Parasites 2 Flashcards

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1
Q

Nematodes

General Aspects

A
• Roundworms
– Enormously prevalent and successful phylum, exceeded only by arthropods in diversity
– 138 species infect humans
– True gut cavity, cuticle
• Enormously prevalent diseases
– billions and billions served…
– high morbidity, modest mortality
– associated with and contribute to poverty, malnutrition, underdevelopment
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2
Q

Nematodes

A
The Major GI Nematodes
– Enterobious vermicularis (pinworm)
– Tricuris triciuria (whipworm)
– Ascaris lumbricoides
– Hookworms
– Strongyloides stercoralis
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3
Q
Enterobius vermicularis (pinworm) 
Epidemiology
A
Enormously widespread.
– 200 million infections worldwide
– Temperate parts of the world
• Primarily a parasite of young children
– Adults in households with infected kids
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4
Q
Enterobius vermicularis (pinworm)
Life Cycle & Transmission
A
• Ova laid on the perianal
skin by females
• Become infective in 4-6h
• May remain infective in cool, moist conditions for up to a week
• Infective by ingestion or inhalation
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5
Q
Enterobius vermicularis (pinworm) 
Diagnosis and Therapy
A

• A cellophane tape prep of the perianal skin may be used to
detect the eggs or adults
• The eggs are elongate and
flattened on one side, 50-60 um long by 20-40 um wide.
• Adult females are 8-13 mm long and may be detected visually,
particularly during the night and early morning
• Treated with mebendazole,
albendazole, or pyrantal pamoate

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6
Q
Trichuris trichiura (whipworm)
Epidemiology
A

• Distribution is cosmopolitan in
warm, moist regions.
• The world prevalence is thought to be 350 million or more. In
parts of the SE US 20-25% of children may be infected.

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7
Q
Tricuris trichiura (whipworm)
Life Cycle and Transmission
A
• Eggs produced at a rate of
1,000 to 7,000 per female
per day
• Infective after about 21d in
soil
• Infection is via swallowing
infective eggs
• Following infection there is
an ~3 month prepatent period
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8
Q
Trichuris trichiura (whipworm)
Clinical Presentation
A
• Adults are 30-50 mm in
length and can live for up to 10 years
• Symptoms depend on the worm load
– Many infections asymptomatic
– Diarrhea with dysentery,
cramping, dehydration, weight loss, or anemia can occur in heavy infections.
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9
Q
Trichuris trichiura (whipworm)
Diagnosis and Therapy
A
• The eggs are barrelshaped
and brown, with thick shells, and
measure 50-55 um long by 22-24 um wide. At each end of the egg is a lucent mucoid plug
• Treated with mebendazole,
albendazole, or pyrantal pamoate
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10
Q

Ascaris lumbricoides

Epidemiology

A

• The largest and most prevalent of the intestinal nematodes
– Over 1 billion infected worldwide
– 20-60% of children infected in parts of SE US
– 90% in parts of Indonesia

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11
Q

Ascaris lumbricoides

Life Cycle & Transmission

A
• Eggs produced at a rate of upto 200,000 per female per day
– Develop in soil for ~3 weeks
before becoming infective
– Exceptionally resistant forms,
can embryonate successfully in
2% formalin or 50% nitric acid
• Can infect a host after 10 years
of storage.
• Have been found in windblown
dust and on circulating banknotes.
• Prepatent period is about 2
months.
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12
Q

Ascaris lumbricoides

Clinical Presentation – Larvae

A

• Pathology caused both by
larvae and adult worms.
• Migrating larvae can cause
granulomatous pneumonitis

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13
Q

Ascaris lumbricoides Clinical Presentation – Adult Worms

A
• adult females are 20-35 cm
long; males from 15-30
• adults live 12-20 months
– in large numbers can cause
bowel obstruction
– malnutrition and decreased
growth
• individuals can migrate
– especially during febrile
illnesses, anesthesia, or trauma
– biliary obstruction or cholangitis
– intestinal perforation/peritonitis
– out nose or mouth
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14
Q

Ascaris lumbricoides

Diagnosis & Therapy

A
• Detection of ova in stool
– fertile eggs are 55-75 um
long by 35-50 um wide, with
a thick transparent shell and
a ruffled outer layer. Unfertilized eggs are elongated and lack the thick shell of the fertilized egg.
• Treated with mebendazole,
albendazole, or pyrantal pamoate
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15
Q

