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Preventive And Social Medicine II > CN1 Nematodes > Flashcards

CN1 Nematodes Flashcards

1
Q

Living together of unlike organisms

A

Symbiosis

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2
Q

What may also involve protection or other advantages to one or both partners?

A

Symbiosis

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3
Q

What is a symbiotic relationship in wc 2 species live together (naol) and one species benefits from the relationship and the other not being harmed or benefiting?

A

Commensalism

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4
Q

What is an example of commensalism?

A

Entamoeba coli in intestinal lumen is supplied w nourishment and is protected from harm, while it doesn’t cause any damage to tissues of host

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5
Q

What is an example of mutualism?

A

Termites and flagellates in their digestive system, wc synthesize cellulose to aid in the breakdown of ingested food

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6
Q

What parasite can cause amoebic dysentery?

A

Entamoeba histolytica

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7
Q

What may exist in a free-living state or may become parasitic when the need arises?

A

Facultative

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8
Q

What needs a host at some stage of their life cycle to complete their development and to propagate thei species?

A

Obligate

E.g., tapeworms

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9
Q

What is considered as such when the parasite is found in an organ wc isn’t its usual habitat?

A

Erratic

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10
Q

What is a parasite wc established itself in a host where it doesn’t ordinarily live?

A

Accidental or incidental

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11
Q

What is a free-living organism that passes through the digestive tract without infecting the host?

A

Spurious

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12
Q

What is responsible for transmitting the parasite from one host to another?

A

Vectors

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13
Q

What transmits the parasite only after the latter has completed its development w/in the host?

A

Biologic vector

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14
Q

What only transports the parasite?

A

Mechanical/phoeretic vector

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15
Q

What is an example of mechanical/phoeretic vector?

A

Flies and cockroaches that feed on fecal material may carry enteric organisms and transfer these to food, wc could be the eaten by humans

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16
Q

What host harbors the sexual or adult stage of parasite?

A

Definitive or final host

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17
Q

What host harbors the asexual or larval stage of the parasite?

A

Intermediate host

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18
Q

Its prevalence is 80-90% (public elementary school children)

A

Ascaris lumbricoides

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19
Q

29% pvt schl children; 56% public school children
10% rural; 75% crowded urban areas

Prevalence: F(16%) than in M(9%)

A

Enterobius vermicularis

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20
Q

Prevalence: 80-84% (co-extensive w Ascaris)
Higher infxn rates than Ascaris in 2001 survey

Children 5-15 y.o. more frequently infected
70-80% both rural and urban areas

A

Trichuris trichiura

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21
Q

Prevalence: 40-45%; 5-60% depends on geo loc and type of rainfall

Over 900 million ppl in tropical and subtropical countries

A

Ancylostoma duodenale/Necator americanus

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22
Q

Parasites: soil polutted with human excreta

A

A. lumbricoides
T. trichiura
Hookworms
S. stercoralis

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23
Q

Contaminated water may contain

A

Viable cysts of parasitic amebae, intestinal flagellates, T. solium eggs, infective cercarial stage of human bld flukes

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24
Q

Food containing the immature infective stage of the parasite

A 
Freshwater fish 
Crabs and crayfishes 
Raw pork 
Beef 
Buffalo nuts 
Watercress
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25
Q

Freshwater fish

A

D. latum, intestinal and liver flukes

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26
Q

Crabs and crayfishes

A

Oriental lung fluke

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27
Q

Raw pork

A

Trichinella spiralis, Taenia solium

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28
Q

Beef

A

T. saginata

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29
Q

Buffalo nuts

A

Fasciolopsis buski

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30
Q

Watercress

A

Fasciola hepatica

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31
Q

Blood sucking insect

A 
Malarial parasites
Leishmania
Trypanosomes
Filariae
Viruses
Rickettsia
Bacteria
Spirochetes
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32
Q

Direct source with the hydatid cyst of Echinococcus granulosus and visceral larva migrans dt Toxocara canis

A

Doggie

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33
Q

Parasite: herbivores

A

Trichostrongylus spp.

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34
Q

Parasite: cats

A

Toxoplasma spp.

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35
Q

Parasite: rats

A

Hymenolepis nana

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36
Q

Another person, his clothing, bedding, or immediate environment that he has contaminated, food handlers

A

Entamoeba histolytica
Enterobius vermicularis
Hymenolepis nana

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37
Q

What can cause autoinfection?

A

E. verm
H. nana
S. stercoralis
C. philippinensis

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38
Q

In taeniasis, human is considered as?

A

Definitive or final host

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39
Q

Intermediate host of Taenia spp and Schistosoma spp.

A

Taenia spp. - Pigs or cattle

Schistosoma spp. - Snails

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40
Q

One in wc the parasite doesn’t dev further to later stages

A

Paratenic host

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41
Q

The parasite remains alive and is able to infect another susceptible host

A

Paratenic host

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42
Q

What is an example of paratenic host?

A

Metacercariae of Paragonimus in raw wild boar meat can pass thru the intestinal wall of humans and complete its development

Wild boar is the paratenic host

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43
Q

What allows the parasite’s life cycle to continue and become additional sources of human infection?

A

Reservoir host

Pigs - B. coli
Field rats - P. westermani
Cats - B. malayi

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44
Q

In Falciparum malaria, possession of what confers some protection?

A

Sickle cell trait

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45
Q

What increases the susceptibility of an individual to Plasmodium vivax infections?

A

Presence of Duffy blood factor

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46
Q

What is not suitable for the development of intestinal protozoans?

A

Diet rich in protein

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47
Q

What favors the appearance of symptoms of amoebiasis and complications of the dse of high carb diet - favors the development of some tapeworms?

A

Low protein diet

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48
Q

What may be v impt in modifying the severity of dse in endemic areas?

A

Acquired immunity

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49
Q

What are the mechanisms by which parasites cause injury to the host?

A

(1) Interference with the vital processes of the host through enz sys
(2) Invasion and destruction of host tissue
(3) Deprivation of the hosts from essential nutrients and substances

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50
Q

What allows the parasites to metabolize nutrients obtained from the host and store these for energy?

