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
Freshwater fish
D. latum, intestinal and liver flukes
26
Crabs and crayfishes
Oriental lung fluke
27
Raw pork
Trichinella spiralis, Taenia solium
28
Beef
T. saginata
29
Buffalo nuts
Fasciolopsis buski
30
Watercress
Fasciola hepatica
31
Blood sucking insect
``` Malarial parasites Leishmania Trypanosomes Filariae Viruses Rickettsia Bacteria Spirochetes ```
32
Direct source with the hydatid cyst of Echinococcus granulosus and visceral larva migrans dt Toxocara canis
Doggie
33
Parasite: herbivores
Trichostrongylus spp.
34
Parasite: cats
Toxoplasma spp.
35
Parasite: rats
Hymenolepis nana
36
Another person, his clothing, bedding, or immediate environment that he has contaminated, food handlers
Entamoeba histolytica Enterobius vermicularis Hymenolepis nana
37
What can cause autoinfection?
E. verm H. nana S. stercoralis C. philippinensis
38
In taeniasis, human is considered as?
Definitive or final host
39
Intermediate host of Taenia spp and Schistosoma spp.
Taenia spp. - Pigs or cattle | Schistosoma spp. - Snails
40
One in wc the parasite doesn't dev further to later stages
Paratenic host
41
The parasite remains alive and is able to infect another susceptible host
Paratenic host
42
What is an example of paratenic host?
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
43
What allows the parasite's life cycle to continue and become additional sources of human infection?
Reservoir host Pigs - B. coli Field rats - P. westermani Cats - B. malayi
44
In Falciparum malaria, possession of what confers some protection?
Sickle cell trait
45
What increases the susceptibility of an individual to Plasmodium vivax infections?
Presence of Duffy blood factor
46
What is not suitable for the development of intestinal protozoans?
Diet rich in protein
47
What favors the appearance of symptoms of amoebiasis and complications of the dse of high carb diet - favors the development of some tapeworms?
Low protein diet
48
What may be v impt in modifying the severity of dse in endemic areas?
Acquired immunity
49
What are the mechanisms by which parasites cause injury to the host?
(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
50
What allows the parasites to metabolize nutrients obtained from the host and store these for energy?
Secretory and excretory products
51
What parasite secretes cysteine proteinases wc digest cellular materials and degrade epithelial basement?
Trophozoites of E. histolytica
52
What invades RBCs, and after multiplication, the host's rbc rupture resulting in the release of merozoites?
Plasmodium
53
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?
Schistosoma japonicum
54
They have cutting plates wc cab attach to the intestinal mucosa and destroy the villi
Hookworms
55
Form tangled masses that can lead to intestinal obstruction and may invade other organs like appendix and bile ducts
Ascaris
56
What can cause massive intestinal bleeding wc results in chronic bld loss and IDA?
Heavy hookworm infxn
57
What parasite competes w its host for available supply of vit B12 that leads to Megaloblastic Anemia?
D. latum
58
What makes the helminthic parasites resistant to cytotoxic effects of both neutrophils and macrophages?
Their cuticle and integument
59
What can destroy non-human trypanosomes except Trypanosoma brucei wc has evolved resistance thru expression of serum resistance-associated protein?
Trypanolytic factors s/a apolipoprotein L-1 (APOL1)
60
What enables a non-human trypanosome (T. evansi) to infect human, and addition of recombinant APOL1 restored tryoanolytic activity?
A frameshift mutation in the APOL1 gene
61
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?
Protozoa and helminthic parasites
62
What reduce the immune fxn of macrophages that lower their capacity of phagocytosis? Also cause the defective processing of antigen (Immune suppression)
Plasmodium spp.
63
What can produce large amounts of surface glycoproteins? | Immune suppression
Trypanomastigotes
64
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)
Decrease lymphokines and immunoglobulin production
65
What parasite produces suppressor factor that can inhibit movement of monocytes to the site of invasion? (Immune suppression)
Entamoeba histolytica
66
Down-regulation of lymphocytes | Immune suppression
Fasciola spp.
67
Polyclonal hypergammaglobulinemia where Ab lack specificity against these parasites (Immune suppression)
W. bancrofti B. malayi Plasmodium spp.
68
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)
Necator americanus
69
Immune complexes produced in cysticercus cellulosae infxn supress inflammatory response thru inhibition of complement activity (Immune suppression)
Plasmodium spp. T. cruzi Schistosoma spp.
