[DISCUSSION] MODULE 3 UNIT 2 AND UNIT 3 Flashcards
1
Q
The phylum Nematoda is divided into classes based on the presence or absence of “(?)’, which are caudal chemoreceptors.
A
phasmids
2
Q
The two (2) classes were earlier called Aphasmidia and Phasmidia, but now have been renamed as (?), respectively.
A
Adenophorea and Secernentea
3
Q
The origin of the name (Gr. trichos = hair + oura = the tail), is not quite correct because it is the (?) of the worm that is hair-like and not the tail.
A
anterior end
4
Q
Whipworm
A
A. Trichuris trichiura
5
Q
Infection is caused by ingestion of embryonated eggs.
A
A. Trichuris trichiura
6
Q
Eggs – hatch in the small intestine.
A
A. Trichuris trichiura
7
Q
larvae (L1) – released and penetrate the intestinal villi and undergo 4 molts in 3-10 days.
A
A. Trichuris trichiura
8
Q
young adult – passively migrate to the cecum (also in the ascending colon) and mature in about 2-3 months
A
A. Trichuris trichiura
9
Q
usually asymptomatic, except in heavy infection
A
Trichuriasis
10
Q
Heavily infected individuals - those with a high worm burden (greater than 200 worms, >5,000 EPG)- are most likely to
develop clinical disease.
A
Trichuriasis
11
Q
hypochromic, microcytic type
A
Iron-deficiency anemia
12
Q
results from chronic blood loss at the attachment site coupled with the long life span of the worms
A
Iron-deficiency anemia
13
Q
Small amounts of blood (0.005 ml per worm) are lost each day at the ulceration in the intestinal mucosa
A
Iron-deficiency anemia
14
Q
worm may be found even up to the rectum in heavy infection
A
Rectal prolapse
15
Q
mucosa of the rectum protrudes through the anal opening associated with the loss of muscle tone of the anus
A
Rectal prolapse
16
Q
Children with severe trichuriasis have:
o growth retardation
o impaired mental development
o cognitive function
A
Sever Trichuriasis
17
Q
Pudoc worm
A
B. Capillaria philippinensis
18
Q
In 1967, an epidemic of Capillariasis took place in
Pudoc West, Tagudin, Ilocos Sur
A
B. Capillaria philippinensis
19
Q
Infection is caused by ingestion of larvae in raw or
undercooked infected fish
A
B. Capillaria philippinensis
20
Q
larvae - develop into adults in the small intestine
(jejenum) where they burrow into the mucosa
A
B. Capillaria philippinensis
21
Q
Female worms - may produce two types of eggs:
o Unembryonated shelled eggs –
passed in the feces
o Embryonated eggs – hatches
within human host
A
B. Capillaria philippinensis
22
Q
larvae - will re-invade and cause autoinfection.
A
B. Capillaria philippinensis
23
Q
unembryonated eggs - ingested by fish when
passed into water.
A
B. Capillaria philippinensis
24
Q
malabsorption syndrome with severe diarrhea
A
Intestinal capillariasis
25
borborygmi (gurgling stomach)
Intestinal capillariasis
26
abdominal pain (can become serious if not treated
because of autoinfection)
Intestinal capillariasis
27
Capillary liver worm
C. Capillaria hepatica
28
The nematode (roundworm) Capillaria hepatica (=Calodium
hepaticum) causes hepatic capillariasis in humans.
C. Capillaria hepatica
29
Nomenclature varies in use globally and by discipline; Capillaria
hepatica is most frequently used in medical literature.
C. Capillaria hepatica
30
zoonotic parasite with a low host specificity
o primarily exists in rodent and carnivore hosts
o Both true and spurious infections occur in
humans
C. Capillaria hepatica
31
Infection is caused by ingestion of embryonated eggs in fecally-
contaminated food, water, or soil
C. Capillaria hepatica
32
Adult worms - are located deep within the liver parenchyma of
the host, and lay hundreds of eggs in the surrounding
parenchymal tissue.
C. Capillaria hepatica
33
eggs - trapped in the parenchyma; can not be passed in the feces
of the host, and remain in the liver until the animal dies, or more
likely, is eaten by a predator or scavenger
C. Capillaria hepatica
34
o Eggs ingested by scavengers are
unembryonated (not infectious) and are passed
in through the digestive tract into and out in
feces, providing an efficient mechanism to
release eggs back into the environment
C. Capillaria hepatica
35
o Eggs embryonate in the environment, where
they require air and damp soil to become
infective.
C. Capillaria hepatica
36
Under natural conditions, embryonation is slow and may take
between 6 weeks and 5 months.
C. Capillaria hepatica
37
The cycle continues when embryonated eggs are eaten by a
suitable mammalian host.