A

Secretory and excretory products

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51
Q

What parasite secretes cysteine proteinases wc digest cellular materials and degrade epithelial basement?

A

Trophozoites of E. histolytica

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52
Q

What invades RBCs, and after multiplication, the host’s rbc rupture resulting in the release of merozoites?

A

Plasmodium

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53
Q

What is the cumulative deposition of eggs in the liver that stimulates an immune response resulting in granuloma formation and then fibrosis wc leads to portal HPN and massive hemorrhage in the venules?

A

Schistosoma japonicum

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54
Q

They have cutting plates wc cab attach to the intestinal mucosa and destroy the villi

A

Hookworms

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55
Q

Form tangled masses that can lead to intestinal obstruction and may invade other organs like appendix and bile ducts

A

Ascaris

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56
Q

What can cause massive intestinal bleeding wc results in chronic bld loss and IDA?

A

Heavy hookworm infxn

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57
Q

What parasite competes w its host for available supply of vit B12 that leads to Megaloblastic Anemia?

A

D. latum

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58
Q

What makes the helminthic parasites resistant to cytotoxic effects of both neutrophils and macrophages?

A

Their cuticle and integument

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59
Q

What can destroy non-human trypanosomes except Trypanosoma brucei wc has evolved resistance thru expression of serum resistance-associated protein?

A

Trypanolytic factors s/a apolipoprotein L-1 (APOL1)

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60
Q

What enables a non-human trypanosome (T. evansi) to infect human, and addition of recombinant APOL1 restored tryoanolytic activity?

A

A frameshift mutation in the APOL1 gene

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61
Q

What are parasites that enter the bld stream or tissue that often able to survive and replicate bcs they’re resistant to the host innate immune response?

A

Protozoa and helminthic parasites

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62
Q

What reduce the immune fxn of macrophages that lower their capacity of phagocytosis?

Also cause the defective processing of antigen

(Immune suppression)

A

Plasmodium spp.

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63
Q

What can produce large amounts of surface glycoproteins?

Immune suppression

A

Trypanomastigotes

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64
Q

Trypanosoma gambiense; this will affect the processing of the proteins dt antongenic competition and impair the B and T lymphocyte activity causing them to:

(Immune suppression)

A

Decrease lymphokines and immunoglobulin production

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65
Q

What parasite produces suppressor factor that can inhibit movement of monocytes to the site of invasion?

(Immune suppression)

A

Entamoeba histolytica

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66
Q

Down-regulation of lymphocytes

Immune suppression

A

Fasciola spp.

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67
Q

Polyclonal hypergammaglobulinemia where Ab lack specificity against these parasites

(Immune suppression)

A

W. bancrofti
B. malayi
Plasmodium spp.

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68
Q

Immune response is directed against the deeper layers of the cuticle but the immune response is diverted to the rapidly changing surface of its integument

(Immune suppression)

A

Necator americanus

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69
Q

Immune complexes produced in cysticercus cellulosae infxn supress inflammatory response thru inhibition of complement activity

(Immune suppression)

A

Plasmodium spp.
T. cruzi
Schistosoma spp.

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70
Q

Antigenic variation

A

Trypanosoma gambiense and Giardia lamblia

Plasmodium falciparum

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71
Q

Parasites changes the antigenic profile off its surface coat –> variant surface glycoproteins (SVG)

(Antigenic variation)

A

Trypanosoma gambiense and Giardia lamblia

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72
Q

They exhibit antigenic diversity

Antigenic variation

A

P. falciparum

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73
Q

Mechanism is thru repeat variation of the encoded polypeptides wc contain tandem sequences of amino acids as observed in:
• MSA - Merozoites surface ag
• RESA - Ring infected rbc surface ag

(Antigenic variation)

A

P. falciparum

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74
Q

These repeat sequences are Ag-ic epitopes, wc stimulate Ab prod.
With variation, Ab fail to recognize the Ag
(Antigenic variation)

A

P. falciparum

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75
Q

These can acquire antigenic mol from the host (host mimicry)

A

Larval stage of Echinococcus granulosus (hydatid cyst)

Tegument of Schistosoma spp. adult

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76
Q

Ab produced against the parasite fail to recognize nonself from self Ag

A

Host mimicry

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77
Q

This saves the parasite from splenic filtration and the action of Ab

A

Intracellular sequestration

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78
Q

Proliferate inside macrophages to escape the host immune response

(Intracellular sequestration)

A

T. cruzi
Leishmania spp.
T. gondii - also in other nucleated cells

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79
Q

Sequestered from the circulation into the deep vasculature

A

P. falciparum (late intracellular stages)

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80
Q

Mediated by the presence of knobs on infected rbc that enable them to be attached to the endothelial cells of tiny capillaries

A

P. falciparum (late intracellular stages)

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81
Q

Its muscle arrangement is polymarian (numerous cells project well into the body cavity)

A

A. lumbricoides

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82
Q

Its color is whitish or pinkish

And has a length of:
10-30cm (male)
22-35cm (female)

A

A. lumbricoides

Parts: terminal mouth, 3 lips, sensory papillae

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83
Q

Difference between male and female A. lumbricoides

A

Males: ventrally curved posterior end with 2 spicules; single, long, tortois tubule

Females: paired reproductive organs (posterior 2/3)

84
Q

What does Ascaris produce that protects worms from digestion?

