[DISCUSSION] MODULE 3 UNIT 2 AND UNIT 3 Flashcards

1
Q

 The phylum Nematoda is divided into classes based on the presence or absence of “(?)’, which are caudal chemoreceptors.

A

phasmids

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2
Q

 The two (2) classes were earlier called Aphasmidia and Phasmidia, but now have been renamed as (?), respectively.

A

Adenophorea and Secernentea

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3
Q

 The origin of the name (Gr. trichos = hair + oura = the tail), is not quite correct because it is the (?) of the worm that is hair-like and not the tail.

A

anterior end

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4
Q

 Whipworm

A

A. Trichuris trichiura

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5
Q

Infection is caused by ingestion of embryonated eggs.

A

A. Trichuris trichiura

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6
Q

 Eggs – hatch in the small intestine.

A

A. Trichuris trichiura

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7
Q

 larvae (L1) – released and penetrate the intestinal villi and undergo 4 molts in 3-10 days.

A

A. Trichuris trichiura

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8
Q

 young adult – passively migrate to the cecum (also in the ascending colon) and mature in about 2-3 months

A

A. Trichuris trichiura

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9
Q

 usually asymptomatic, except in heavy infection

A

Trichuriasis

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10
Q

 Heavily infected individuals - those with a high worm burden (greater than 200 worms, >5,000 EPG)- are most likely to
develop clinical disease.

A

Trichuriasis

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11
Q

 hypochromic, microcytic type

A

Iron-deficiency anemia

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12
Q

 results from chronic blood loss at the attachment site coupled with the long life span of the worms

A

Iron-deficiency anemia

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13
Q

 Small amounts of blood (0.005 ml per worm) are lost each day at the ulceration in the intestinal mucosa

A

Iron-deficiency anemia

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14
Q

 worm may be found even up to the rectum in heavy infection

A

Rectal prolapse

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15
Q

 mucosa of the rectum protrudes through the anal opening associated with the loss of muscle tone of the anus

A

Rectal prolapse

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16
Q

 Children with severe trichuriasis have:
o growth retardation
o impaired mental development
o cognitive function

A

Sever Trichuriasis

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17
Q

 Pudoc worm

A

B. Capillaria philippinensis

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18
Q

 In 1967, an epidemic of Capillariasis took place in
Pudoc West, Tagudin, Ilocos Sur

A

B. Capillaria philippinensis

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19
Q

Infection is caused by ingestion of larvae in raw or
undercooked infected fish

A

B. Capillaria philippinensis

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20
Q

 larvae - develop into adults in the small intestine
(jejenum) where they burrow into the mucosa

A

B. Capillaria philippinensis

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21
Q

 Female worms - may produce two types of eggs:
o Unembryonated shelled eggs –
passed in the feces
o Embryonated eggs – hatches
within human host

A

B. Capillaria philippinensis

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22
Q

 larvae - will re-invade and cause autoinfection.

A

B. Capillaria philippinensis

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23
Q

 unembryonated eggs - ingested by fish when
passed into water.

A

B. Capillaria philippinensis

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24
Q

 malabsorption syndrome with severe diarrhea

A

Intestinal capillariasis

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25
Q

 borborygmi (gurgling stomach)

A

Intestinal capillariasis

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26
Q

 abdominal pain (can become serious if not treated
because of autoinfection)

A

Intestinal capillariasis

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27
Q

 Capillary liver worm

A

C. Capillaria hepatica

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28
Q

 The nematode (roundworm) Capillaria hepatica (=Calodium
hepaticum) causes hepatic capillariasis in humans.

A

C. Capillaria hepatica

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29
Q

 Nomenclature varies in use globally and by discipline; Capillaria
hepatica is most frequently used in medical literature.

A

C. Capillaria hepatica

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30
Q

 zoonotic parasite with a low host specificity
o primarily exists in rodent and carnivore hosts
o Both true and spurious infections occur in
humans

A

C. Capillaria hepatica

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31
Q

Infection is caused by ingestion of embryonated eggs in fecally-
contaminated food, water, or soil

A

C. Capillaria hepatica

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32
Q

 Adult worms - are located deep within the liver parenchyma of
the host, and lay hundreds of eggs in the surrounding
parenchymal tissue.

A

C. Capillaria hepatica

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33
Q

 eggs - trapped in the parenchyma; can not be passed in the feces
of the host, and remain in the liver until the animal dies, or more
likely, is eaten by a predator or scavenger

A

C. Capillaria hepatica

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34
Q

o Eggs ingested by scavengers are
unembryonated (not infectious) and are passed
in through the digestive tract into and out in
feces, providing an efficient mechanism to
release eggs back into the environment

A

C. Capillaria hepatica

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35
Q

o Eggs embryonate in the environment, where
they require air and damp soil to become
infective.