70
Antigenic variation
Trypanosoma gambiense and Giardia lamblia | Plasmodium falciparum
71
Parasites changes the antigenic profile off its surface coat --> variant surface glycoproteins (SVG) (Antigenic variation)
Trypanosoma gambiense and Giardia lamblia
72
They exhibit antigenic diversity | Antigenic variation
P. falciparum
73
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)
P. falciparum
74
These repeat sequences are Ag-ic epitopes, wc stimulate Ab prod. With variation, Ab fail to recognize the Ag (Antigenic variation)
P. falciparum
75
These can acquire antigenic mol from the host (host mimicry)
Larval stage of Echinococcus granulosus (hydatid cyst) | Tegument of Schistosoma spp. adult
76
Ab produced against the parasite fail to recognize nonself from self Ag
Host mimicry
77
This saves the parasite from splenic filtration and the action of Ab
Intracellular sequestration
78
Proliferate inside macrophages to escape the host immune response (Intracellular sequestration)
T. cruzi Leishmania spp. T. gondii - also in other nucleated cells
79
Sequestered from the circulation into the deep vasculature
P. falciparum (late intracellular stages)
80
Mediated by the presence of knobs on infected rbc that enable them to be attached to the endothelial cells of tiny capillaries
P. falciparum (late intracellular stages)
81
Its muscle arrangement is polymarian (numerous cells project well into the body cavity)
A. lumbricoides
82
Its color is whitish or pinkish And has a length of: 10-30cm (male) 22-35cm (female)
A. lumbricoides Parts: terminal mouth, 3 lips, sensory papillae
83
Difference between male and female A. lumbricoides
Males: ventrally curved posterior end with 2 spicules; single, long, tortois tubule Females: paired reproductive organs (posterior 2/3)
84
What does Ascaris produce that protects worms from digestion?
Pepsin inhibitor 3 (PI-3)
85
* 88-94 um by 39-44 um * Longer and narrower than fertile eggs * Thin shell and irregular mammilated coating filled w refractile granules
Infertile eggs (A. lumbricoides)
86
* 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
Fertile eggs (A. lumbricoides)
87
* 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
Embryonated egg (A. lumbricoides)
88
* Cuticular alar expansion at the anterior end * Prominent posterior esophageal bulb
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
Difference of femal and male adult E. verm
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
* 140-150 by 10 um * Characteristic esophageal bulb * No cuticular expansion on the anterior end
Rhabditiform larva of E. vem
91
* Asymmetrical * One side flattened, other side convex * 50-60 by 20-30 um (ave 55 by 36 um) * Translucent shell
Eggs of E. verm
92
What is the outer, triple albuminous covering of the eggs of E. verm for?
Mechanical protection
93
What is the inner, embryonic lipoidal membrane of the eggs of E. verm for?
Chemical protection
94
Its somatic muscle arrangement is holomyarian (small nucleus cells are closely packed in a narrow zone)
Trichuris trichiura
95
* 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
Adult T. trichiura
96
Male and female differences of T. trichiura
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
Soon after the embryonated eggs are ingested, the larvae escape and penetrate intestinal villi where they remain for 3-10 days
Trichuris trichiura larvae
98
* 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
Trichuris trichiura eggs
99
Somatic muscle arrangement: meromyarian (fewer cells 2-5 per dorsal or ventral half)
Ancylostoma duodenale
100
* 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
Adult Ancylostoma duodenale
101
* 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
Filariform larvae of Ancylostoma duodenale
102
* Bluntly rounded ends * Single transparent hyaline shell * Unsegmented at oviposition and in the 2- to 8-cell stages of division in fresh feces
Eggs of Ancylostoma duodenale
103
LC of Ascaris lumbricoides: When the eggs are ingested, where does larva hatch and penetrate?
Small intestine and penetrate to the intestinal wall
104
LC of Ascaris lumbricoides: What happens after they hatch and penetrate to the intestine?
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
LC of Ascaris lumbricoides: What happens after they hatch and penetrate to the intestine?
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
LC of Ascaris lumbricoides: What does larvae undergo before migrating to the larynx and oropharynx to be swalloew into digestive tract?
Molting
107
How many days is migration and molting phase in the lungs?
7-10 days
108
Prepatent period takes about how many days?
60-70 days
109
Bogitsh LC of Ascaris lumbricoides: When fertilized eggs are deposited, what happens to the zygote?
Uncleaved until the eggs reach soil
110
Bogitsh LC of Ascaris lumbricoides: Eggs deposited in soil are:
1) resistant to dessication | 2) very sensitive to environmental temperatures
111
Bogitsh LC of Ascaris lumbricoides: The zygote within the eggshell develops at what?