A

Pepsin inhibitor 3 (PI-3)

85
Q
  • 88-94 um by 39-44 um
  • Longer and narrower than fertile eggs
  • Thin shell and irregular mammilated coating filled w refractile granules
A

Infertile eggs (A. lumbricoides)

86
Q
  • 45-70 um by 35-50 um
  • Outer, coarsely mammilated albuminous covering (lost in decorticated eggs)
  • Thick transparent hyaline shell w thick outer layer
  • Delicate vitelline, lipoidal, inner membrane - higly impermeable
  • At oviposition, ovoid mass of protoplasm - dev into larvae in abt 14 dayz
A

Fertile eggs (A. lumbricoides)

87
Q
  • Infective stage
  • Can survive in moist shaded soil for a few mos to abt 2 yrs in tropical and sub-tropical, but much longer in temperate regions
A

Embryonated egg (A. lumbricoides)

88
Q
  • Cuticular alar expansion at the anterior end
  • Prominent posterior esophageal bulb
A

Adult E. verm

Female: winglike expansion (alae) of the body wall at anterior end, distention of body dt large number of eggs in uteri, and a pointed tail

Male: curved tail

89
Q

Difference of femal and male adult E. verm

A

Female: 8-13 by 0.4 mm
Long pointed tail
Uteri gravid females are distended w eggs

Male: 2-5 by 0.1-0.2 mm
Curved tail and a single spicule
Usually die after copulation

90
Q
  • 140-150 by 10 um
  • Characteristic esophageal bulb
  • No cuticular expansion on the anterior end
A

Rhabditiform larva of E. vem

91
Q
  • Asymmetrical
  • One side flattened, other side convex
  • 50-60 by 20-30 um (ave 55 by 36 um)
  • Translucent shell
A

Eggs of E. verm

92
Q

What is the outer, triple albuminous covering of the eggs of E. verm for?

A

Mechanical protection

93
Q

What is the inner, embryonic lipoidal membrane of the eggs of E. verm for?

A

Chemical protection

94
Q

Its somatic muscle arrangement is holomyarian (small nucleus cells are closely packed in a narrow zone)

A

Trichuris trichiura

95
Q
  • Attenuated anterior 3/5 traversed by a narrow esophagus
  • Resembles a string of beads
  • Robust posterior 2/5 contains the intestine and a single set of reproductive organs
A

Adult T. trichiura

96
Q

Male and female differences of T. trichiura

A

Male: 30-45 mm, slightly shorter than female
Coiled posterior w a single spicule and refractile sheath

Female: 35-50 mm long
Blunt, rounded posterior end
Lays approx. 3,000-10,000 eggs per day

97
Q

Soon after the embryonated eggs are ingested, the larvae escape and penetrate intestinal villi where they remain for 3-10 days

A

Trichuris trichiura larvae

98
Q
  • 50-55 by 23 um
  • lemon-shaped w plug-like translucent polar prominences
  • yellowish outer and a transparent inner shell
  • fertilized eggs are unsegmented at oviposition
A

Trichuris trichiura eggs

99
Q

Somatic muscle arrangement: meromyarian (fewer cells 2-5 per dorsal or ventral half)

A

Ancylostoma duodenale

100
Q
  • single-paired male and female reproductive organs
  • the shape is such that the head continues in the same direction as the curvature of the body
  • the buccal capsule has 2 pairs of curved ventral teeth
A

Adult Ancylostoma duodenale

101
Q
  • inconspicuous buccal spears and transverse striations on the sheath in the tail region
  • infective stage to humans; infxn is by penetration thru the exposed skin
A

Filariform larvae of Ancylostoma duodenale

102
Q
  • Bluntly rounded ends
  • Single transparent hyaline shell
  • Unsegmented at oviposition and in the 2- to 8-cell stages of division in fresh feces
A

Eggs of Ancylostoma duodenale

103
Q

LC of Ascaris lumbricoides:

When the eggs are ingested, where does larva hatch and penetrate?

A

Small intestine and penetrate to the intestinal wall

104
Q

LC of Ascaris lumbricoides:

What happens after they hatch and penetrate to the intestine?

A

Larva enters the venules to go to liver (portal vein), on to the heart and pulmonary vessels where they break out of capillaries to enter the air sacs

105
Q

LC of Ascaris lumbricoides:

What happens after they hatch and penetrate to the intestine?

A

Larva enters the venules to go to liver (portal vein), on to the heart and pulmonary vessels where they break out of capillaries to enter the air sacs

106
Q

LC of Ascaris lumbricoides:

What does larvae undergo before migrating to the larynx and oropharynx to be swalloew into digestive tract?

A

Molting

107
Q

How many days is migration and molting phase in the lungs?

A

7-10 days

108
Q

Prepatent period takes about how many days?

A

60-70 days

109
Q

Bogitsh LC of Ascaris lumbricoides:

When fertilized eggs are deposited, what happens to the zygote?

A

Uncleaved until the eggs reach soil

110
Q

Bogitsh LC of Ascaris lumbricoides:

Eggs deposited in soil are:

A

1) resistant to dessication

2) very sensitive to environmental temperatures

111
Q

Bogitsh LC of Ascaris lumbricoides:

The zygote within the eggshell develops at what?

A

Soil temp (25°C) > body temp host (37°C)

112
Q

Bogitsh LC of Ascaris lumbricoides:

Development ceases at what temp?

A

15.5°C

113
Q

Can eggs survive at temps more than slightly above 38°C?

A

Nope

114
Q

After 2-4 wks in moist soil at optimal temp and O2 lvls, what happens to the embyro?

A

It molts at least once and develops to an infective second-stage larva

115
Q

Bogitsh LC of Ascaris lumbricoides:

Duodenum to heart that takes approx 1 week

A

Mucosal lining –> circulatory sys –> venous system –> liver –> right side of heart –> lungs (propelled by pulmo arterial flow)

116
Q

The larvae remain in the lungs for several days, molting twice, and eventually rupture from the pulmonary capillaries to enter the?

A

Alveoli

117
Q

Bogitsh LC of Ascaris lumbricoides:

What is essential to the worms’ survival in the small intestine? Those who undergo this develop to sexual maturity

A

Fourth molt

118
Q

What is the interval from ingestion of infective eggs to the appearance of sexually mature worms in the smol intestine?

A

3 months

119
Q

LC of E. verm:

Where are adult worms found?

A

Ileum and cecum

120
Q

LC of E. verm:

Single female lays how many eggs per day?

A

4,672 to 16,888 eggs/day

Ave: 11,105

121
Q

LC of E. verm:

Eggs on the perianal region become fully embryonated within how many hrs?

