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Parasitology Lab > Lab 9 > Flashcards

Lab 9 Flashcards

Nematodes I

1
Q

protective covering of nematodes

A

external cuticle

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2
Q

alae

A

lateral thickenings of cuticle

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3
Q

what body systems are well developed in nematodes? (3)

A

muscular, nervous, digestive

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4
Q

nematode oral cavity is also known as a

A

buccal cavity

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5
Q

nematode buccal cavity is lined with:

A

cuticle

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6
Q

what muscular pumping organ is after the buccal cavity

A

esophagus

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7
Q

nematode gut is lined with:

A

columnar epithelial cells with microvilli

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8
Q

nematodes digest food in the ______ region

A

midgut

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9
Q

where is waste expelled from a nematode?

A

anus

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10
Q

Pseudocoel:

A

body cavity that is fluid filled that acts like a hydrostatic skeleton

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11
Q

nematodes excrete both ____ and ____ wastes

A

fluid and solid

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12
Q

nematodes excrete solids out of _____ and fluids out of _____

A

anus; excretory pore

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13
Q

most nematodes are monecious or dioecious?

A

dioecious

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14
Q

large part of body of female devoted to:

A

reproduction

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15
Q

what reproductive organs do females have?

A

1 or 2 ovaries; uterus; vulva

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16
Q

male reproductive organs are:

A

single testis; copulatory spicules; gubernaculum

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17
Q

what stage is typically infective?

A

J3

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18
Q

molting is also known as:

A

ecdysis

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19
Q

hypobiosis-

A

a developmental arrest in parasite cycle

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20
Q

when does hypobiosis end and development continue?

A

usually favorable

environmental conditions—conducive to parasite survival

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21
Q

what does a nematode live on while in hypobiosis?

A

food reserves

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22
Q 
pinworm characteristics
tail shape:
esophagous has prominent:
eggs:
life cycle:
A

pointed
posterior bulb
thin shelled with flattened side
direct

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23
Q

roundworm characteristics
___ prominent lips
lateral external ______ on cephalic end
eggs:

A

3
papillae
thick shelled with rough coating;very resistant

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24
Q

hookworm characteristics
body shape:
_____ esophagus
eggs:

A

long and slender
club
thin shelled

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25
Q

threadworm characteristics
size:
size of buccal cavity:
what kind of esophagus:

A

tiny
small
filariform (J3 and adult female) or rhabditiform (free living stages)

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26
Q 
trichurida characteristics
body shape:
size of buccal cavity:
what kind of esophagus:
eggs:
A

anterior more slender than posterior
reduced or absent
stichosome
polar plugs

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27
Q

Enterobius vermicularis
what kind of worm:
distribution:
niche:

A 
pinworm
world wide (very common in elementary schools and day care centers)
large intestine and rectum
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28
Q 
Enterobius vermicularis morphology
\_\_\_\_\_ alae
\_\_\_\_\_\_ esophagus
female tail:
male tail:
A

cephalic
bulbed
very pointy
blunt and curled

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29
Q

Enterobius vermicularis eggs
size:
shape:

A

50x25 micrometers

ovoid, thin shelled, flattened on 1 side

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30
Q 
Enterobius vermicularis life cycle
direct or indirect?
how does female lay eggs?
how long does it take for eggs to embryonate?
eggs are so light that....?
A
  • direct
  • female migrates out anus at night and lays eggs in perineal regions -expels all the eggs and then dies
  • eggs rapidly embryonate and develop to the infective J3 stage (wn 6 hrs)
  • they can become airborne
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31
Q

Enterobius vermicularis retroinfection is possible how?

A

J3 hatches on perineum and crawls right back into rectum and up to colon.

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32
Q

Enterobius vermicularis will rarely but sometimes do what?

A

J3 larvae crawl into vagina in female instead of anus - an aberrant infection
- most will die quickly

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33
Q

Enterobius vermicularis clinical symptoms:

A

-most pinworm infections are asymptomatic -some develop intense itching in perineal regions

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34
Q

Enterobius vermicularis diagnosis:

A

“scotch tape” test
tape applied to perineum first thing in morning (before going to bathroom or bathing) remove immediately and put on slide to see eggs under microscope. No fecal smears!

