fluke (trematode) species
Schistosoma sp
55
Soil transmitted helminthiasis
Among the most common infections worldwide
Affect the poorest and most deprived communities
Transmitted by eggs present in human faeces which in turn contaminate soil in areas where sanitation is poor.
56
Soil transmitted helminthiasis main species
Ascaris lumbricoides
Strongyloides stercoralis (threadworm)
Trichuris trichiura (whipworm)
Necator americanus and Ancylostoma duodenale (hookworms)
57
Soil transmitted helminthiasis - Morbidity
Morbidity is directly related to worm burden
58
Soil transmitted helminthiasis - short term symptoms
Often ‘asymptomatic’
When present, symptoms include intestinal manifestations (diarrhoea, abdominal pain), general malaise and weakness
Nutritional status often impaired, sometimes causing death by
- intestinal bleeding,
- anaemia,
- loss of appetite,
- anorexia, diarrhoea or dysentery,
- reducing absorption of micronutrients
59
Soil transmitted helminthiasis - complications
Complications that require surgical intervention (intestinal obstruction and rectal prolapse).
Worsening school performance – cognitive defects
60
Concomitant infections
Concomitant infections with other parasite species are frequent
- may have additional effects on nutritional status and organ pathology.
61
Ascaris lumbricoides
Nematoda – roundworm
62
The lifecycle of Ascaris
Eggs are highly resistant to harsh environmental conditions
must mature in the soil for a few weeks before becoming infective.
(Worms are not directly transmitted between human hosts.)
63
Symptoms of Ascaris lumbricoides
Clinical ascariasis can include fever, wheezing, shortness of breath.
Heavy worm loads can cause malabsorption of nutrients, obstruction of ducts (bile, pancreatic)
64
Diagnosis
Fertilised eggs rounded - thick shell with an external mammillated (rounded lumps) layer
Fertile eggs 45 to 75 µm in length.
Unfertilised eggs elongated and larger (up to 90 µm).
Shell is thinner
Contain a mass of refractile granules.
65
Trichuris trichiura - lifecycle
66
unembryonated eggs
The unembryonated eggs are passed with the stool .
In the soil, the eggs develop into a 2-cell stage , an advanced cleavage stage , and then they embryonate
67
Embryonated eggs
eggs become infective in 15 to 30 days.
After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvae that mature and establish themselves as adults in the colon
68
Adult worms
The adult worms (approximately 4 cm in length) live in the cecum and ascending colon.
The adult worms are fixed in that location, with the anterior portions threaded into the mucosa.
The females begin to oviposit 60 to 70 days after infection.
Female worms in the cecum shed between 3,000 and 20,000 eggs per day.
The life span of the adults is about 1 year.
69
Trichuris trichiura - diagnosis
70
Strongyloides stercoralis lifecycle
The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host.
71
Free-living cycle
The rhabditiform larvae passed in the stool can either become infective filariform larvae (direct development), or free-living adult males and females that mate and produce eggs from which rhabditiform larvae hatch and eventually become infective filariform larvae .
The filariform larvae penetrate the human host skin to initiate the parasitic cycle
72
Parasitic cycle
Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine .
In the small intestine they mote twice and become adult female worms .
The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs, which yield rhabditiform larvae.
73
rhabditiform larvae
The rhabditiform larvae can either be passed in the stool or can cause autoinfection .
In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body.
74
Autoimmunity
To date, occurrence of autoinfection in humans with helminthic infections is recognized only in Strongyloides stercoralis and Capillaria philippinensis infections.
In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals.
75
Migration of L3 larvae
Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed.
However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues
76
Strongyloides stercoralis acute infection symptoms
Infection with S stercoralis often mild or asymptomatic – may be increased peripheral blood eosinophil count as only marker.
Acute infection may give a characteristic cutaneous reaction as the larvae penetrate the skin, known as ground itch.
77
Symptoms as larvae migrate
As the larvae migrate through the lungs they can produce respiratory symptoms, such as a dry cough or wheeze.
78
Symptoms associated adult worms
Once adult worms reach the small intestine - vague gastrointestinal symptoms such as diarrhoea, anorexia, and vomiting, and epigastric pain worsened by eating.
79
Chronic strongyloidiasis
common – lifelong infections
80
Strongyloides stercoralis; Diagnosis
Diagnosis rests on the microscopic identification of larvae (rhabditiform and occasionally filariform) in the stool or duodenal fluid.
81
Hookworms Lifecycle
82
Hatching of larvea
Eggs are passed in the stool , and under favorable conditions (moisture, warmth, shade), larvae hatch in 1 to 2 days.
83
rhabditiform larvae
The released rhabditiform larvae grow in the feces and/or the soil,
and after 5 to 10 days (and two molts) they become filariform (third-stage) larvae that are infective .
These infective larvae can survive 3 to 4 weeks in favorable environmental conditions.
84
infecting humans
On contact with the human host, the larvae penetrate the skin and are carried through the blood vessels to the heart and then to the lungs.
They penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed .
The larvae reach the small intestine, where they reside and mature into adults.
85
Adult worms
Adult worms live in the lumen of the small intestine, where they attach to the intestinal wall with resultant blood loss by the host .
Most adult worms are eliminated in 1 to 2 years, but the longevity may reach several years.
Some A. duodenale larvae, following penetration of the host skin, can become dormant (in the intestine or muscle).
86
Transmission
In addition, infection by A. duodenale may probably also occur by the oral and transmammary route. N. americanus, however, requires a transpulmonary migration phase.
