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Intestinal Parasites Flashcards

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USMLE® Step 1 flashcards Biology 101 flashcards
1
Q

Protozoa

A

single celled animals – eukaryotes
2-100nm in length
Many species free-living, some are important parasites of humans.

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2
Q

Classification of Protozoa

A

Classified according to their means of locomotion

Amoebae, Flagellates, Cilliates, Sporozoa (coccidia)

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3
Q

Three species of particular importance

A

Cryptosporidium parvum / hominis
Entamoeba histolytica
Giardia intestinalis (aka lamblia/duodenalis)

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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)

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5
Q

Cryptosporidium

A

Domestic animals can be reservoirs

Organism arranges itself along microvilli of intestinal tract

Becomes intracellular – covered by host cell membrane

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6
Q

Cryptosporidium life cycle

A
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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.

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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.

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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.

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10
Q

Cryptosporidium organisms

A
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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.

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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

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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

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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
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15
Q

Cryptosporidium infection

A

no specific treatment

supportive treatment for symptoms that appear

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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.

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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.

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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.

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19
Q

Three main groups of Helminths important in humans

A

Tapeworms (Cestoda)

Flukes (Trematoda or Digenea)

Roundworms (Nematoda)

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20
Q

Flatworms or platyhelminths

A

Tapeworms or flukes

Flatworms have flattened bodies with muscular suckers and/or hooks for attachment to the host.

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21
Q

Roundworms

A

Roundworms have long cylindrical bodies and generally lack specialised attachment organs.

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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

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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.

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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

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25
Q

Why use a wet mount identification technique.

A

Protozoan trophozoites, cysts, oocysts, and helminth eggs and larvae may be seen and identified

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26
Q

Stained smears used in identification x5

A 
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
Q

Why is it important for microscopist to be able to measure objects in the microscopic field?

A

Size might be a major diagnostic feature, when morphology very similar,
eg Trematode eggs
using a calibrated measuring scale in the eyepiece

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28
Q

Testing faecal samples

A

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

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29
Q

Detection of Parasite Antigens

A

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.

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30
Q

Molecular methods of detection of parasite antigens

A

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

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31
Q

Pathogenic amoebae; Entamoeba histolytica

A

Obligate intracellular parasites

Invades intestinal mucosa (or occasionally blood, via the liver)

Trophozoites can feed on bacteria as well host tissue

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32
Q

Transmission of Entamoeba histolytica

A

Person-to-person spread, faecal oral route (eg contaminated water)

Both trophozoites and cysts can be passed in diarrhoea

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33
Q

Entamoeba histolytica symptoms

A

10% to 20% of people who are infected withE. histolyticabecome 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)

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34
Q

E. Histolytica life cycle

A
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35
Q

Entamoeba diagnosis using faecal samples

A

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.

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36
Q

Detecting E. histolyticatrophozoites

A

E. histolyticatrophozoites can also be identified in aspirates or biopsy samples obtained during colonoscopy or surgery.

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37
Q

Antigen detection

A

Antigen detection by EIA may be useful as an adjunct; can distinguish between pathogenic and nonpathogenic infections.

PCR for confirmation

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38
Q

E. Histolytica Stains

A
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39
Q

Giardia

A

the first intestinal parasite to be observed under a microscope -
Anton van Leeuwenhoek described it in 1681.

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40
Q

Giardia life cycle stages

A
  1. Flagellate binucleate trophozoite

2. Resistant four nucleate cyst

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41
Q

Giardia Lifecycle

A
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42
Q

Cysts

A

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.

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43
Q

trophozoites

A

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.

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44
Q

excystation

A

In the small intestine, excystation releases trophozoites (each cyst produces two trophozoites).

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45
Q

Encystation

A

occurs as the parasites transit toward the colon. The cyst is the stage found most commonly in nondiarrheal feces.

46
Q

Giardia symptoms

A

spectrum varies from asymptomatic carriage to severe diarrhoea and malabsorption.

47
Q

Acute giardiasis

A

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
Q

chronic giardiasis

A

symptoms recurrent and malabsorption and debilitation may occur.

49
Q

Giardia diagnosis

A

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
Q

Identifying cysts

A

Cysts typically seen in wet mount preparations, while trophozoites are seen in permanent mounts (i.e. trichrome).

51
Q

Identifying trophozoites

A

Samples of duodenal fluid or duodenal biopsy may demonstrate trophozoites.

52
Q

Soil transmitted helminths: Nematodes species

A

Ascaris lumbricoides
Strongyloides stercoralis (threadworm)
Trichuris trichiura (whipworm) and
Necator americanusandAncylostoma duodenale (hookworms)

53
Q

Tapeworms (cestodes) species

A

Taenia saginata

Taenia solium

54
Q

Fluke (trematode) species

A

Schistosoma sp

55
Q

Soil transmitted helminthiasis

A

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
Q

Soil transmitted helminthiasis main species

A

Ascaris lumbricoides
Strongyloides stercoralis (threadworm)
Trichuris trichiura (whipworm)
Necator americanusandAncylostoma duodenale (hookworms)

57
Q

Soil transmitted helminthiasis - Morbidity

A

Morbidity is directly related to worm burden

58
Q

Soil transmitted helminthiasis - short term symptoms

A

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
Q

Soil transmitted helminthiasis - complications

A

Complications that require surgical intervention (intestinal obstruction and rectal prolapse).