A

C. Capillaria hepatica

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36
Q

 Under natural conditions, embryonation is slow and may take
between 6 weeks and 5 months.

A

C. Capillaria hepatica

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37
Q

 The cycle continues when embryonated eggs are eaten by a
suitable mammalian host.

A

C. Capillaria hepatica

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38
Q

 Infective eggs hatch in the intestine, releasing first stage larvae.

A

C. Capillaria hepatica

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39
Q

 The larvae penetrate the intestinal wall and migrate via the portal
vein to the liver parenchyma within 3-4 days.

A

C. Capillaria hepatica

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40
Q

 Larvae take about 3-4 weeks to mature into adults and mate.

A

C. Capillaria hepatica

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41
Q

 rare in humans

A

Hepatic capillariasis

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42
Q

 typically manifests as an acute or subacute hepatitis with:
o peripheral leukocytosis and eosinophili
o hepatomegaly
o persistent fever (which may be as high as 40°C)

A

Hepatic capillariasis

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43
Q

 Trichina worm

A

D. Trichinella spiralis

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44
Q

 The name Trichinella is derived from the minute size of the adult (Gr. trichos =hair, ella suffix for diminutive) and spiralis refers to the spirally coiled
appearance of larvae in muscles.

A

D. Trichinella spiralis

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45
Q

Infection is caused by ingestion of raw/rare or undercooked meat containing encysted larvae

A

D. Trichinella spiralis

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46
Q

 Adult worms and encysted larvae develop within:
o 1 vertebrate host
o definitive host and potential intermediate host : infected animal
o A second host is required to perpetuate the life cycle of Trichinella.

A

D. Trichinella spiralis

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47
Q

 domestic cycle
o pigs
o anthropophilic rodents
o other domestic animals
 horses

A

D. Trichinella spiralis

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48
Q

 sylvatic cycle
o bear
o moose
o wild boar

A

D. Trichinella spiralis

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49
Q

 After exposure to gastric acid and pepsin, the larvae are released from the cysts (excystation) invade the small bowel mucosa, molt four times and
rapidly develop into adults, either male or female, by the 2nd day of infection.

A

D. Trichinella spiralis

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50
Q

 Within 5 days, they become sexually mature

A

D. Trichinella spiralis

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51
Q

 The male dies after fertilizing the female.

A

D. Trichinella spiralis

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52
Q

 After 1 week of infection, the fertilized females release larvae.

A

D. Trichinella spiralis

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53
Q

 Larvae continue to be discharged during the remaining part of the lifespan of the female worm, which ranges from 4 weeks to 4 months.

A

D. Trichinella spiralis

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54
Q

 These larvae enter the intestinal lymphatics or mesenteric venules and are transported in circulation to different parts of the body.
o They get deposited in the muscles, central nervous system and other sites.

A

D. Trichinella spiralis

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55
Q

 The larvae die in most other situations, except in the skeletal muscles, where they grow.

A

D. Trichinella spiralis

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56
Q

 Within 20 days after entering the muscle cells, the larvae encyst within nurse cells.

A

D. Trichinella spiralis

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57
Q

 Encysted larvae lie parallel to the muscles of host and can survive for months to years and eventually calcify and die.

A

D. Trichinella spiralis

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58
Q

 In man, the life cycle ends here.
o Man is a dead-end host of the parasite, as the cysts in human muscles are unlikely to be eaten by another host.

A

D. Trichinella spiralis

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59
Q

 Trichinella spiralis has an unusual life cycle in that the same individual animal serves as both definitive and intermediate host, adults and larvae
located in different organs.

A

D. Trichinella spiralis

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60
Q

 autoheteroxenous parasite

A

D. Trichinella spiralis

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61
Q

Cysts develop preferentially in muscles relatively poor in glycogen and in hypoxic environment.
o Therefore, the biceps, deltoid, gastrocnemius, pectoralis, masseter, extraocular muscles, intercostal muscles and diaphragm, which
are constantly active, are the ones mostly affected.

A

D. Trichinella spiralis

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62
Q
  • gastrointestinal symptoms
     diarrhea
     abdominal pain
     vomiting
A

Intestinal phase

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63
Q

 high fever
 periorbital and facial edema
 conjunctivitis
 blurred vision
 myalgias
 splinter hemorrhages
 rashes
 peripheral eosinophilia lasting 1 month in heavy infection
Occasional life-threatening manifestations:
 myocarditis
 central nervous system involvement
 pneumonitis

A

Migration phase

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64
Q

 myalgia and weakness o followed by subsidence of symptoms

A

Larval encystment

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65
Q

 abdominal tenderness and pain
 weight loss
 weakness
 mucoid or bloody stool

A

A. Trichuris trichiura

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66
Q

 Cosmopolitan
 Tropical and subtropical countries with warm and moist soil.