The Hookworms - Epidemiology

A
• Two major species
– Necator americanus worldwide,
– Ancylostoma duodenale Africa, China, Japan, India
• Nearly 1 billion infected worldwide
• Most pathology produced in children
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16
Q

Hookworms

Life Cycle & Transmission

A

• Eggs produced at a rate of about 9,000 eggs/female/day (Necator) or 25-30,000/day (Ancylostoma)
– hatch in the soil, infective larvae
develop in about a week
• Larvae
– penetrate the skin, migrate to the lungs, and are swallowed
– mature within the intestine, attached to the mucosa
• The prepatent period is ~5 weeks

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17
Q

Hookworms

Clinical Presentation

A
• The adults have teeth or cutting
plates anteriorly to anchor themselves to the mucosa
– Necator adults are 7-11 mm long,
while Ancylostoma are 8-13 mm long
– Live for 1-2 years, but occasionally as
long as 10.
• Pathogenesis related to worm burden
– a major cause of iron-deficiency
anemia worldwide
– liver function abnormalities;
hypoproteinemia, hepatosplenomegaly
– developmental delay and malnutrition
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18
Q

Hookworms

Dignosis and Therapy

A

• Detection of ova in stool
– eggs of species are indistinguishable
– range from 55-75 um long by 36-40 um wide
– Lucent shell with early embryo inside
– Usually in the 4-16-cell stage when shed
• Treated with mebendazole,
albendazole, or pyrantal pamoate

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19
Q

Strongyloides stercoralis

Epidemiology

A

• Widely distributed in the tropics and subtropics, as well as into moist temperate regions
• Maintenance in an area requires
continuously moist soil
• 10-20% prevalence in areas of Africa, S. America, and Asia, but usually <1%

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20
Q

Strongyloides stercoralis

Life Cycle & Transmission

A

• Several dozen eggs produced per female per day.
– Hatch, first larval stage passed in the feces
• Larvae in the soil
– become mature infectious larvae…
– …or undergo sexual differentiation and mate
• may also mature and become
infectious within the gut and
autoinfect
• Penetrate skin, migrate to the lungs, up the trachea, and are swallowed to mature in the small intestine.

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21
Q

Strongyloides stercoralis

Clinical Presentation 1 – Normal Host

A

• The adults are 2-2.5 mm long and live within the intestinal
mucosa. Because of autoinfection, infections can last for decades
• Initial infection can cause ground itch & pneumonitis
• Chronic eosinophilia

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22
Q

Strongyloides stercoralis
Clinical Presentation 2 –
Immunocompromised

A

• Autoinfection with progressive
increase in worm burden
– presents as pneumonia or as
massive diarrhea.
– invade any organ of the body, and dispose to gramnegative
sepsis, meningitis, and other infections.

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23
Q

Strongyloides stercoralis

Diagnosis

A

• The first-stage larvae (in
the stool) are .18 to .38 mm long
• In latent infections few larvae may be present and multiple specimens required
• Serology is helpful in O&P negative cases, but does not reflect disease activity.
• Treat with thiabendazole,
ivermectin or albendazole

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24
Q

Strongyloides vs. Hookworm

Larvae

A

• Hookworm
– Long buccal canal
– No genital primordium

• Strongyloides
– Short buccal canal
– Prominent genital primordium

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25
Q

Trematodes and Cestodes

A
• Trematodes
– General aspects
– Schistosomes
– Other flukes
• Cestodes
– Taenia infections
– Diphyllobothrium latum
– Other tapeworms
• 173 species isolated from humans
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26
Q

Trematodes – General

A

• Flatworms without a true gut
• All have a snail in the life cycle
somewhere
• “Some molluscs (not many) can have children merely by sitting around and thinking about it…
others are like us, dioecious, possessed of only one sexual nature but thankful for small favors.”
-James Thurber, Is Sex Necessary?