A

4-6 hrs

122
Q

LC of E. verm:

When ingested, eggs containing the 3rd stage larvae hatch where?

A

Duodenum, pass down the SI to the cecum, and develop into adults

123
Q

What condition is more favorable for E. verm?

A

Moist (eggs remain viable for 13 days)

124
Q

LC of T. trichiura:

Embryonic development takes place outside the host when eggs are deposited in

A

Clayish soil

125
Q

LC of T. trichiura

An unhatched, infective, third-stage larva develops within

A

3-6 wks

126
Q

LC of T. trichiura:

Where does the larva hatch?

A

Upper portion of SI and quickly burrow into the cells of intestinal villi near the Crypts of Lieberkuhn

127
Q

LC of hkworms:

In the soil, embryo within the egg develops rapidly and hatches after 1-2 days into?

A

Rhabditiform larva

128
Q

LC of hkworms:

After 7-10 days, larva is tranformed into?

A

Non-feeding filariform larvae (infective)

129
Q

LC of hkworms:

Filariform larvae to SI

A

Filariform larvae –> skin –> venules –> heart –> lungs –> alveoli –> trachea –> swallowed –> SI

130
Q

What are the clinical manifestations in Larval Stage of A. lumbricoides?

A
  1. During lung migration:
    • allergy (lung infiltration, asthma attacks, lip edema)
    • pneumonia-like dt penetration of lung capillaries
  2. Vague abdominal pain (MOST FREQ COMPLAINT)
  3. Eosinophilia during larval migration
  4. Lactose intolerance in children (moderate infxns)
  5. Bowel obstruction (heavy infxn)
131
Q

What are the clinical manifestations in Adult Stage of A. lumbricoides?

A
  1. Severe colicky abdo pain; px w biliary ascariasis, by worm movement in biliary tract
  2. Acute appendicitis
  3. Pancreatitis
  4. Peritonitis
  5. Intestinal volvulus, intussusception obstruction
  6. High fever
  7. Intestinal spasm –> intestinal obstruction
132
Q

What are the clinical manifestations in Larval Stage of E. verm?

A
  1. Pruritus
  2. Insomnia
    - poor appetite
    - wt loss
    - irritability
    - grinding of teeth
    - abdominal pain
133
Q

What are the clinical manifestations in Adult Stage of E. verm?

A
  1. Mild catarrhal inflammation of intestinal mucosa (dt attachment of worms)
  2. Inflamm of deeper layers of the intestine (mechanical irritation and secondary bacterial infxn)
  3. Irritation of the perineal region (migration of egg-laying females to the anus)
  4. Due to adult worm migration
    - appendicitis
    - vaginitis
    - endometritis
    - salpingitis
    - peritonitis
134
Q

What are the clinical manifestations in Larval Stage of T. trichiura?

A

Over 5,000 eggs (symptomatic)

  1. Severe diarrhea or dysenteric syndrome (more than 20,000 eggs per gram feces)
  2. Heavy chronic trichuriasis
    - frequent bld-streaked diarrheal stools
    - abdominal pain and tenderness
    - nausea and vomiting
    - anemia
    - wt loss
135
Q

What are the clinical manifestations in Adult Stage of T. trichiura?

A
  1. Petechial hemorrhage
    - anterior portions of the worm embedded in the mucosa, wc may predispose to amoebic dysentery (E. histolytica)
  2. Hyperaemic and edematous mucosa
  3. Enterorrhagia (COMMON)
  4. Rectal prolapse (HEAVY INFXNS)
  5. Appendicitis/granulomas (lumen of appendix filled w worms; consequent irritation and inflammation)
136
Q

What are the clinical manifestations in Larval Stage of Ancylostoma duodenale?

A
  1. Maculopapular lesions and localized erythema
    - penetration of filariform larva thru skin
  2. “Ground itch” or “dew itch” (severe itching; related to contact w soil esp. on dewy morning)
  3. Itching, edema, erythema, papulovesicular eruption lasting for 2 weeks
  4. Bronchitis/pneumonitis (abundant larva migration to lungs)
  5. Minute hemorrhage w eosinophilic and leukocytic infiltration (rare in the tropics)
137
Q

What are the clinical manifestations in Adult Stage of A. duodenale?

A
  1. Maturation of worm in int
    • abdo pain
    • steatorrhea
    • diarrhea w bld and mucus
    • bld eosinophilia (30-60%)
  2. Progressive, secondary, microcytic, hypochromic anemia of the iron-def type (chronic moderate/heavy infxn; dt primarily continuous bld loss)
  3. Hypoalbuminemia
  4. Symptoms: exertional dyspnea, weakness, dizziness, and lassitude
  5. Signs: rapid pulse, edema, albuminuria
138
Q

What are the diagnostic procedures for A. lumbricoides?

A
  1. DFS
  2. Kato technique/cellophane smear mtd
  3. Kato-katz technique
139
Q

What is a quanti tech to make egg cts of parasite per gram of feces and to determine egg redxn rate after tx?

A

Kato-katz technique

140
Q

What is a qualitative mtd recommended for mass examination of feces for diagnosis?

A

Kato-thick or cellophane smear mtd

141
Q

What are the diagnostic procedures for T. trichiura?

A
  1. DFS
  2. Kato thick smear mtd (20-60mg)
  3. Kato katz (simple low cost)
    4 Conc techniques (acid-ether and formalin-ether mtds)
142
Q

Highly recommended in dx of trichuriasis

Useful in dx clinic px and mass exam in community surveys

A

Kato thick smear mtd

143
Q

Quantitative mtd for egg counting to determine cure rate (CR), egg redxn rate (ERR), and intensity of infxn

Can be used to assees the success or failure of a ctrl program

A

Kato-katz technique

144
Q

What are the diagnostic procedures for Ancylostoma duodenale?

A
  1. DFS
  2. Kato technique or Kato-katz
  3. Conc mtds (ZnSO4 centrifugal floatation and Formalin-ether)
  4. Culture mtds (Harada-Mori)
145
Q

What is the most effective time to intervene in the prevention of parasitic worm infxns?