A

A. Trichuris trichiura

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67
Q

Global
 604 to 795 million
o Children

A

A. Trichuris trichiura

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68
Q

Phlippines
 4.5 to 55.1%
o preschool children
 8.1 to 57.9%
o school-age children

A

A. Trichuris trichiura

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69
Q

 Natural host: Humans

A

A. Trichuris trichiura

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70
Q

 morphologically similar worms are found to infect:
o pigs
o dogs
o some monkeys

A

A. Trichuris trichiura

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71
Q

 At risk: ↑ children

A

A. Trichuris trichiura

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72
Q

 Area: poor sanitation practices are common
o open defecation
o night soil as fertilizer

A

A. Trichuris trichiura

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73
Q

 Mechanical vectors:
o House flies
o Cockroaches

A

A. Trichuris trichiura

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74
Q

Symptoms
 severe protein-losing enteropathy and hypoalbuminemia
 malabsorption of fats and sugars
 decreased excretion of xylose
 low serum potassium, sodium and calcium
 high levels of IgE
 Serious cases may be fatal in 2 weeks to 2 months.

A

B. Capillaria philippinensis

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75
Q

 Endemic
o Ilocos Norte, Ilocos Sur, Cagayan, La Union, Pangasinan, Zambales, Agusan del Norte, Leyte
o More:  Zamboanga del Norte
o Few:
 Zamboanga del Sur
 Agusan del Sur
 Misamis Occidental.

A

B. Capillaria philippinensis

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76
Q

 Twice as many males as females become infected.

A

B. Capillaria philippinensis

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77
Q

 Males are mostly fishermen who partake of the days catch.

A

B. Capillaria philippinensis

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78
Q

 Definitive host/Reservoir: Fish-eating birds
 Intermediate host
o fresh or brackish water fish

A

B. Capillaria philippinensis

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79
Q

 Migratory birds
o parasite is widely distributed throughout Asia and elsewhere

A

B. Capillaria philippinensis

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80
Q

 deposition of eggs in the liver parenchyma causes:
o granuloma formation and liver necrosis, which in heavy infections can lead to potentially fatal liver dysfunction

A

C. Capillaria hepatica

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81
Q

 Cosmopolitan in wildlife
o Human cases have originated from all inhabited continents except for Australia, although it exists in wildlife

A

C. Capillaria hepatica

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82
Q

 The prevalence in humans may be underestimated due to the nonspecific clinical presentation and difficulty of diagnosis

A

C. Capillaria hepatica

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83
Q

 Typical host: rodents such as rats
o has a low host specificity

A

C. Capillaria hepatica

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84
Q

 Infections have also been identified in:
o wild and domestic carnivores o humans

A

C. Capillaria hepatica

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85
Q

 contaminated food is ingested
 human feces are not the source of contamination
 feces of carnivores or flesh-eating rodents are involved

A

C. Capillaria hepatica

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86
Q

 Other symptoms vary depending on the location and number of larvae present

A

D. Trichinella spiralis

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87
Q

 Cosmopolitan
o most common in Europe and America
o rarely reported in the tropics

A

D. Trichinella spiralis

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88
Q

 It occurs particularly in members of the meat-eating population but the prevalence is low

A

D. Trichinella spiralis

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89
Q

 pig
 deer
 bear
 walrus
 rat

A

D. Trichinella spiralis

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90
Q

 ingestion of contaminated pork scraps by pigs

A

D. Trichinella spiralis

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91
Q

 ingestion of contaminated infected rats by pigs – ubiquitous in pig farms

A

D. Trichinella spiralis

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92
Q

 ingestion of contaminated meat by other animals

A

D. Trichinella spiralis

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93
Q

 ingestion of contaminated pork meat by humans
o Cooking meat to 60ºC or freezing (20 days in a normal freezer or at - 20°C for 3 days) will kill larvae.
o Smoking, salting or drying the meat does not destroy the infective larvae.

A

D. Trichinella spiralis

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94
Q

The Trichinella cycle that is maintained in nature occurs among cannibalistic and carrion-feeding carnivores

A

D. Trichinella spiralis

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95
Q

 Giant intestinal worm

A

A. Ascaris lumbricoides

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96
Q

Infection is caused by ingestion of embryonated eggs.

A

A. Ascaris lumbricoides

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97
Q

 Larvae invade the intestinal mucosa, and are carried via the portal, then systemic circulation on to the heart, then into the lungs

A

A. Ascaris lumbricoides

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98
Q

 The larvae break out of the capillaries into the alveoli.