Soil temp (25°C) > body temp host (37°C)
112
Bogitsh LC of Ascaris lumbricoides: Development ceases at what temp?
15.5°C
113
Can eggs survive at temps more than slightly above 38°C?
Nope
114
After 2-4 wks in moist soil at optimal temp and O2 lvls, what happens to the embyro?
It molts at least once and develops to an infective second-stage larva
115
Bogitsh LC of Ascaris lumbricoides: Duodenum to heart that takes approx 1 week
Mucosal lining --> circulatory sys --> venous system --> liver --> right side of heart --> lungs (propelled by pulmo arterial flow)
116
The larvae remain in the lungs for several days, molting twice, and eventually rupture from the pulmonary capillaries to enter the?
Alveoli
117
Bogitsh LC of Ascaris lumbricoides: What is essential to the worms' survival in the small intestine? Those who undergo this develop to sexual maturity
Fourth molt
118
What is the interval from ingestion of infective eggs to the appearance of sexually mature worms in the smol intestine?
3 months
119
LC of E. verm: Where are adult worms found?
Ileum and cecum
120
LC of E. verm: Single female lays how many eggs per day?
4,672 to 16,888 eggs/day Ave: 11,105
121
LC of E. verm: Eggs on the perianal region become fully embryonated within how many hrs?
4-6 hrs
122
LC of E. verm: When ingested, eggs containing the 3rd stage larvae hatch where?
Duodenum, pass down the SI to the cecum, and develop into adults
123
What condition is more favorable for E. verm?
Moist (eggs remain viable for 13 days)
124
LC of T. trichiura: Embryonic development takes place outside the host when eggs are deposited in
Clayish soil
125
LC of T. trichiura An unhatched, infective, third-stage larva develops within
3-6 wks
126
LC of T. trichiura: Where does the larva hatch?
Upper portion of SI and quickly burrow into the cells of intestinal villi near the Crypts of Lieberkuhn
127
LC of hkworms: In the soil, embryo within the egg develops rapidly and hatches after 1-2 days into?
Rhabditiform larva
128
LC of hkworms: After 7-10 days, larva is tranformed into?
Non-feeding filariform larvae (infective)
129
LC of hkworms: Filariform larvae to SI
Filariform larvae --> skin --> venules --> heart --> lungs --> alveoli --> trachea --> swallowed --> SI
130
What are the clinical manifestations in Larval Stage of A. lumbricoides?
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
What are the clinical manifestations in Adult Stage of A. lumbricoides?
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
What are the clinical manifestations in Larval Stage of E. verm?
1. Pruritus 2. Insomnia - poor appetite - wt loss - irritability - grinding of teeth - abdominal pain
133
What are the clinical manifestations in Adult Stage of E. verm?
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
What are the clinical manifestations in Larval Stage of T. trichiura?
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
What are the clinical manifestations in Adult Stage of T. trichiura?
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
What are the clinical manifestations in Larval Stage of Ancylostoma duodenale?
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
What are the clinical manifestations in Adult Stage of A. duodenale?
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
What are the diagnostic procedures for A. lumbricoides?
1. DFS 2. Kato technique/cellophane smear mtd 3. Kato-katz technique
139
What is a quanti tech to make egg cts of parasite per gram of feces and to determine egg redxn rate after tx?
Kato-katz technique
140
What is a qualitative mtd recommended for mass examination of feces for diagnosis?
Kato-thick or cellophane smear mtd
141
What are the diagnostic procedures for T. trichiura?
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
Highly recommended in dx of trichuriasis | Useful in dx clinic px and mass exam in community surveys
Kato thick smear mtd
143
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
Kato-katz technique
144
What are the diagnostic procedures for Ancylostoma duodenale?
1. DFS 2. Kato technique or Kato-katz 3. Conc mtds (ZnSO4 centrifugal floatation and Formalin-ether) 4. Culture mtds (Harada-Mori)
145
What is the most effective time to intervene in the prevention of parasitic worm infxns?