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27
Q

The Schistosomes

Epidemiology – S. mansoni

A
• Schistosoma mansoni
– Africa, the Middle East, South
America, and the Caribbean
– Roughly 83 million cases
– Some animal reservoirs
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28
Q

The Schistosomes Epidemiology – S. japonicum/mekongi

A
• Schistosoma japonicum
and mekongi
– Found in Southeast Asia,
China, and the Philippines
– Roughly 1.5 million cases of
S. japonicum, 900,000 S.
mekongi
– Many animal reservoirs; cattle, horses, pigs, dogs, cats, rodents, and deer
29
Q

The Schistosomes

Epidemiology – S. hematobium

A

• Schistosoma haematobium
– Large areas of Africa and the Middle East
– Roughly 114 million human cases

30
Q

The Schistosomes

Life Cycle and Transmission

A
• Direct contact with water
harboring infected snails
– Infective cerceriae penetrate
skin
– migrate to venules
• Gi tract (mansoni, japonicum, mekongi)
• bladder and ureters (hematobium)
• larvae mature in venues
31
Q

The Schistosomes

Life Cycle and Transmission (cont.)

A
• Adults reside in the bloodstream of the
patient
– relatively little morbidity
– ova laid, most pass out
in stool or urine
• Prepatent period is 5-8
weeks
• Ova hatch in water and
infect snail vector
32
Q

The Schistosomes

Clinical presentation – acute syndromes

A
• Swimmer’s itch
• Systemic disease 4-8 weeks after exposure
– fever, malaise, aches
– lymphadenopathy and
hepatomegaly
– abdominal pain & diarrhea
– eosinophilia
– specific syndromes related to ectopic worms
33
Q

S. mansoni/japonicum

Clinical Presentation – chronic

A
• Disease related to the ova
• Each female releases ~300
(S. mansoni) or 3000 (S.
japonicum) eggs/day
– some migrate through the
intestinal mucosa to be excreted in the feces
– others swept up in portal
blood and carried to liver
– induce a granulomatous
periportal response
34
Q

S. mansoni/japonicum

Clinical Presentation – chronic

A
– heavily infected individuals --
periportal fibrosis (Symmer's
fibrosis)
– synthetic and detoxification
function is initially wellpreserved
• portal hypertension
• variceal bleeding
• hypersplenism
• hepatic failure
• cor pulmonale, glomerulonephritis from immune complex shunting
35
Q

S. hematobium

Clinical Presentation – chronic

A
•  Initially
– hematuria and dysuria
– an intense inflammatory
response around entrapped eggs
– urinary obstruction
– bladder or ureters -- mass lesion and ulceration are seen
36
Q

S. hematobium

Clinical Presentation – chronic

A
• Later manifestations
– host response changes
• fibrosis increased, less
inflammation
– fibrotic lesions may calcify
– relatively few patients go on to
chronic obstruction and renal
failure.
– eggs passing into the
pulmonary circulation may
induce pulmonary hypertension
– increase in Salmonella UTIs
and prolonged carriage
– squamous cell carcinoma of the
bladder
37
Q

The Schistosomes

Morphologic Diagnosis

A
• Ova identified from stool or
urine
• S. mansoni
– 118-180 um
– Prominent lateral spine

• S. hematobium
– 112-170 um
– Terminal spine

• S. japonicum
– Smaller (70-100 um) and
rounder than the others
– Small or absent lateral spine

38
Q

The Schistosomes

Diagnosis/Therapy

A

• In chronic disease, particularly with severe fibrosis, excretion of eggs may decline or stop
– Rectal/ bladder biopsy in these patients.
• Serology useful (90% sensitivity) where eggs cannot be found
– positive in both active and cured infections
• Treat with praziquantel

39
Q

Clonorchis and Opisthorchis

Epidemiology

A
• Prevalent in Japan, Korea,
China, Taiwan, and Vietnam
• Clonorchis sinensis infects
more than 7 million people.
• Related flukes of the Opisthorchis group are
clinically similar
– affect persons in Siberia as
well as the Far East 
– 10 million affected
40
Q

Clonorchis and Opisthorchis

Life Cycle & Transmission

A
• Adults reside in the biliary tree
and shed eggs
– Eggs must be ingested by a
freshwater snail
– Cercariae released by the
snail penetrate fish and encyst
– Fish eaten uncooked, larvae
released in duodenum
– Migrate into the bile ducts,
where they mature in about a
month
• Dogs, rats, pigs, and cats
serve as reservoir hosts.
41
Q