A

A. Ascaris lumbricoides

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99
Q

 The larvae (L4s) mature further in the lungs (10-14 days), after a molt, penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed.

A

A. Ascaris lumbricoides

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100
Q

 Upon reaching the small intestine, they develop into adult worms.

A

A. Ascaris lumbricoides

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101
Q

 Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female.

A

A. Ascaris lumbricoides

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102
Q

 Adult worms can live 1 to 2 years.

A

A. Ascaris lumbricoides

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103
Q

 Unfertilized eggs may be ingested but are not infective.

A

A. Ascaris lumbricoides

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104
Q

 Larvae develop to infectivity within fertile eggs after 18 days to several weeks, depending on the environmental conditions (optimum: moist, warm, shaded soil).

A

A. Ascaris lumbricoides

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105
Q

Clinical manifestations of ascariasis are caused by the (?) of the:
o Larvae
o adult worms in the small intestine
o wandering adult worms

A

pulmonary migratory phase

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106
Q

The (?) causes allergic reaction.

A

larval migration

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107
Q

The initial exposure to larvae during the (?) is usually asymptomatic, except when the larval load is heavy.

A

lung migration phase

108
Q

 asthmatic respiration
 cough with bronchial rales
 chest pain

A

A. Ascaris lumbricoides

109
Q

These symptoms may be due to the petechial hemorrhages and massive destruction of the lung parenchyma as the larvae break through the capillaries on their way to the alveolar sacs, in massive infection, the hemorrhage may give rise to Ascaris pneumonitis.

A

A. Ascaris lumbricoides

110
Q

The pulmonary clinical features subside in 1 or 2 weeks after infection. Due to (?) in the blood stream, the larvae may lodge in vital organs such as the brain and spinal cord, the eyeball and the kidney.

A

larval migration

111
Q

Clinical manifestations due to adult worm vary from asymptomatic infection to severe and even fatal consequences.

A

A. Ascaris lumbricoides

112
Q

The (?), when present, are caused by spoliative action, toxic action, mechanical effects and wandering effects

A

pathological effects

113
Q

 The adult worms in the lumen of the small intestine feed on the liquid nutrient in the intestinal fluids.

A

A. Ascaris lumbricoides

114
Q

 The nutritional effects are usually seen when there is heavy worm burden.

A

A. Ascaris lumbricoides

115
Q

 The worms interfere with proper digestion and absorption of food.

A

A. Ascaris lumbricoides

116
Q

 Ascariasis may contribute to protein-energy malnutrition and vitamin A deficiency.

A

A. Ascaris lumbricoides

117
Q

The (?) are due to hypersensitivity to the worm antigens and may be manifested as fever, urticaria and edema.

A

toxic effects

118
Q

Ascariasis may cause complications due to (?). Masses of worms (Ascaris bolus) may cause intestinal obstruction.

A

mechanical effect

119
Q

(?) is a complication of ascariasis due to a few factors, e.g. fever, use of anesthesia during surgery, and worms seeking mates.

A

Ectopic migration

120
Q

 The worm may migrate up or down along the intestine.
o It may block the biliary or pancreatic ducts causing acute biliary obstruction or pancreatitis.

A

A. Ascaris lumbricoides

121
Q

 It may enter the liver parenchyma causing liver abscesses.

A

A. Ascaris lumbricoides

122
Q

 The worm may go up the esophagus and come out through the mouth, nose, or ears.
o It may obstruct the appendix causing appendicitis. It may lead to peritonitis when it perforates the intestine.

A

A. Ascaris lumbricoides

123
Q

 This tendency makes preoperative deworming necessary before gastrointestinal surgery in endemic areas. The wandering worm may also reach kidneys.

A

A. Ascaris lumbricoides

124
Q

 most common human helminthic infection

A

A. Ascaris lumbricoides

125
Q

 ↑ tropical and subtropical regions o embryonated eggs
 can survive in moist shaded soil for a few months to about 2 years in tropical and subtropical areas, but for much longer in temperate regions

A

A. Ascaris lumbricoides

126
Q

 inadequate sanitation

A

A. Ascaris lumbricoides

127
Q

 rare to absent in developed countries

A

A. Ascaris lumbricoides

128
Q

 sporadic cases may occur in rural, impoverished regions of those countries

A

A. Ascaris lumbricoides

129
Q

 Some cases in these areas where human transmission is negligible have direct epidemiologic associations to pig farms.