A

When the infective stage of the worm is in the soil

146
Q

S-shaped
Buccal capsule has a ventral pair of semilunar cutting plate

Bipartite (2 digits)
Barbed Bristle-like copulatory bursa

A

N. americanus

147
Q

C-shaped
2 pairs of teeth

Tripartite (3 digits)
Simple, not barbed copulatory bursa

A

A. duodenale

148
Q

Tx for E. verm

A

Pyrantel pamoate

Mebendazole

149
Q

Tx for T. trichiura

A

Mebendazole

Albendazole

150
Q

Tx for Ascaris lumbricoides

A

Pyrantel pamoate
Mebendazole
Piperazine citrate (int obs)

151
Q

Tx of Ancylostoma duodenale

A

Pyrantel pamoate

Mebendazole/albendazole

152
Q

MOA of Mebendazole

A

Depolymerizing effect on microtubules

153
Q

MOA of Pyrantel Pamoate

A

Neuromuscular blocking agent causing paralysis of the helminths; do not kill the parasite

154
Q

MOA of Albendazole

A

Larvicidal agent (kills parasite)

155
Q

What is the infective stage of Intestinal Taeniasis

A

Cysticerci Larvae

156
Q

What is the common & largest Nematode?

A

A. lumbricoides

157
Q

What is the longest tapeworm?

A

D. latum

158
Q

Microcytic Anemia

A

A. duodenale

159
Q

Cobalamin Deficiency

A

D. latum

160
Q

Small, cylindrical, fusiform, grayish-white nematodes

A

N. americanus

161
Q

True or false. N. americanus adult Females are larger then Males.

A

True.

Female: 9-11mm by 0.35mm
Male: 5-9mm by 0.30mm

162
Q

Posterior end of a Male N. americanus

A

Broad, membranous caudal bursa with rib-like rays (used for copulation)

163
Q

What is larger, A. duodenal or N. americanus?

A

A. duodenale

164
Q

Buccal capsule of A. duodenale

A

2 pairs of curved ventral teeth

165
Q

Which genital primordium is smaller, hkwrm or S. stercoralis?

A

Hookworms

166
Q

Conspicuous transverse striations on the sheath in the tail region

A

N. americanus Filariform larvae

167
Q

Kay kinsa ning life cycle?

  1. Adult worms copulate while attached to the mucosa of the SI
  2. Female oviposit in intestinal lumen
  3. Eggs on feces
  4. In soil, embryo within the eggs are passed out
  5. Egg rapidly develops and hatches into Rhabditiform larva (after 1-2 days)
  6. After 7-10 days, larva undergoes 2 stages of molting (shed)
  7. Transforms into non-feeding Filariform (L3)
A

Hookworm

168
Q

Since filariform larva penetrate the skin and enter the venules, how to they go to the small intestine?

A

They migrate to the heart and lungs, and into the alveoli. Larva ascends to trachea and get swallowed, and passed down to the SI where the worms become sexually mature and female will start laying eggs.

169
Q

Pathology of Hookworm

A

1) skin
2) lungs - larval migration
3) small intestine - habitat

170
Q

Clinical manifestations of hookworm

A
  • maculopapular lesions
  • localized erythema
  • itching (“ground itch” or “dew itch”) - contact w soil on a dewy morning
  • edema
  • papulovesicular eruptions (2 wks)
  • bronchitis, pneumonitis (if abundant sa lungs)
  • hypoalbuminemia (d/t loss of blood, lymph and protein)
  • minute hemorrhages with eosinophilic and leukocytic infiltration

Other symptoms: exertional dyspnea, weak, dizzy, lassitude
Other signs: rapid pulse, edema, albuminuria

Stage of maturation of worm in intestine:
- abdominal pain
- steatorrhea
- diarrhea w blood and mucus
- eosinophilia

171
Q

Results in a progressive, secondary, microcytic, hypochromic anemia of iron-deficient type, d/t continuous blood loss

A

Chronic moderate or heavy hookworm infxn

172
Q

Diagnosis of hookworm

A

Ova in feces

  1. DFS - if heavy infxns
  2. Kato thick or Kato-Katz mtd - inc detection rates since more stools
    [kato - quanti diagnosis by det intensity of infxn in terms of number of helminth eggs per gram of feces]
    Disadv: rapid clearance of hkwm eggs after 30-60 mins w the use of glycerine (clearing agent)
  3. Conc method: greater stool quantity = inc sensitivity
    - zinc sulfate centrifugal flotation
    - formalin-ether/ethyl acetate conc
    - FLOTAC (centrifugal flotation mtd) - higher sensi
  4. Culture methods (Harada-Mori) - sp. identification
    - hatching of larva from eggs on strips of filter paper one end immersed in water
  5. Molecular approach, PCR-based detection of hkwm DNA in feces and ELISA
    - detect of secretory/excretory coproantigens
173
Q

Tx for hkwm

Mass drug administration (once a yr)

A

Albendazole
- single dose 400mg

Mebendazole
- 500mg

Both these are benzimidazole derivatives that uptake of glucose by most intestinal and tissue nematodes

174
Q

Local distribution of human hkwm infxn is greater where?

A

Agricultural areas: Farmers (rice fields and veggie gardens) no proper protection against contact w infective soil

175
Q

Difference in the method of human infxn in Necatoriasis and Ancylostomiasis

A

Necatoriasis: percutaneous
Ancylostomiasis: perc and oral route (eating raw vegetables w contaminated larva, or raw meat)

176
Q

Can infect humans causing “creeping eruption,” AKA cutaneous larva migrans

A

Ancylostoma braziliense (cat hkwm)
Ancylostoma caninum (dog)

177
Q

T. saginata adult worm inhabits the upper jejunum and can live for up to how many yrs?

A

25 yrs

178
Q

Difference between parasite, predator, and scavenger

A

Parasite: one harm the host w/o killing immediately
Predator: organism that lives by victimizing for one’s own gain
Scavenger: organism that feeds on dead plants/animals or other orgs and decaying organic matter

179
Q

A host in wc the parasite doesn’t develop further to later stages, but the parasite remains alive and able to infect another susceptible host

A

Paratenic host

180
Q

Example of paratenic host

A

Paragonimus metacercaria in ras wild boar meat can pass thru the int wall of humans and complete its development.