Clonorchis and Opisthorchis

Clinical Presentation

A
• Light infections usually
asymptomatic
• 500+ flukes can cause fever,
chills, jaundice, and eosinophilia
• Biliary fibrosis and recurrent
suppurative cholangitis
– obstruction by dead flukes
– increased Salmonella typhi
carriage with gallstones
– long-standing infections --
cholangiocarcinoma.
• Acute pancreatitis
42
Q

Clonorchis and Opisthorchis

Diagnosis and Therapy

A
• Adult flukes produce up to
4000 eggs per day
• Detect ova in stool
– The prepatent period is
about 1 month
– The ova are 26-30 um
long by 15-17 um wide.
There is a wide, prominent operculum
• Treat with praziquantel
43
Q

Fasciola hepatica

A

• Worldwide, nearly anywhere sheep are raised
– 2.4 million infected
• Adult worms dwell in the bile ducts, live up to 11 years
• Acquired by eating larvae with edible water plants
• Chronic biliary fibrosis and obstruction
• Late invasion of liver parenchyma and ectopic
migration

44
Q

Fasciolopsis buski

A

• Found in China, Thailand, and elsewhere in the Far East
• A disease of pigs with humans serving as a less important reservoir.
• Acquired by eating any of a number of water plants
(including the water chestnut)
• It probably infects over 210,000 persons
• Adult worms dwell in the small intestine, attached to the
mucosa
– usually asymptomatic unless very heavy (500 flukes).
– Diarrhea with excess mucous, abdominal pain, hemorrhage, and
obstruction

45
Q

Fasciola & Fasciolopsis

A
• Hermaphrodite worms
• Morphologically similar
ova
• 130-159 um long
• Small operculum, may pop open when cover slip pressed
46
Q

Paragonimus spp.

A
• The lung fluke
– Several species in various parts
of the world
– Far East, the East Indies, Pacific
islands, western Africa, Latin
America
• Acquired from poorly cooked
shellfish
• Adults encysted in the lungs
• Chronic bronchitis and sputum
production with hemoptysis
– Radiographically, diffuse
infiltrates replaced by nodules
which may cavitate
• Ectopic adults
47
Q

Paragonimus spp.

Diagnosis

A
• adult flukes overall resemble
coffee beans, may live 10-20 years
• Eggs found in feces or sputum
– Prominent operculum
– 68-118 um long
48
Q

Cestodes – General

A
• Tapeworms
• GI worms with segmented bodies
• Tissue cysts in intermediate hosts
• "Peckish is not the word. I felt like a homeless tapeworm"
-P.G. Wodehouse
49
Q

Diphyllobothrium latum

Epidemiology

A

• The fish tapeworm
• Most common in areas with cold freshwater lakes
– Scandinavia, northern Europe, Russia, northern Japan, and northern North America
• 9 million cases worldwide

50
Q

Diphyllobothrium latum

Life Cycle & Transmission

A
• Adult worms can be more
than 10m
– live for up to 20 years
– may release up to a million
eggs per day
• Egg hatches and infects
freshwater crustacean
– Crustacean eaten by a fish.
• Tapeworm acquired by
eating undercooked fish
51
Q

Diphyllobothrium latum

Clinical Presentation

A
• Like most tapeworm
infections, symptoms usually
slight
– Rarely, more severe pain
– diarrhea or constipation
– vomiting, and weight loss.
• Tapeworm pernicious anemia,
mostly in Finland
– The worm successfully
competes for B12 with the
host, absorbing 80-100% of a
labeled dose
– Attachment to proximal
jejunum
52
Q

Diphyllobothrium latum

Diagnosis

A

• Eggs are 60-75 um in length and 40-50 um wide
– Operculum, sometimes
difficult to visualize
– Small knob on the abopercular end, may or may not be evident;
sometimes only a roughening or
thickening of the egg wall

53
Q

Taenia species Epidemiology

A

• Beef tapeworm – T. saginata
– sub-Saharan Africa, the Balkans and Middle East, Latin America, and Russia
– 77 million infected
• Pork tapeworm – T. solium
– Latin America (especially Mexico), Africa, southeast Asia, and eastern Europe
– 10 million infected

54
Q

Taenia species

Life cycle/transmission

A
• Adults live in human GI tract
– eggs passed in the stool of
patients eaten by cattle or pig
– eggs hatch, and larva migrates
to muscle and encysts
• Encysted form -- cysticercus
– human ingests cysticercus in
undercooked meat
– larva is activated in response
to bile salts
– prepatent 2-12 weeks
55
Q