A

A. Ascaris lumbricoides

130
Q

Global
 billion
 ↑ children
 co-exists with Trichuris trichiura

A

A. Ascaris lumbricoides

131
Q

Phlippines
 80-90%
 Risk group: public elementary school children

A

A. Ascaris lumbricoides

132
Q

 Ascaris lumbricoides – humans

A

A. Ascaris lumbricoides

133
Q

 Ascaris suum – humans and pigs

A

A. Ascaris lumbricoides

134
Q

 Fecal-oral route
 ↑ children
 Night-soil
 House-flies and cockroaches

A

A. Ascaris lumbricoides

135
Q

 Resistance of Ascaris eggs to chemicals – lipid layer of their eggshell
o 2%
 Formalin
 potassium dichromate
o 50%
 Hydrochloric
 Nitric
 Acetic
 Sulfuric acid

A

A. Ascaris lumbricoides

136
Q

 Pinworm, seatworm
 Former name: Oxyuris vermicularis

A

B. Enterobius vermicularis

137
Q

Infection occurs from ingestion of infective eggs

A

B. Enterobius vermicularis

138
Q

 These eggs hatch in the small intestine, and the adults establish themselves in the colon, usually in the cecum

A

B. Enterobius vermicularis

139
Q

 The time interval from ingestion of infective eggs to oviposition by the adult females is about one month.

A

B. Enterobius vermicularis

140
Q

 At full maturity adult females measure 8-13 mm, and adult males 2-5 mm; the adult life span is about two months.

A

B. Enterobius vermicularis

141
Q

 Gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area.

A

B. Enterobius vermicularis

142
Q

 The larvae contained inside the eggs develop (the eggs become infective) in 4 to 6 hours under optimal conditions

A

B. Enterobius vermicularis

143
Q

? – infected individuals may reinfect themselves
 infective eggs are ingested via hand-to-mouth contamination due to scratching of perianal area with fingers → deposition of eggs under the nails.
o ↑ children

A

Autoinfection

144
Q

 eggs laid on the perianal skin immediately hatch into the infective stage larva and migrate through the anus → develop into worms in the cecum

A

Retroinfection

145
Q

 one-third are asymptomatic

A

Enterobiasis or oxyuriasis

146
Q

 worm produces intense itching of the perianal area (pruritus ani) and also the perineal area, when it crawls out of the anus to lay eggs
o scratching and irritation of the skin around the anus
o may give rise to secondary bacterial infection
o Children infected – insomnia due to the pruritus

A

Enterobiasis or oxyuriasis

147
Q

 poor appetite
 weight loss
 irritability
 nocturnal enuresis (involuntary urination)
 grinding of teeth
 abdominal pain

A

B. Enterobius vermicularis

148
Q

not associated with eosinophilia or with elevate lgE

A

B. Enterobius vermicularis

149
Q

In female patients
 worms may cause (?) when they crawl into the vulva and vagina causing irritation

A

ectopic migration

150
Q

 It may migrate up to the uterus and fallopian tubes

A

B. Enterobius vermicularis

151
Q

 This may cause symptoms of:
o Cervicitis o chronic salpingitis o peritonitis o recurrent urinary tract infections

A

B. Enterobius vermicularis

152
Q

 The worm is sometimes found in surgically removed appendix and has been claimed to be responsible for appendicitis.

A

B. Enterobius vermicularis

153
Q

 Cosmopolitan
o both temperate and tropical areas

A

B. Enterobius vermicularis

154
Q

Global
 ↑ temperate regions and urban areas
 Enterobiasis – most common helminth infection in the United States

A

B. Enterobius vermicularis

155
Q

Phlippines
 29% - schoolchildren from exclusive private schools
 56% - public schools
 16% - females
 9% - males

A

B. Enterobius vermicularis

156
Q

 Natural host: Humans

A

B. Enterobius vermicularis

157
Q

 Rare: airborne – inhaled and swallowed

A

B. Enterobius vermicularis

158
Q

 anus-to-mouth
o contaminated fingers or other objects in the mouth
o inhalation of dust containing Enterobius eggs

A

B. Enterobius vermicularis

159
Q

 cool moist conditions – eggs remains viable for about 2 weeks

A

B. Enterobius vermicularis

160
Q

 warm, dry conditions – eggs begin to lose their infectivity within 2 days

A

B. Enterobius vermicularis

161
Q

Factors:
 Overcrowding
 wearing soiled clothing
 lack of adequate bathing and poor personal hygiene
o especially among young school-aged children
 Finger sucking and nail biting
o may be sources of recurrent infection in children
 sexual activity o oral and anal sex
 extremely contagious and can easily spread among members of a family or in institutions o familial or a group disease

A

B. Enterobius vermicularis

162
Q

Two (2) species of hookworms are human parasites:
 Necator americanus - New world hookworm
 Ancylostoma duodenale - Old world hookworm