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35
Q

Ascaris lumbricoides
Aka:
distribution:
highest prevalence distribution:

A
  • human roundworm
  • worldwide
  • tropical, rural areas where sanitation is low or absent.
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36
Q

Ascaris lumbricoides

niche:

A

upper small intestine in human host.

-adults live in upper small intestine on predigested food and host cellular debris

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37
Q

Ascaris lumbricoides mechanism for staying in intestine:

A

-stay in place by continually moving against peristalsis

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38
Q

Ascaris lumbricoides
size:
female tail:
male tail:

A

huge; can be 30 cm long
straight
curled

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39
Q 
Ascaris lumbricoides eggs
size:
shell:
how resistant:
what will kill egg?
A
  • 45-75x35-50 micrometers
  • thick shelled and rough surface
  • -very resistant
  • -can survive for years in warm, moist soil
  • -can survive sub-arctic conditions
  • -resistant to most chemicals
  • -ubiquitous in regions where infections are common
  • heat will kill eggs
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40
Q

Ascaris lumbricoides
life cycle:
infective stage:

A

direct

J3 stage

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41
Q

Ascaris lumbricoides infection

  • embryonated egg containing ___ stage which immediately molts to the __ stage in the intestine before it hatches.
  • eggs shed in feces are not ________(eggs require ______ to embryonate)
  • J1 molts to J2 within the egg (will remain as J2 until egg is ingested)
  • J2 molts to J3 when egg is ingested and J3 hatches out in small intestine
A
  • J2
  • J3
  • embryonated
  • oxygen
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42
Q

Ascaris lumbricoides
-round worms have a migratory phase that goes from ___ to ____ to ____ and back to ____:
-___ penetrates gut wall to capillary to ____
-In ____, ___ migrates through tissue, feeds on _______ and grows
-J3 migrates to _____ via bloodstream
-in _____, ____ molts to ______, which breaks out of ______ and migrates up bronchi
to pharyngeal area and is swallowed
(lung migration stage may cause signs of ______)
-J4 molts to adult stage in _____ intestine
-adults mate
-female produces about _______ eggs per day

A

Ascaris lumbricoides
-round worms have a migratory phase that goes from gut to liver to lung and back to gut:
-J3 penetrates gut wall to capillary to liver
-In liver, J3 migrates through tissue, feeds on liver parenchyma and grows
-J3 migrates to lungs via bloodstream
-in Lungs J3 molts to J4, which breaks out of alveolus and migrates up bronchi
to pharyngeal area and is swallowed
(lung migration stage may cause signs of pneumonitis)
-J4 molts to adult stage in small intestine
-adults mate
-female produces about 200,000 eggs per day

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43
Q

Ascaris lumbricoides eggs require certain conditions to hatch:

A

37 degrees C, pH 7, low oxygen, high CO2

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44
Q

Ascaris lumbricoides host reaction
_______ Phase – causes most host response
-______ substances very antigenic
-_______ and ________ occur
-Intensity of host reaction related to:
-heavy infections = enlarged ____, and _________ in lung

A
  • Migratory
  • molting
  • eosinophilia and increased levels of IgE
  • the number of worms migrating at any one time
  • liver; pneumonitis
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45
Q

Ascaris lumbricoides intestinal phase
symptoms:
obstruction, and there are cases on record where what happened?

A
  • few

- worms migrated to stomach and were vomited up

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46
Q

Ascaris lumbricoides intestinal phase

heavy infection can cause what:

A
  • obstruction
  • perforate intestine and cause peritonitis
  • obstruct biliary tree causing a peritonitis
  • malabsorption
  • stunting
  • cholecystitis
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47
Q

Ascaris lumbricoides Dx:

A

eggs in feces

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48
Q

Ascaris lumbricoides

although rare, juveniles can enter placenta and migrate to fetus, causing:

A

neonatal ascariasis

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49
Q

Toxocara canis

host:

A

dogs and other canids

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50
Q

Toxocara canis life cycle is dependent on age and immune status of host

  • young puppy or adult never before infected:
  • adult, reinfected dog:
  • Adult reinfected female that becomes pregnant
  • puppies can also get J3’s via a _________ route
A
  • life cycle in dog like A. lumbricoides in man with migratory phase from gut to liver to lung and back to gut
  • parasite does not complete the lung migration. J3’s wander through body and eventually go into developmental arrest
  • the dormant J3’s become active and migrate to placenta and to the fetus. In the fetus, the J3’s complete the lung migration back to gut. Puppies can be born with T canis infections.
  • transmammary
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51
Q