Taenia species

Clinical Presentation

A
• Most patients have few
symptoms
– mild abdominal pain, nausea
– mild hunger sensations and
loss of appetite is also common.
– syndrome of dizziness,
abdominal pain, headache,
hyperesthesia, and rarely delirium thought to be a toxic reaction in heavy infections.
• The adult worm may live for
up to 25 years and is typically 5-10m long.
56
Q

Taenia species

Clinical Presentation

A

• Proglottids: often the presenting symptom of tapeworm infection
– typically pass intact out the anus and crawl actively about

  • T. solium: 7-13 uterine branches
  • T. saginata: 15-30 branches
57
Q

Taenia species

Diagnosis and Therapy

A

• Detection of proglottids
• Detection of ova in stool or Scotch tape prep
– 30-45 um in diameter
• Recovery of scolex provides proof of cure
• Treat with praziquantel

58
Q

Taenia solium

Cysticercosis – transmission

A
• Ova (from an infected human) ingested
– fecal-oral route
– reverse peristalsis & autoinfection
– larvae migrate to tissues
and encyst
• Endemic in rural Mexico, and elsewhere
59
Q

Taenia solium

Cysticercosis – pathology

A

• Cysticerci
– most in subcutaneous connective tissue, then eye, brain, muscles, heart, and liver
– 1-2 cm in diameter surrounded by a fibrous capsule of host origin.
– inflammatory response to
the live larva becomes severe when it dies or is killed.

60
Q

Taenia solium

Cysticercosis – clinical presentation

A
Seizures: the most common
cause of adult-onset seizures
in endemic areas.
• Obstructive hydrocephalus
• Meningoencephalitis
– massive infestations
– patients inadvertently treated
in the course of therapy for
other parasitic infestations
• Ocular disease
61
Q

Taenia solium

Cysticercosis – diagnosis and therapy

A
• Diagnosis requires a high
degree of suspicion
– nodules on head imaging,
or in soft tissues.
• Serology helpful -- new
CDC immunoblot test
• Treat with albendazole/
praziquantel +/- steroids
– Don’t treat asymptomatic
calcified nodules
– supportive and symptomatic care
62
Q

Echinococcosis/Hydatid disease

Epidemiology

A

• Humans incidental participants in the canine/herbivore life cycle of E. granulosus or E. multilocularis
• E. granulosus – 2.7 million infected
– places where sheep and cattle are tended with the
help of dogs
– Middle East, Australia, New Zealand, east and south Africa, South America, and central Europe
• E. multilocularis
– a rare infection, mainly of northern temperate zones.

63
Q

Echinococcosis/Hydatid disease

Life Cycle & Transmission

A

• Usually acquired by ingestion of infective eggs from the feces
of dogs which carry the adult worm
• Larval stage typically develops within the liver or lung, though it may be found
anywhere

64
Q

Echinococcosis/Hydatid disease

Clinical Presentation

A

• The E. granulosus hydatid forms a slowly growing cyst containing numerous larval forms
– liver & lung 80%
– other assorted organs
• E. multilocularis forms an
invasive, infiltrating growth in the liver which may be mistaken for a malignancy

65
Q

Echinococcosis/Hydatid disease

Diagnosis & Therapy

A
• Typically radiographic for
E. granulosus
– serology may be helpful if
positive
• Clinical manifestations vary
depending on the site of
the cyst and upon whether
it ruptures
– anaphylaxis to ruptured cyst
contents
• Therapy -- albendazole +
drainage
66
Q

Hymenolepis nana

A
• The dwarf tapeworm
– the most common both
worldwide and in the US
– spread by the direct fecal-oral route or by internal autoinfection
• Usually asymptomatic
– cramping and diarrhea
observed
– Rarely, dizziness and seizures in children attributed to a neurotoxin
67
Q

Hymenolepis nana

A
• Adults 15-40 mm long
• Diagnosis
– Ova in stool
– 40-60 x 30-40 um
– Oval with polar filaments
68
Q

Hymenolepis diminuta

A
• The rat tapeworm
• Rare in humans
– Acquired by ingesting
infected insects
– Mostly asymptomatic
• Ova
– 70 - 86 um X 60 - 80 um
– Striated outer wall, could be confused with Taenia but is larger, with a space between embryo and striations