181
Q

Period between infxn and evidence of symptoms

A

Clinical incubation pd

182
Q

Period between infxn or acquisition of parasite and evidence or demonstration of infxn

A

Pre-patent pd, AKA biological incubation pd

183
Q

Bullastra snails are associated with what infection?

A

Artyfechinostomum malayanum

184
Q

involves individual-level deworming with selection for treatment based on a diagnosis of infection or an assessment of the intensity of infection, or based on presumptive grounds. This strategy can be used in whole populations, or in defined risk groups.

A

Selective treatment

185
Q

is group-level deworming where
the (risk) group to be treated (without prior
diagnosis) may be defined by age, sex, or other
social characteristics irrespective of infection
status.

A

Targeted Tx

186
Q

is population-level
deworming in which the community is treated
irrespective of age, sex, infection status, or other
social characteristics.

A

Universal Tx

187
Q

inability of the parasite to synthesize certain
cellular components and the need of the parasite
to obtain these from a host

A

Streamlining

188
Q

What does Ascaris produce that suppresses lymphocyte proliferation?

A

Phosphorylcholine

189
Q

● Bilaterally symmetrical, unsegmented pseudoceolomates
● Body generally elongate, cylindrical, covered by cuticle
● Terminal mouth is surrounded by lips
● Sexes are separate
● Anterior body characteristically with 16 setiform or
papilliform sensory organs and two amphids
(chemoreceptors)
● Digestive tract complete, with subterminal anus
● Excretory system, when present, empties waste through
anterior, ventromedian pore
● Body musculature limited to longitudinally oriented muscles
● No respiratory system
● Eggs with determinate cleavage
● Oviparous or ovoviviparous
● Stages in life cycle are egg, four juvenile (larval) stages,
and adult

A

phylum nematoda

190
Q

Epidemiologic triad

A

A harmful agent that comes into contact w a susceptible host in the proper environment

191
Q

E. verm bogitsh epidemiology

A

● Children, especially of early school-age, are most
vulnerable to E. vermicularis infection.
● The geographic distribution of the worm is global. Infections
are especially prevalent in temperate zones, where an
estimated 500 million persons are infected.
● However, prevalence varies in each locale.
○ Alaskan Inuits displays a 51% prevalence
○ Elementary students in and around Tallahassee,
Florida, 27%
○ Preschoolers in San Francisco, 58%
○ Sicilian children, 77%
○ Children overall in the United States, 33%
● Enterobius vermicularis is the most common nematode
parasitizing humans in the United States.
● Infections occur in one of four ways:
○ Retroinfection - when hatched larvae migrate back
into the large intestine.
○ Self-infection - when the patient is reinfected by
hand-to-mouth transmission.
○ Cross-infection - when infective eggs are ingested,
either with contaminated surface or body parts from
infected humans.
○ Inhalation of airborne eggs.
● In households with heavily infected individuals, infective
eggs have been found in samples of dust taken from chairs,
tabletops, dresser tops, floors, baseboards, etc.
● In a survey to determine the distribution of airborne pollens
in public places, pinworm eggs were found in theaters, not only arm rest and baseboards but also on chandeliers high
above the seats; most of these eggs, however, were no
longer viable.
● Experiments show that at room temperature or above, fewer
than 10% of such eggs survive more than 2 days, probably
accounting for the less than the unusual infection in such
public places.

191
Q

LC of E. verm (bogitsh)

A

● Sexually mature worms usually inhabit the ileocaecal area
of the human intestinal tract, but they can spread to adjacent
regions of the small and large intestines (Fig. 16-21).
● Adhering to the mucosa, the worms feed on bacteria and
epithelial cells.
● Males die following copulation, while egg-bearing females,
with up to 15,000 eggs in their uteri, migrate to the perianal
and perineal regions.
○ There, stimulated by the lower temperature and
aerobic environment, they deposit their eggs and
then also die. More eggs are released when the
female’s body ruptures.
● The elongate eggs, each measuring approximately 50-60
um by 20-30 um, are characteristically flattened on one
side. Upon deposition, each contains an immature larva.
● The infective, third-stage larva completes development
within the egg several hours after leaving the body of the
female worm.
● Infection and reinfection occur when eggs containing the
infective larvae are ingested by the host.
○ This may happen when eggs are picked up on the
hands from bed- clothes or beneath fingernails
contaminated with the host scratches the perianal
zone to relieve itching caused by nocturnal migration
of the female worms.
○ However, the lightweight eggs are sometimes
airborne and, therefore, can also be inhaled.
● Retroinfections occur when third-stage larvae hatch from
perianally located eggs and enter the host’s intestinal tract
through the anus.
● Ingested eggs usually hatch shortly after reaching the
duodenum.
● The escaping larvae molt and develop as they migrate
posteriorly, reaching sexual maturity by the time they arrive
at the colon.
● The life cycle of E. vermicularis spans about 2 months.
● Although vulnerable to even moderately high temperatures,
eggs are highly resistant to drying and remain viable for a
week or more under cool, humid conditions. Some
researchers claim that eggs can remain viable for years
under favorable conditions.

192
Q

E verm Gravid females may also migrate up the female reproductive
tract, become trapped in the tissues and cause _________ in the uterus and fallopian tubes

A

granulomata

193
Q

E. verm diagnosis

A

● Diagnosis is verified when the adult worms and/or eggs
are detected.
● Female worms emerge at night and are frequently visible in
the perianal and perineal regions.
● Adult worms can often be observed on feces as well;
however, eggs are found in feces in only about 5% of cases.
● The most reliable procedure for finding eggs is to apply a
strip of cellophane tape to the perianal skin, remove the
tape, and place it on a clean microscope slide for
examination.
● Negative results from this protocol for seven consecutive
days constitute confirmation that the patient is free of
infection.