Toxocara cati
host:
life cycle is similar to T. canis except:

A
  • cats

- there is no transplacental transmission

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52
Q
  • human infection with Toxocara cati or Toxocara canid can lead to:
  • what areas of human body are most seriously affected?
A
  • Visceral Larval Migrans, Ocular Larval Migrans

- CNS, liver, lungs, and eyes most seriously affected

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53
Q

what is human host response to T. cati and canid?

A

inflammatory and formation of eosinophilic granulomas

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54
Q

what age human is most affected by T. cati and canid?

how do they get it?

A
  • children

- get eggs from soil while they play

55
Q

whether you get VLM or OLM depends on your sensitization to T. canis and cati
Immunologically naive people get:
sensitized people get:

A
  • OLM

- VLM

56
Q

OLM
-severity will depend on:
-retinal granulomas that form around the larvae were initially mistaken in 40’s and
50’s for:

A

-number and location within eye
-aggressive malignant tumors- retinoblastomas
-

57
Q

VLM host inflammatory responses and granuloma formation in organs infected severity will depend upon:

A

specific organ and level of involvement.

58
Q

VLM and OLM Dx.:

A

immunological tests such as ELISA using J2 antigens

59
Q

Baylisascaris procyonis

  • host:
  • aka:
  • we now know that ____ are also definitive hosts
  • has predilection for _____ in humans
A
  • raccoons
  • raccoon roundworm
  • dogs
  • CNS
60
Q

Baylisascaris procyonis
egg strength:
what humans are most often affected?
Rx.:

A
  • very resistant
  • small children
  • none, usually fatal
61
Q

what 3 hookworms are we studying?

A 
Necator americanus (New World hookworm)
Ancylostoma duodenale(Old World hookworm)
Ancylostoma caninum (canine hookworm)
62
Q

Hookworms
distribution:
niche:

A
  • North America, South America, Africa, SE Asia, Pacific Islands, China, Europe, India, Caribbean
  • small intestine
63
Q 
Hookworms
-feed on \_\_\_\_\_ in host
-can cause:
-can affect \_\_\_\_\_\_\_\_ in children
--may contribute to\_\_\_\_\_\_\_\_\_\_\_\_\_ when pregnant women
are infected
A
  • intestinal mucosa and blood
  • anemia and iron deficiency
  • physical and mental development
  • low birth weight and fetal development
64
Q 
Hookworms adult morphology
-"hooked" \_\_\_\_\_\_ end
-\_\_\_\_\_ esophagus
-female size:
-female tail shape:
-male size:
(female has vulvar slit. male has copulatory bursa on posterior end)
A
  • anterior
  • club
  • 10-15 mm
  • pointed
  • 8-12 mm
65
Q

Hookworms eggs
size:
shell:
unembryonated in:

A
  • 70x40 micrometers
  • thin shelled
  • fresh feces
66
Q

Hookworms life cycle
-____ hatches from egg in soil and develops to ____, which penetrates host skin and enters bloodstream, migrates to ____, breaks out of _____ and is swallowed. Molts to ___ in small intestine, attaches to epithelium and starts going to town with eating and making eggs

A

Hookworms life cycle
-J1 hatches from egg in soil and develops to J3, which penetrates host skin and enters bloodstream, migrates to lungs, breaks out of alveoli and is swallowed. Molts to J4 then adult in small intestine, attaches to epithelium and starts going to town with eating and making eggs

67
Q

Hookworm eggs are passed embryonated/unembryonated?