A

C. Hookworms

163
Q

Infection occurs from penetration of filariform larvae (L3) larvae

A

C. Hookworms

164
Q

 Infective stage are filariform larvae (L3) that penetrate the skin and are carried through the blood vessels to the heart and then to the lungs.
o penetrate into the pulmonary alveoli
o ascend the bronchial tree to the pharynx
o are swallowed o reach the jejunum of the small intestine
 reside and mature into adults

A

C. Hookworms

165
Q

 Adult worms live in the lumen of the small intestine, typically the distal jejunum, where they attach to the intestinal wall by means of well-developed mouth parts (cutting plates in N. americanus and teeth in A. duodenale)

A

C. Hookworms

166
Q

 Eggs are passed in the stool, and under favorable conditions

A

C. Hookworms

167
Q

 Larvae hatch in 1 to 2 days and become free-living in contaminated soil.
o These released rhabditiform (L1) 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

A

C. Hookworms

168
Q

Hookworm disease (?) manifests three main phases of pathogenesis

A

necatoriasis or ancylostomiasis

169
Q

 filariform larvae penetrate skin

A

the invasion or cutaneous period

170
Q

 do little damage to superficial layers, since they seem to slip unbroken skin through hair follicles, or pores

A

the invasion or cutaneous period

171
Q

 usual sites of infection:
o the dorsum of the feet or between the toe
o the hands, especially interdigital spaces

A

the invasion or cutaneous period

172
Q

 Once in the dermis, however, their attack on blood vessels initiates a tissue reaction.

A

the invasion or cutaneous period

173
Q

 If, as it usually happens, pyogenic bacteria are introduced into skin with the invading larva, a severe local itching known as ground itch, dew itch, or coolie itch will result

A

the invasion or cutaneous period

174
Q

 Erythematous papular rash develops when a large number of larvae penetrate the skin.
o This is a self-limiting condition, lasting for 2 to 4 weeks

A

the invasion or cutaneous period

175
Q

 larvae break out of the lung capillary bed into alveoli and progress up bronchi to the throat.

A

the migration or pulmonary phase

176
Q

 Each site hemorrhages slightly, with serious consequences in massive infections; however, very large numbers of larvae migrating through the lungs simultaneously are rare

A

the migration or pulmonary phase

177
Q

 The phase is usually asymptomatic, although there may be some dry coughing and sore throat.

A

the migration or pulmonary phase

178
Q

 A pneumonitis and Loeffler’s syndrome may occur in heavy larvae infection

A

the migration or pulmonary phase

179
Q

 Asymptomatic

A

the intestinal phase

180
Q

 Attachment of the worms to the mucosa with their strong buccal capsule and teeth or cutting plates may stimulate:
o Abdominal pain
o Nausea
o Anorexia

A

the intestinal phase

181
Q

 Adult worms suck blood aided by the anticoagulant that they secrete.

A

the intestinal phase

182
Q

 The worms change feeding sites and the old biting sites will continue to bleed.

A

the intestinal phase

183
Q

 Blood loss per worm is about 0.03 ml per day for N. americanus and about 0.15-0.25 ml per day for A. duodenale.

A

the intestinal phase

184
Q

 Thus, in heavy infection, a substantial amount of blood can be lost, and a severe iron-deficiency (microcytic, hypochromic) anemia may develop in a short time.

A

the intestinal phase

185
Q

 Nevertheless, a moderate hookworm infection will gradually produce an iron-deficiency anemia as body reserves of iron are used up

A

the intestinal phase

186
Q

 Patients have reported vague gastrointestinal disturbances and eosinophilia (sometimes referred to as Wakana syndrome) following peroral infection

A

the intestinal phase

187
Q

 Cosmopolitan

A

C. Hookworms

188
Q

 N. americanus – tropical Africa and the Americas

A

C. Hookworms

189
Q

 A. duodenale – Europe and Southwestern Asia

A

C. Hookworms

190
Q

 But now, both species have become widely distributed throughout the tropics and subtropics, and rigid demarcations are no longer present

A

C. Hookworms

191
Q

Global
 25%

A

C. Hookworms

192
Q

Phlippines
 5-45%

A

C. Hookworms

193
Q

 N. americanus – 97%
 A. duodenale – 1%
 mixed infections – 2%

A

C. Hookworms

194
Q

 Principal host: Humans

A

C. Hookworms

195
Q

 percutaneous transmission of filariform larvae from the soil

A

necatoriasis and ancylostomiasis

196
Q

 oral route
o eating raw vegetables contaminated with infective filariform larvae
o A. duodenale may remain dormant in the intestines or in the muscles, resulting in a prolonged incubation period and creating problems in treatment.
 Transmammary
o larvae are able to pass into the mammary glands of the mother, so that the newborn baby can receive a large dose of infective larvae through its mother’s milk
o cases of heavy and sometimes fatal hookworm infections in children a month or so of age

A

ancylostomiasis

197
Q

 Ancylostoma caninum (dog hookworm)
 Ancylostoma braziliense (cat hookworm)

A

D. Zoonotic hookworms

198
Q

 The larvae produce itching papules, which develop into serpigenous tracks in the epidermis called (?) or creeping eruption.
o These tracts can elongate by several centimeters a day; larvae can migrate for upto one year until they die, but the lesions usually heal spontaneously within weeks to months.
o Secondary pyogenic infection may occur at these sites.