194
Q

In both sexes, a capillary-like esophagus extends two-thirds
of the body length and is encircled along much of its length by
a series of unicellular glands, the stichocytes.
● The posterior extremity of males is characteristically coiled
and equipped with a single spicule enclosed in a spinose,
retractile, cuticular sheath.

A

Trichuris trichiura

195
Q

LC of T. trichuria

A

● Adult Whipworms occur primarily in the human host’s colon
but also inhabit the appendix and rectum (Fig 16-2).
● The female deposits up to 5000 eggs daily; these are
typically barrel-shaped with two polar plugs.
○ The eggs measure 50 µm by 22 µm and
contain uncleaved zygote at oviposition,
after which the unembryonated eggs pass
to the exterior in feces and develop slowly
in warm, damp soil.
○ An unhatched, infective, third-stage larva
develops in three to six weeks.
● New human hosts become infected when these
embryonated eggs are ingested with contaminated food or
water or from fingers.
● The larvae hatch in the upper portions of the small
intestine and quickly burrow into the cells of the intestinal
villi near the crypts of Lieberkuhn, where they mature,
undergoing two molts in about 3-10 days.
● Subsequently, they migrate to the caecal region and
develop to sexual maturity in 30-90 days from the time the
eggs ingested.
● Adult worms embed the long, slender, anterior ends of their
bodies deeply into the colon submucosa.
● Little is known about the parasites nutritional requirements,
but there is no evidence that they feed on host blood.
● While these worms normally survive approximately 2 years
in the human host, there have been reports of infections
lasting 8 years or longer.

196
Q

They are believed to have a depolymerizing effect of
cytoskeletal elements, such as microtubules.

A

T. trichiuria DOC Meb and Alb

197
Q

A. lum LC

A

● Adult worms inhabit the lumen of the small intestine and
draw nourishment from the semidigested food of the host
(Fig. 16-17).
● Copulation occurs at this site, and eggs are passed with
host feces.
● The outer, albuminous coat of the fertilized eggs is golden
brown due to bile pigment adsorbed from feces.
○ Among the oval, fertilized eggs are found numerous
unfertilized eggs, identifiable by their elongated shape
and the absence of the albuminous coat.
● When fertilized eggs are deposited, the zygote is uncleaved,
and it remains in this state until the eggs reach soil.
5
● Eggs deposited in soil are resistant to desiccation but are
very sensitive to environmental temperature at this stage of
development.
● The zygote within the eggshell develops at a soil
temperature of about 25
oC. Development ceases at
temperature more than slightly above 38
oC.
● After 2-4 weeks in moist soil at optimal temperatures and
oxygen levels, the embryo molts at least once in the shell
and develops to an infective second-stage larva.
● Eggs containing infective larvae may remain viable in the
soil for years or longer.
● After being ingested by a human, eggs containing infective
larvae hatch in the duodenum.
○ The larvae actively burrow into mucosal lining, enter
the circulatory system, and are carried via the portal
circulation to the liver, through the right side of the
heart, and to the lungs by the pulmonary artery.
○ This migration requires one week. The larvae remain
in the lungs for several days, molting twice, and
eventually rupture from the pulmonary capillaries to
enter the alveoli.
○ From there, they move up the respiratory tree and
trachea to the epiglottis to be coughed up,
swallowed, and passed again to small intestine.
● During this complex migratory process, individual worms
grow from 200-300 gm in length to ten times that length.
● A fourth molt in the small intestine is essential to the
worms’ survival, and only those worms that undergo this
final molt develop to sexual maturity.
● The interval from the ingestion of infective eggs to the
appearance of sexually mature worms in the small intestine
is about 3 months.

198
Q

Hkwm LC

A

● Humans almost exclusively are hosts for A. duodenale,
while dogs also are common hosts for N. americanus.
● Eggs are expelled in feces (Fig. 16-13); under optimal
conditions (temperature of 23-33
oC, shade, and sandy soil
rich in organic materials), a rhabditiform larva matures in
1 — 2 days and from the thin-shelled egg.
● The newly emerged larva, about 275 um long, feeds on
bacteria and organic materials in the soil and doubles its
size in 5 days.
● After two molts, the rhabditiform larva becomes a
non-feeding, infective, filariform larva. During the last
molt, the article is retained and encloses the larva as a
sheath.
● The active ensheathed, filariform larvae inhabit the upper
10 cm of soil, usually remaining within 50 cm of the initial
size of oviposition, where they can live up to 6 weeks.
● Human infection occurs when these larvae penetrate the
skin, usually of the feet and legs.
○ Entry is most often gained through hair follicles,
pores, and skin abrasions.
○ Upon penetration, the larvae enter the host’s
lymphatic system, migrate to the right side of the
heart, and enter the lungs via the pulmonary artery.
○ Rupturing from the capillaries, they enter the alveoli
and migrate up the respiratory tree, molting en route,
and then are coughed up and swallowed. The
migratory period lasts about one week.
● At the third molt, larva develops a temporary buccal
capsule enabling it to develop into a feeding worm.
○ Once the larvae reach the small intestine, they actively
burrow into the intervillous spaces where, at about
the 13th day, they undergo their fourth molt. They
become sexually mature adults 5 — 6 weeks.
● Ancylostoma duodenale infection can also be acquired
orally by humans and in some endemic regions this is the
primary means of transmission.
○ Following ingestion, the filariform larva is swallowed and
develops to sexual maturity in the small intestine, molting
twice en route.

199
Q

Who is primarily concerned with the
curative aspect and eradication of the parasite from the host
by prescribing drugs specifically to combat the spread of the
parasitic infection.
○ He also treats whatever complications the host may
have

A

Private practitioner

200
Q

Tx hkwms

A

● Treatment generally targets alleviation of symptoms, such
as the itching, rather than destroying the larvae.
● A topical ointment consisting of a 10% suspension of
thiabendazole has proven effective, and light infections
often respond to chilling of the portion of the lesion with
ethyl chloride.
○ The latter treatment must be administered with extreme
caution, as prolonged exposure to ethyl chloride can
produce second-degree bums.
● Any accompanying microbial infection should be treated with
antibiotics and/or fungicides.