A

unembryonated

68
Q
  • Hookworm J3 are ______ larvae that do not feed.
  • They “quest” by doing what?
  • live on ___________, so limited time to find and penetrate a host before they die
A
  • filariform
  • climbing onto grass blades
  • stored reserves
69
Q

Ancylostoma duodenale

-differs from Necator americanus in three ways:

A

1) Morphology
2) Transmission
3) Pathogenicity

70
Q

Anclyostoma duodenale’s buccal cavity has ______, whereas Necator has _______

A

cutting teeth; cutting plates

71
Q 
Anclyostoma duodenale in comparison to N. americanus
pathogenicity:
size:
blood loss:
egg production:
number of methods of transmission:
A
  • more pathogenic
  • bigger
  • more blood loss
  • more egg production (28,000 compared to 10,000)
  • several more than americanus
72
Q

A. duodenale can infect humans 4 different ways:

A

1) penetration of skin by J3 and
2) oral ingestion of J3 orally ingested larvaestay in GI tractundergo two molts to
adults – No tissue migration!
3) Transplacental J3’s can cross placenta
4) Transmammary J3’s migrate to mammary glands and pass through into breast milk “vertical transmission” to neonate.

73
Q

-Ancylostoma duodenale can under go _________: ability to undergo arrested development in host tissues (Necator americanus cannot do this)

A

Hypobiosis

74
Q

Ancylostoma duodenale hypobiosis
what stage does this and where?
when does this occur?

A
  • J3 in muscle

- time of year when parasite development in soil would not be favorable

75
Q

A. duodenale has ___ life span, N. americanus has ____ life span

A

1 year

5 year

76
Q

Anclyostoma duodenale pathology in gut:

A

-attach by “biting” a plug of mucosa
-ingest both tissue and blood from attachment lesion
-adults produce an anticoagulant to obtain blood at attachment site
when move to new site, old lesion will continue to bleed

77
Q

does hookworm immunity exist in humans?

A

no

78
Q

Anclyostoma duodenale clinical disease
-repeated infections can create a:
-this condition often called “________”
-migratory phase: may see ______ symptoms with heavy infections
-Intestinal Phase:
heavy infection can cause severe illness:

A
  • dermatitis that is very pruritic (itchy)
  • ground itch or dew itch; NOTE: This is not CLM!!!
  • pneumonia
  • can vary from asymptomatic to pain and discomfort
  • iron-deficiency–>anemia–>heart palpitations–>congestive heart problems
79
Q
  • Infantile ancylosomiasis can occur from _______ or ________ route
  • Infantile symptoms from this:
A
  • transplacental; transmammary

- severe anemia, blood in stool and failure to thrive

80
Q

Anclyostoma duodenale Dx:

A

eggs in feces

81
Q

Anclyostoma duodenale prevention:

A

1) sanitation
2) education
3) wear shoes

82
Q

when you are the wrong host for a hookworm, _____ can occur.

A

CLM (cutaneous larval migrans)

83
Q

What species’ cause CLM

A

Ancylostoma braziliense (most often)

  • Uncinaria stenocephala
  • Ancylostoma caninum
84
Q

What stage of hookworm that causes CLM infects humans?

A

Filariform J3 in soil

85
Q

“wrong host” hookworms (CLM) crawl around in epidermis and cause lesions called “_______”

A

creeping eruptions

86
Q 
Strongyloides stercoralis
distribution:
size:
host:
res. host:
infective stage:
niche:
A
  • worldwide
  • very small (3 mm)
  • dogs, cats, humans and other primates
  • dogs and primates
  • J3
  • small intestine
87
Q

Strongyloides stercoralis

has 2 adult stages in life cycle:

A

free living and parasitic

88
Q

Strongyloides stercoralis

-Parasitic females reproduce by:

A

-parthenogenesis

89
Q

Strongyloides stercoralis eggs

-embryonated eggs released into _______ by adult female, and hatch _____ stage during ______

A
  • gut lumen
  • J1
  • passage in gut lumen
90
Q

Strongyloides stercoralis

once J1 is in the soil, it will develop into one of 2 types of J3’s to go into one of which 2 cycles?

A

heterogonic or homogonic

91
Q

Strongyloides stercoralis heterogonic life cycle

-J1 in warm moist soil will undergo 4 molts to become adults of both sexes and continue the cycle.

A

no answer

92
Q

Strongyloides stercoralis homogonic life cycle

-if juvenile develops into ______, then it must enter homogonic life cycle and ________ within 3 days or die.

A
  • filariform J3

- penetrate the skin

93
Q

Strongyloides stercoralis parasitic phase
J3 travels in circulation to ______, where it penetrates into _____ and becomes J4, then gets swallowed to SI to become adult

A
  • lungs

- alveoli

94
Q

Strongyloides stercoralis modes of transmission: (4)

A

1) skin penetration by J3
2) Ingestion of J3 from contaminated soil or water (J3 can swim if get into water)
3) Autoinfection
4) Transmammary in pregnant/lactating women

95
Q

Strongyloides stercoralis autoinfection

How does this happen?