87
Symptoms
Iron deficiency anemia (caused by blood loss at the site of intestinal attachment of the adult worms) is the most common symptom of hookworm infection, and can be accompanied by cardiac complications.
Gastrointestinal and nutritional/metabolic symptoms can also occur.
In addition, local skin manifestations (‘ground itch’) can occur during penetration by the filariform (L3) larvae, and respiratory symptoms can be observed during pulmonary migration of the larvae.
88
Diagnosis
The eggs of Ancylostoma and Necator cannot be differentiated microscopically.
The eggs are thin-shelled, colourless and measure 60-75 µm by 35-40 µm.
89
Tapeworm (cestodes) species
Taenia saginata
Taenia solium
T. asiatica.
Humans are the only definitive hosts for these three species.
90
how tapeworm infection is acquired
Adult tapeworms are acquired by eating undercooked or raw meat containing larval stages.
91
tapeworm infection
Tapeworms frequently infect humans, but are relatively harmless, despite their potential for reaching a large size.
Humans can also act as the intermediate hosts for certain species and the development of larval stages can cause severe disease.
92
Transmission of tapeworms
Eggs or gravid proglottids are passed with feces
the eggs can survive for days to months in the environment.
Cattle (T. saginata) and pigs (T. solium and T. asiatica) become infected by ingesting vegetation contaminated with eggs or gravid proglottids .
93
Lifecycle in animal intestine
In the animal’s intestine, the oncospheres hatch , invade the intestinal wall, and migrate to the striated muscles, where they develop into cysticerci.
A cysticercus can survive for several years in the animal.
94
Lifecycle stage in human intestine
Humans become infected by ingesting raw or undercooked infected meat .
In the human intestine, the cysticercus develops over 2 months into an adult tapeworm, which can survive for years.
The adult tapeworms attach to the small intestine by their scolex and reside in the small intestine .
Length of adult worms is usually 5 m or less for T. saginata (however it may reach up to 25 m) and 2 to 7 m for T. solium.
95
proglottids
The adults produce proglottids which mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool (approximately 6 per day).
T. saginata adults usually have 1,000 to 2,000 proglottids, while T. solium adults have an average of 1,000 proglottids.
The eggs contained in the gravid proglottids are released after the proglottids are passed with the feces. T. saginatamay produce up to 100,000 and T. solium may produce 50,000 eggs per proglottid respectively.
96
Cysticercosis
Cysticercosis is a tissue infection caused by larval cysts of the tapeworm Taenia solium.
97
How Cysticercosis is acquired
People infected by swallowing eggs found in the faeces of a person with an intestinal tapeworm.
98
How eggs develop
Eggs develop into larval stages and form cysts in the brain, muscle or other tissue.
99
complications
An important cause of adult onset seizures in several low income countries where sanitation is poor.
100
Several species of fluke (trematodes) can mature in humans
Three main species
101
Where fluke develop in humans
developing in the intestines, lungs, liver and blood vessels.
102
the parasite in the environment
Infection occurs when skin comes in contact with contaminated freshwater in which certain types of snails that carry the parasite are living.
Freshwater becomes contaminated by Schistosoma eggs when infected people urinate or defecate in the water.
103
eggs hatching
The eggs hatch, and if the appropriate species of snails are present in the water, the parasites infect, develop and multiply inside the snails.
The parasite leaves the snail and enters the water where it can survive for about 48 hours.
104
Penetrating and migrating in humans
Schistosoma parasites can penetrate the skin of persons who come in contact with contaminated freshwater, typically when wading, swimming, bathing, or washing.
Over several weeks, the parasites migrate through host tissue and develop into adult worms inside the blood vessels of the body.
105
maturing worms
Once mature, the worms mate and females produce eggs.
Some of these eggs travel to the bladder or intestine and are passed into the urine or stool.
106
cause of symptoms of schistosomiasis
are caused not by the worms themselves but by the body’s reaction to the eggs.
Eggs shed by the adult worms that do not pass out of the body can become lodged in the intestine or bladder, causing inflammation or scarring.
107
repeat infections
Children who are repeatedly infected can develop anemia, malnutrition, and learning difficulties.
After years of infection, the parasite can also damage the liver, intestine, spleen, lungs, and bladder.
108
Common Symptoms
Most people have no symptoms when they are first infected.
However, within days after becoming infected, they may develop a rash or itchy skin.
Within 1-2 months of infection, symptoms may develop including fever, chills, cough, and muscle aches.
The acute phase is coincident with first egg release and is characterised by allergic responses (overwhelming immune complex formation), resulting in pyrexia, fatigue, aches, lymphadenopathy, gastrointestinal discomfort and eosinophilia.
109
Chronic schistosomiasis
Without treatment, schistosomiasis can persist for years.
The chronic phase occurs in response to the cumulative deposition of fluke eggs in tissues and the host reactions that develop against them.
Signs and symptoms of chronic schistosomiasis include: abdominal pain, enlarged liver, blood in the stool or blood in the urine, and problems passing urine.
Chronic infection can also lead to increased risk of bladder cancer.
Rarely, eggs are found in the brain or spinal cord and can cause seizures, paralysis, or spinal cord inflammation.
110
Schistosomiasis (or bilharzia) course of infection
divided into three phases: migratory, acute and chronic.
The migratory phase occurs when cercariae penetrate and migrate through the skin.
This is often asymptomatic, but in sensitized patients, it may cause transient dermatitis
(‘swimmers itch’), and occasionally pulmonary lesions and pneumonitis.
111
Evidence that chronic infection predisposes to cancer
S. haematobium – bladder cancer
| S. mansoni – colorectal cancer??