A

cutaneous larva migrans (CLM)

199
Q

 Definitive host: dogs and cats

A

D. Zoonotic hookworms

200
Q

 Threadworm
o UK and Australia – pinworm or seatworm (Enterobius vermicularis)

A

E. Strongyloides stercoralis

201
Q

 Free-living cycle - Heterogonic cycle
 Parasitic cycle - Homogonic

A

E. Strongyloides stercoralis

202
Q

 Rhabditiform larvae in the gut become infective filariform larvae that can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal and perineal area (external autoinfection).

A

Autoinfection

203
Q

 They ultimately enter the lymphatics or venules and are carried to the right heart and the lungs to complete the life cycle as earlier, or disseminate throughout the body

A

Autoinfection

204
Q

 benign and asymptomatic

A

Strongyloidiasis

205
Q

 only indications of infection
o Eosinophilia and larvae in stool

A

Strongyloidiasis

206
Q

 In immunocompromised individuals, it may cause clinical manifestations which may be severe and even fatal

A

Strongyloidiasis

207
Q

 filariform larvae may enter blood circulation and lodge in various organs, e.g. heart, lungs, brain, kidneys, pancreas, liver and lymph nodes

A

Disseminated strongyloidiasis

208
Q
  • dermatitis, with erythema and itching at the site of penetration of the filariform larva, particularly when large numbers of larvae enter the skin
A

Cutaneous manifestations

209
Q
  • larva currens (meaning racing larvae) has been applied to the rapidly progressing linear or serpiginous urticarial tracks caused by migrating filariform larvae
A

Cutaneous manifestations

210
Q
  • often follow autoinfection and start perianally
A

Cutaneous manifestations

211
Q
  • This rash usually advances very rapidly (up to 10 cm/hr)
A

Cutaneous manifestations

212
Q
  • When the larva escape from the pulmonary capillaries into the alveoli, small hemorrhages may occur in the alveoli and bronchioles.
    Pneumonia and Loeffler’s syndrome may be present in some patients.
A

Pulmonary manifestations

213
Q
  • This may present as malabsorption syndrome.
    Diarrhea is often present.
A

Intestinal manifestations

214
Q
  • In heavy infection, there may be extensive sloughing of the intestinal mucosa.
A

Intestinal manifestations

215
Q

 internal autoinfection in immunocompromised

A

Hyperinfection

216
Q

 large number of worms in the intestine and lungs

A

individuals

217
Q

 Other manifestations include:
o protein losing enteropathy
o paralytic ileus

A

E. Strongyloides stercoralis

218
Q

 Clinical manifestations depend on the sites affected:
o Brain abscess
o meningitis and peritonitis

A

E. Strongyloides stercoralis

219
Q

 Cosmopolitan
o tropics and subtropics
o Europe and the USA
o follows a distribution pattern similar to hookworm

A

E. Strongyloides stercoralis

220
Q

Global
 Unknown
 Estimate: 30–100 million

A

E. Strongyloides stercoralis

221
Q

Phlippines
 relatively rare

A

E. Strongyloides stercoralis

222
Q

Host
 Humans

A

E. Strongyloides stercoralis

223
Q

 Rarer human-infecting species of Strongyloides zoonotics:
o S. fuelleborni (fülleborni) subsp. fuelleborni
o S. fuelleborni subsp. kellyi

A

E. Strongyloides stercoralis

224
Q

 direct contact with soil contaminated by Strongyloides larvae

A

E. Strongyloides stercoralis

225
Q

 area: poor sanitation
o feces are disposed in the warm moist soil
o provide an optimal atmosphere for the organism to exist

A

E. Strongyloides stercoralis

226
Q

 allows for maintenance of the parasite within the host for years following the initial exposure

A

Autoinfection

227
Q

 Toxocara canis - dog ascarid
 Toxocara cati - cat ascarid

A

F. Toxocara spp.

228
Q

Ingesting infective eggs or undercooked meat/viscera of infected paratenic hosts

A

F. Toxocara spp.

229
Q

 Humans are accidental hosts

A

F. Toxocara spp.

230
Q

 eggs hatch

A

F. Toxocara spp.

231
Q

 larvae penetrate the intestinal wall and are carried by the circulation to a variety of tissues (liver, heart, lungs, brain, muscle, eyes)

A

F. Toxocara spp.

232
Q

Toxocara spp. can follow a [?] (one host) or [?] (multiple host) life cycle.