201
Q

,has the responsibility
to act as medical resource, educator and social
mobilizer/community leader to be able to control the
parasitic infection of the residents of the community.
○ As medical resource, the physician makes the
diagnosis and prescribes the proper treatment for the
intestinal parasitism.
○ As educator, the physician must see to it that the family
understands the transmission of parasites, the possible
complications and prevention of parasitism, so that
compliance with the treatment and preventive
measures can be assured.
○ As community leader/social mobilizer, the public
practitioner can request the help and coordinate work
with the City Health Officer and the barangay health
workers to have a sanitary inspector visit the locality.
Advise proper waste disposal.

A

public practitioner

202
Q

wellness plan for px

A
  1. Diagnostic
    ○ Stool examination to determine what parasitic infection
    JT and other family members may be having.
  2. Therapeutic
    ○ Give the appropriate antihelminthic drug, give pain
    reliever for abdominal pain, Iron supplement to correct
    anemia.
    ○ Boost immune status: administer whatever
    immunization is appropriate for age.
  3. Preventive
    ○ Teach personal hygiene- proper handwashing
    ○ Hygienic food preparation.
    ○ Proper waste disposal.
    ○ Refrain from playing in the soil which may be highly
    contaminated with parasitic ova or other
    disease-causing organisms.
    ○ Inform/teach the patient / parents on how they can get
    parasitic infections- modes of transmission, lifecycle
203
Q

further on antihelminthics

A

Benzimidazoles
● History:
○ Are broad spectrum anthelmintic agents against
parasites of both veterinary and human medical
importance.
○ Of the hundreds of derivatives tested, those most
therapeutically useful have modifications at the 2
and/or 5 positions of the benzimidazole ring system.
○ 3 compounds, thiabendazole, mebendazole and
albendazole.
■ Thiabendazole contains a thiazole ring at position
2, is active against a wide range of nematodes
that infect the GIT.
■ Mebendazole, the prototype benzimidazole
carbamate.
■ Albendazole is a newer benzimidazole that is
used worldwide, primarily against a variety of
intestinal and tissue nematodes.
Anthelmintic action:
● Mebendazole and Albendazole are versatile anthelmintic
agents,particularly against GI nematodes, where their
action is not dictated by the systemic drug concentration.
○ These drugs are active against both larval and adult
stages and they are ovicidal for ascaris and trichuris.
○ Albendazole is highly effective against the hookworms
9
that cause cutaneous larval migrans, although
thiabendazole can be used topically.
● Benzimidazoles produce many biochemical changes in
susceptible nematodes, e.g., inhibition of mitochondrial
fumarate reductase, reduced glucose transport, and
uncoupling of oxidative phosphorylation.
● The primary action of these drugs is to inhibit
microtubule polymerization by binding to B-tubulin.
● The selective toxicity of these agents derives from the
specific, high affinity binding to parasite B-tubulin occurs at
much lower concentration than does binding to the
mammalian protein.

204
Q

absorption, fate, excretion

A

Thiabendazole
● Absorbed rapidly after oral ingestion.
● Peak concentration in plasma - after 1 hour.
● Excreted in urine within 24 hours as hydroxythiabendazole,
conjugated either as the glucuronide or as the sulfate.
Mebendazole
● Tablet formulation are poorly absorbed and erratically
absorbed.
● Concentration in plasma are low.
● Conjugates and its metabolites have been found in bile, but
little unchanged it appears in urine.
Albendazole
● Variably and erratically absorbed aner oral administration.
● Absorption is enhanced by the presence of fatty foods and
bile salts.
● It is metabolized in the liver and in the intestine to
albendazole sulfoxide.
● Plasma half life range from 4 to 15 hours

205
Q

Therapeutic uses

A

Thiabendazole
● Topical cream 15% applied to affected area 2 to 3X per
day for 55 days (for creeping eruptions).
Mebendazole
● Valuable for treatment of mixed infection.
● Taken orally, and the same dosage schedule applies to
adults and children more than 2 years of age.
● For enterobiasis, a single 100 mg tab. is taken.
● For ascariasis, trichuriasis and hookworm, the
recommended regimen is 100 mg taken in the morning and
evening for 3 consecutive days. If not cured under 3
weeks, a second course should be given.
Albendazole
● Provides safe and highly effective therapy against infections
with Gl nematodes, including mixed infections of ascaris,
trichuria and hookworms
● It is taken as a single oral 400 mg dose by adults and
children more than 2 years of age.
● Cure rates for light to moderate ascaris infection are
typically over 97%, although heavy infection may require
therapy for 2 to 3 days.
TOXICITY, SIDE EFFECTS, PRECAUTION AND
CONTRAINDICATIONS
Thiabendazole
● Side effects: Anorexia, nausea, vomiting and dizziness.
○ Less frequently, diarrhea, weariness, drowsiness,
giddiness and headache.
○ Occasional fever, rashes, erythema multiforme,
hallucinations, sensory disturbances and StevensJonhson Syndrome.
● Precautions: CNS effects occur frequently, activities
requiring mental alertness should be avoided during therapy
● It has hepatotoxic potential, it should be used with caution
with hepatic disease or decreased hepatic function
● Should be used in pregnancy only when the potential benefit
justifies the potential risk.
Mebendazole
● Side effects: Allergic reaction, alopecia, reversible
neutropenia, agranulocytosis, hypospermia.
● Contraindications: Pregnancy and children less than 2
years of age.
○ Patients who have allergic reactions to the agent.
Albendazole
● Side effects: Transient abdominal pain, diarrhea, nausea,
dizziness and headache, increase in serum
aminotransferase activity.
● Contraindications: Patient with hepatic cirrhosis and
pregnant women.

Preventive And Social Medicine II (32 decks)

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