A
  • -J1retained in gut long enough to molt twice to J3 (think constipation)
  • -J3 burrow into colonic mucosa, enter bloodstream and go to lungs
  • -Break out of alveoli, up bronchi and swallowed
  • -in small intestine, females embed in epithelium and reproduce
96
Q

Strongyloides stercoralis hyperinfection

how does this occur and what are the consequences?

A
  • amplified autoinfection in compromised individuals
  • individuals who have been given levels of corticosteroids high enough to immumosuppress them.
  • this level of steroids actually speed up the molting process of the parasite
  • leads to disseminated infection with parasites in ectopic sites
97
Q

Strongyloides stercoralis pathology
adult damage in intestine:
if heavy infection:
immunity?

A
  • usually none, just some local inflammation
  • watery, mucosal diarrhea which varies in intensity
  • yes, in 6 weeks immunity develops and adults are expelled
98
Q

Stronglyoides stercoralis can cause “_____” if larvae migrate to skin

A

creeping eruption

99
Q 
Strongyloides fulleborni
distribution:
disease:
symptoms of disease:
treatment?
A
  • new guinea and africa
  • swollen belly syndrome in children
  • diarrhea, abdominal distention, malabsorption, effect on mental and physical development
  • yes, it is reversible with treatment
100
Q

Strongyloides fulleborni Dx.:

A

eggs in stool

101
Q

Strongyloides stercoralis Dx.:

A

rhabditiform J2 in stool

102
Q

Strongyloides fulleborni Dx.
if a stool sample has been allowed to remain at room temp for 24 hrs or more, then
the problem becomes the ability of distinguish between ____________ that may have hatched out (if the individual has hooks too) and Strongyloides larvae. This is based on two features:

A
  • hookworm larvae
  • length of buccal capsule (cavity) Strongyloides – short buccal capsule,
    hooks: long buccal capsule.
103
Q

Can differentiate a Strongyloides J3 from a hookworm J3 by the:

A

notched tail of the Strongyloides J3.

104
Q 
Trichuris trichiura
what kind of worm?
reservoir host:
infection more severe in what people?
severe infection effects:
infective stage:
A
  • whipworm
  • none
  • children; infection usually heavier than in adults
  • colitis and stunted growth both physical and mental
  • eggs with J3 picked up from soil
105
Q

Trichuris trichiura

which end is long and slender like a whip?

A

-anterior

106
Q

Trichuris trichiura
female size and tail shape:
male size and tail shape:
egg size and shape:

A
  • 35-50 mm/straight tail
  • 30-45 mm/curled tail and 1 spicule
  • 50x25 micrometers; bipolar plugs; thick shell; brown color
107
Q

Trichuris trichiura
infective stage:
life cycle:
number of eggs produced per day:

A
  • J3
  • direct
  • 3000-5000
108
Q

Trichuris trichiura life cycle
J3 hatches in _______, penetrates _______, molts twice and emerges back out into lumen to travel to ______ where it mates and then ______________, where it remains producing eggs till death (2 years). Eggs embryonate in _________.

A
  • small intestine
  • columnar epithelium
  • colon
  • embeds esophagus in columnar epithelium of transverse and descending colon
  • soil
109
Q

Trichuris trichiura pathology
adults feed on:
produce _____ that lets them invade colon epithelium

A
  • mucosal cell contents and blood

- proteins

110
Q

Trichuris trichiura

what can happen due to tenesmus?