A

direct
indirect

233
Q

 Unembryonated eggs are shed in the feces of the definitive host.

A

F. Toxocara spp.

234
Q

 Eggs embryonate over a period of 1 to 4 weeks in the environment and become infective, containing thirdstage (L3) larvae.

A

F. Toxocara spp.

235
Q

 Following ingestion by a definitive host, the infective eggs hatch and larvae penetrate the gut wall

A

F. Toxocara spp.

236
Q

In younger dogs (T. canis) and in cats (T. cati):
 the larvae migrate through the lungs, bronchial tree, and esophagus, where they are coughed up swallowed into the gastrointestinal tract
 adult worms develop and oviposit in the small intestine

A

direct (one host)

237
Q

In older dogs, patent (egg-producing) infections can also occur
 larvae more commonly become arrested in tissues
 Arrested larvae are reactivated in female dogs during late gestation and may infect pups by the transplacental (major) and transmammary (minor) routes in whose small intestine adult worms become established

A

direct (one host)

238
Q

In cats, T. cati:
 larvae can be transmitted via the transmammary route to kittens if the dam is infected during gestation
 somatic larval arrest and reactivation does not appear to be important as in T. canis

A

direct (one host)

239
Q

 ingestion of paratenic hosts

A

indirect (multiple host)

240
Q

 Eggs ingested by suitable paratenic hosts hatch and larvae penetrate the gut wall and migrate into various tissues where they encyst

A

indirect (multiple host)

241
Q

 The life cycle is completed when definitive hosts consume larvae within paratenic host tissue, and the larvae develop into adult worms in the small intestine

A

indirect (multiple host)

242
Q

 preschool children

A

visceral larva migrans (VLM)

243
Q

 larvae invade multiple tissues
o commonly liver
o lung
o skeletal muscle
o occasionally heart

A

visceral larva migrans (VLM)

244
Q

 cause various nonspecific symptoms
o fever
o myalgia
o weight los
o cough
o rashes
o hepatosplenomegaly
 usually accompanied by hypereosinophilia

A

visceral larva migrans (VLM)

245
Q

 Migration to the central nervous system

A

neurotoxocariasis or neural larva migrans

246
Q

 Uncommon

A

neurotoxocariasis or neural larva migrans

247
Q

 eosinophilic meningoencephalitis

A

neurotoxocariasis or neural larva migrans

248
Q

 Death
o severe cardiac
o pulmonary
o neurologic involvement

A

neurotoxocariasis or neural larva migrans

249
Q

 larvae produce various ophthalmologic lesions

A

(OLM)

250
Q

 may cause diffuse unilateral subacute neuroretinitis (DUSN)
o unilateral (affecting one eye) involvement

A

(OLM)

251
Q

associated visual impairment usually presents with
 uveitis, retinitis, or endophthalmitis
 permanent visual damage or blindness

A

F. Toxocara spp.

252
Q

associated larval granulomas
 misdiagnosed as retinoblastoma

A

F. Toxocara spp.

253
Q

 Cosmopolitan
o among domestic dogs and cats

A

F. Toxocara spp.

254
Q

 both animals and people
o ↑ developing countries

A

F. Toxocara spp.

255
Q

 people of lower socioeconomic strata
o ↑ developed countries

A

F. Toxocara spp.

256
Q

 Public places: 10-30%

A

F. Toxocara spp.

257
Q

 western countries: 25% to 30 to 60% (dogs)

A

F. Toxocara spp.

258
Q

 Accidental hosts: Humans

A

F. Toxocara spp.

259
Q

 all wild and domestic canids
 puppies
o patent infections

A

Toxocara canis

260
Q

 wild and domestic felids of all ages
 kittens
o patent infections

A

Toxocara cati

261
Q

Paratenic hosts: mammals and birds; livestock
Paratenic or transport hosts: Cockroaches and earthworms

A

F. Toxocara spp.

262
Q

 soil-transmitted zoonosis

A

Human toxocariasis

263
Q

 ↑ children living in homes and in neighborhoods where dogs and puppies are not dewormed o tendency to play in soil o geophagia or soil eating

A

Human toxocariasis

264
Q

 Poor personal hygiene

A

Human toxocariasis

265
Q

 consumption of inadequately washed vegetables chronic low-dose infections

A

Human toxocariasis

266
Q

 consumption of undercooked beef, lamb, chicken, and duck meat (particularly liver)

A

Human toxocariasis