When the infective stage of the worm is in the soil
146
S-shaped Buccal capsule has a ventral pair of semilunar cutting plate Bipartite (2 digits) Barbed Bristle-like copulatory bursa
N. americanus
147
C-shaped 2 pairs of teeth Tripartite (3 digits) Simple, not barbed copulatory bursa
A. duodenale
148
Tx for E. verm
Pyrantel pamoate | Mebendazole
149
Tx for T. trichiura
Mebendazole | Albendazole
150
Tx for Ascaris lumbricoides
Pyrantel pamoate Mebendazole Piperazine citrate (int obs)
151
Tx of Ancylostoma duodenale
Pyrantel pamoate | Mebendazole/albendazole
152
MOA of Mebendazole
Depolymerizing effect on microtubules
153
MOA of Pyrantel Pamoate
Neuromuscular blocking agent causing paralysis of the helminths; do not kill the parasite
154
MOA of Albendazole
Larvicidal agent (kills parasite)
155
What is the infective stage of Intestinal Taeniasis
Cysticerci Larvae
156
What is the common & largest Nematode?
A. lumbricoides
157
What is the longest tapeworm?
D. latum
158
Microcytic Anemia
A. duodenale
159
Cobalamin Deficiency
D. latum
160
Small, cylindrical, fusiform, grayish-white nematodes
N. americanus
161
True or false. N. americanus adult Females are larger then Males.
True. Female: 9-11mm by 0.35mm Male: 5-9mm by 0.30mm
162
Posterior end of a Male N. americanus
Broad, membranous caudal bursa with rib-like rays (used for copulation)
163
What is larger, A. duodenal or N. americanus?
A. duodenale
164
Buccal capsule of A. duodenale
2 pairs of curved ventral teeth
165
Which genital primordium is smaller, hkwrm or S. stercoralis?
Hookworms
166
Conspicuous transverse striations on the sheath in the tail region
N. americanus Filariform larvae
167
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)
Hookworm
168
Since filariform larva penetrate the skin and enter the venules, how to they go to the small intestine?
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
Pathology of Hookworm
1) skin 2) lungs - larval migration 3) small intestine - habitat
170
Clinical manifestations of hookworm
- 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
Results in a progressive, secondary, microcytic, hypochromic anemia of iron-deficient type, d/t continuous blood loss
Chronic moderate or heavy hookworm infxn
172
Diagnosis of hookworm
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
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Tx for hkwm Mass drug administration (once a yr)
Albendazole - single dose 400mg Mebendazole - 500mg Both these are benzimidazole derivatives that uptake of glucose by most intestinal and tissue nematodes
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Local distribution of human hkwm infxn is greater where?
Agricultural areas: Farmers (rice fields and veggie gardens) no proper protection against contact w infective soil
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Difference in the method of human infxn in Necatoriasis and Ancylostomiasis
Necatoriasis: percutaneous Ancylostomiasis: perc and oral route (eating raw vegetables w contaminated larva, or raw meat)
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Can infect humans causing “creeping eruption,” AKA cutaneous larva migrans
Ancylostoma braziliense (cat hkwm) Ancylostoma caninum (dog)
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T. saginata adult worm inhabits the upper jejunum and can live for up to how many yrs?
25 yrs
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Difference between parasite, predator, and scavenger
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
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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
Paratenic host
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Example of paratenic host
Paragonimus metacercaria in ras wild boar meat can pass thru the int wall of humans and complete its development.
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Period between infxn and evidence of symptoms
Clinical incubation pd
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Period between infxn or acquisition of parasite and evidence or demonstration of infxn
Pre-patent pd, AKA biological incubation pd
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Bullastra snails are associated with what infection?
Artyfechinostomum malayanum
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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.
Selective treatment
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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.
Targeted Tx
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is population-level deworming in which the community is treated irrespective of age, sex, infection status, or other social characteristics.
Universal Tx
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inability of the parasite to synthesize certain cellular components and the need of the parasite to obtain these from a host
Streamlining
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What does Ascaris produce that suppresses lymphocyte proliferation?
Phosphorylcholine
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● 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
phylum nematoda
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Epidemiologic triad
A harmful agent that comes into contact w a susceptible host in the proper environment
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E. verm bogitsh epidemiology
● 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.
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LC of E. verm (bogitsh)
● 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.
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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
granulomata
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E. verm diagnosis
● 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.
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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.
Trichuris trichiura
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LC of T. trichuria
● 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.
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They are believed to have a depolymerizing effect of cytoskeletal elements, such as microtubules.
T. trichiuria DOC Meb and Alb
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A. lum LC
● 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.
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Hkwm LC
● 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.
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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
Private practitioner
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Tx hkwms
● 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.
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,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.
public practitioner
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wellness plan for px
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
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further on antihelminthics
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.
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absorption, fate, excretion
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
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Therapeutic uses
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.