A

prolapsed rectum

111
Q

Trichuris trichiura Dx:

A

eggs in feces characteristic “barrel shaped” eggs with polar plugs (plugs at each end)

112
Q 
Trichuris trichiura eggs are very resistant
resistant to chemical disinfectants
can survive hours in:
days in:
months in:
A
  • direct sun
  • sewage
  • warm, moist soil
113
Q

Trichuris trichiura usually affects children. heavy infection needed for disease. dysentery, chronic colitis are symptoms. with really heavy infections, children can have: (4)

A

clubbing of fingers and toes, weight loss, anemia, and extensive swelling of rectal mucosa leading to rectal prolapse

114
Q

Trichinella spiralis
world’s largest intracellular parasite
-adults live within ________
-larvae live within:

A
  • intestinal epithelium

- nurse cell complex

115
Q

Trichinella spiralis

humans are a “______” host unless eaten by a cannibal or carnivore

A

-dead end

116
Q

Trichinella spiralis

reservoir host:

A

domestic pigs

117
Q

Trichinella spiralis

infective stage:

A

J1 within nurse cell complex, also known as a newborn larvae

118
Q 
Trichinella spiralis adult morphology
anterior/posterior differences:
what kind of esophagus:
female size:
female tail shape:
male size:
male tail shape:
A
  • slightly more slender anterior than posterior
  • stichosome
  • 1.5-4 mm
  • straight tail
  • 1.5-2 mm
  • claspers (pseudobursa) on tail
119
Q

Trichinella spiralis has two phases to life cycle:

A

enteral and parenteral phase

120
Q

Trichinella spiralis enteral phase
Digestive enzymes liberate J1. J1 penetrates columnar epithelium in _________ at base of _______. It then molts ___________ over a ____ hour period.

A
  • upper 2/3 of small intestine
  • villi
  • 4 times in rapid succession
  • 30
121
Q

Trichinella spiralis parenteral phase
NBL are J__. They have a sharp structure called a ______ in their oral cavity that helps penetrate cells. J1 enter bloodstream and distribute into all cells. Most cell types that are invaded will _____, but skeletal muscle fibers will support the larvae.

A
  • 1
  • stylet
  • die
122
Q

Trichinella spiralis enteral phase
5 days post mating, females produce live offspring called _____, and will continue to produce them until _____ about _____ weeks later. Immunity expels the adult

A
  • newborn larvae
  • immunity develops
  • 2 or 3
123
Q

Trichinella spiralis parenteral phase
larvae in skeletal muscle cells induce a process called:
this can last for how long?

A
  • Nurse cell formation

- life of the host

124
Q

Trichinella spiralis

it will change a muscle cell from having contractile capability to functioning solely to:

A

-nourish and support parasite development

125
Q

What cellular changes take place in muscle cells infected with Trichinella spiralis? (5)

A
  1. the cell loses its contractile myofilaments, 2. nuclei enlarge and divide,
  2. smooth endoplasmic reticulum increases, 4. mitochondria degenerate and
  3. entire cell with J1 within, becomes encapsulated with collagen. (walled off)
126
Q

-Trichinella spiralis Nurse cell complex
It alters cell’s gene expression by arresting DNA replication at ___ stage.
-It stimulates _________ to form a _______ which encircles the nurse cell complex

A
  • 4N
  • angiogenesis
  • circulatory rete
127
Q

Trichinella spiralis J1 will undergo developmental arrest until it is liberated by gut enzymes of a new host. Many will only last a few months before:
but some will last a few:

A
  • dying and calcifying

- years

128
Q

Trichinella spiralis predilection sites for NBL
1st:
2nd:
3rd:

A

-striated muscles of eye, tongue, masticatory muscles
-diaphragm and intercostals muscles (muscles needed for breathing)
– heavy muscles of extremities

129
Q

Trichinella spiralis infection of muscle will initiate progressive inflammation, leading to:

A

myositis and edema

130
Q

Trichinella spiralis symptoms
Enteral phase:
Parenteral phase:
Heavy infections in diaphragm:

A
  • gastroenteritis, diarrhea
  • muscle pain and eosinophilia
  • difficulty breathing (dyspnea) and possibly death
131
Q

Trichinella spiralis 2 distinct cycles
_______ cycle- in pigs rats and humans
_______ cycle- wild animals
man is primarily infected by:

A
  • urban
  • sylvan
  • eating raw pork
132
Q

Trichinella spiralis Dx:

A

muscle biopsy and observation of nurse cell-parasite complex in muscle rising and falling cycles of eosinophilia should alert MD to consider Trichinella

133
Q

Trichinella spiralis prevention

A

thoroughly cook pork

134
Q

why should you cook bear meat extra good?

A

their cells resist ice crystal formation so freezing may not kill the parasite

Parasitology Lab (10 decks)

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