Worsening school performance – cognitive defects

60
Q

Concomitant infections

A

Concomitant infections with other parasite species are frequent

  • may have additional effects on nutritional status and organ pathology.
61
Q

Ascaris lumbricoides

A

Nematoda – roundworm

62
Q

The lifecycle of Ascaris

A

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
Q

Symptoms of Ascaris lumbricoides

A

Clinical ascariasis can include fever, wheezing, shortness of breath.
Heavy worm loads can cause malabsorption of nutrients, obstruction of ducts (bile, pancreatic)

64
Q

Diagnosis

A

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
Q

Trichuris trichiura - lifecycle

A
66
Q

unembryonated eggs

A

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
Q

Embryonated eggs

A

eggs become infective in 15 to 30 days.

After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvaethat mature and establish themselves as adults in the colon

68
Q

Adult worms

A

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
Q

Trichuris trichiura - diagnosis

A
70
Q

Strongyloides stercoralis lifecycle

A

TheStrongyloideslife 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
Q

Free-living cycle

A

The rhabditiform larvae passed in the stool can either become infective filariform larvae (direct development), or free-living adult males and femalesthat mate and produce eggsfrom which rhabditiform larvae hatchand eventually become infective filariform larvae.

The filariform larvae penetrate the human host skin to initiate the parasitic cycle

72
Q

Parasitic cycle

A

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
Q

rhabditiform larvae

A

The rhabditiform larvae can either be passed in the stoolor 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
Q

Autoimmunity

A

To date, occurrence of autoinfection in humans with helminthic infections is recognized only inStrongyloides stercoralisandCapillaria philippinensisinfections.

In the case ofStrongyloides, 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
Q

Migration of L3 larvae

A

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
Q

Strongyloides stercoralis acute infection symptoms

A

Infection withS stercoralisoften 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
Q

Symptoms as larvae migrate

A

As the larvae migrate through the lungs they can produce respiratory symptoms, such as a dry cough or wheeze.

78
Q

Symptoms associated adult worms

A

Once adult worms reach the small intestine - vague gastrointestinal symptoms such as diarrhoea, anorexia, and vomiting, and epigastric pain worsened by eating.

79
Q

Chronic strongyloidiasis

A

common – lifelong infections

80
Q

Strongyloides stercoralis; Diagnosis

A

Diagnosis rests on the microscopic identification of larvae (rhabditiform and occasionally filariform) in the stool or duodenal fluid.

81
Q

Hookworms Lifecycle

A
82
Q

Hatching of larvea

A

Eggs are passed in the stool, and under favorable conditions (moisture, warmth, shade), larvae hatch in 1 to 2 days.

83
Q

rhabditiform larvae

A

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
Q

infecting humans

A

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
Q

Adult worms

A

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.

SomeA. duodenalelarvae, following penetration of the host skin, can become dormant (in the intestine or muscle).

86
Q

Transmission

A

In addition, infection byA. duodenalemay probably also occur by the oral and transmammary route.N. americanus, however, requires a transpulmonary migration phase.

87
Q

Symptoms

A

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
Q

Diagnosis

A

The eggs ofAncylostomaandNecatorcannot be differentiated microscopically.
The eggs are thin-shelled, colourless and measure 60-75 µm by 35-40 µm.

89
Q

Tapeworm (cestodes) species

A

Taenia saginata
Taenia solium
T. asiatica.

Humans are the only definitive hosts for these three species.

90
Q

how tapeworm infection is acquired

A

Adult tapeworms are acquired by eating undercooked or raw meat containing larval stages.

91
Q

tapeworm infection

A

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
Q

Transmission of tapeworms

A

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. soliumandT. asiatica) become infected by ingesting vegetation contaminated with eggs or gravid proglottids.

93
Q

Lifecycle in animal intestine

A

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
Q

Lifecycle stage in human intestine

A

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 scolexand reside in the small intestine.

Length of adult worms is usually 5 m or less forT. saginata(however it may reach up to 25 m) and 2 to 7 m forT. solium.

95
Q

proglottids

A

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. saginataadults usually have 1,000 to 2,000 proglottids, whileT. soliumadults 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 andT. soliummay produce 50,000 eggs per proglottid respectively.

96
Q

Cysticercosis

A

Cysticercosis is a tissue infection caused by larval cysts of the tapeworm Taenia solium.

97
Q

How Cysticercosis is acquired

A

People infected by swallowing eggs found in the faeces of a person with an intestinal tapeworm.

98
Q

How eggs develop

A

Eggs develop into larval stages and form cysts in the brain, muscle or other tissue.

99
Q

complications

A

An important cause of adult onset seizures in several low income countries where sanitation is poor.

100
Q

Several species of fluke (trematodes) can mature in humans

A

Three main species

101
Q

Where fluke develop in humans

A

developing in the intestines, lungs, liver and blood vessels.

102
Q

the parasite in the environment

A

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
Q

eggs hatching

A

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
Q

Penetrating and migrating in humans

A

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
Q

maturing worms

A

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
Q

cause of symptoms of schistosomiasis

A

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
Q

repeat infections

A

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
Q

Common Symptoms

A

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
Q

Chronic schistosomiasis

A

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
Q

Schistosomiasis (or bilharzia) course of infection

A

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
Q

Evidence that chronic infection predisposes to cancer

A

S. haematobium – bladder cancer

S. mansoni – colorectal cancer??

medical microbiology (29 decks)

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