C. Capillaria hepatica
38
Infective eggs hatch in the intestine, releasing first stage larvae.
C. Capillaria hepatica
39
The larvae penetrate the intestinal wall and migrate via the portal
vein to the liver parenchyma within 3-4 days.
C. Capillaria hepatica
40
Larvae take about 3-4 weeks to mature into adults and mate.
C. Capillaria hepatica
41
rare in humans
Hepatic capillariasis
42
typically manifests as an acute or subacute hepatitis with:
o peripheral leukocytosis and eosinophili
o hepatomegaly
o persistent fever (which may be as high as 40°C)
Hepatic capillariasis
43
Trichina worm
D. Trichinella spiralis
44
The name Trichinella is derived from the minute size of the adult (Gr. trichos =hair, ella suffix for diminutive) and spiralis refers to the spirally coiled
appearance of larvae in muscles.
D. Trichinella spiralis
45
Infection is caused by ingestion of raw/rare or undercooked meat containing encysted larvae
D. Trichinella spiralis
46
Adult worms and encysted larvae develop within:
o 1 vertebrate host
o definitive host and potential intermediate host : infected animal
o A second host is required to perpetuate the life cycle of Trichinella.
D. Trichinella spiralis
47
domestic cycle
o pigs
o anthropophilic rodents
o other domestic animals
horses
D. Trichinella spiralis
48
sylvatic cycle
o bear
o moose
o wild boar
D. Trichinella spiralis
49
After exposure to gastric acid and pepsin, the larvae are released from the cysts (excystation) invade the small bowel mucosa, molt four times and
rapidly develop into adults, either male or female, by the 2nd day of infection.
D. Trichinella spiralis
50
Within 5 days, they become sexually mature
D. Trichinella spiralis
51
The male dies after fertilizing the female.
D. Trichinella spiralis
52
After 1 week of infection, the fertilized females release larvae.
D. Trichinella spiralis
53
Larvae continue to be discharged during the remaining part of the lifespan of the female worm, which ranges from 4 weeks to 4 months.
D. Trichinella spiralis
54
These larvae enter the intestinal lymphatics or mesenteric venules and are transported in circulation to different parts of the body.
o They get deposited in the muscles, central nervous system and other sites.
D. Trichinella spiralis
55
The larvae die in most other situations, except in the skeletal muscles, where they grow.
D. Trichinella spiralis
56
Within 20 days after entering the muscle cells, the larvae encyst within nurse cells.
D. Trichinella spiralis
57
Encysted larvae lie parallel to the muscles of host and can survive for months to years and eventually calcify and die.
D. Trichinella spiralis
58
In man, the life cycle ends here.
o Man is a dead-end host of the parasite, as the cysts in human muscles are unlikely to be eaten by another host.
D. Trichinella spiralis
59
Trichinella spiralis has an unusual life cycle in that the same individual animal serves as both definitive and intermediate host, adults and larvae
located in different organs.
D. Trichinella spiralis
60
autoheteroxenous parasite
D. Trichinella spiralis
61
Cysts develop preferentially in muscles relatively poor in glycogen and in hypoxic environment.
o Therefore, the biceps, deltoid, gastrocnemius, pectoralis, masseter, extraocular muscles, intercostal muscles and diaphragm, which
are constantly active, are the ones mostly affected.
D. Trichinella spiralis
62
- gastrointestinal symptoms
diarrhea
abdominal pain
vomiting
Intestinal phase
63
high fever
periorbital and facial edema
conjunctivitis
blurred vision
myalgias
splinter hemorrhages
rashes
peripheral eosinophilia lasting 1 month in heavy infection
Occasional life-threatening manifestations:
myocarditis
central nervous system involvement
pneumonitis
Migration phase
64
myalgia and weakness o followed by subsidence of symptoms
Larval encystment
65
abdominal tenderness and pain
weight loss
weakness
mucoid or bloody stool
A. Trichuris trichiura
66
Cosmopolitan
Tropical and subtropical countries with warm and moist soil.
A. Trichuris trichiura
67
Global
604 to 795 million
o Children
A. Trichuris trichiura
68
Phlippines
4.5 to 55.1%
o preschool children
8.1 to 57.9%
o school-age children
A. Trichuris trichiura
69
Natural host: Humans
A. Trichuris trichiura
70
morphologically similar worms are found to infect:
o pigs
o dogs
o some monkeys
A. Trichuris trichiura
71
At risk: ↑ children
A. Trichuris trichiura
72
Area: poor sanitation practices are common
o open defecation
o night soil as fertilizer
A. Trichuris trichiura
73
Mechanical vectors:
o House flies
o Cockroaches
A. Trichuris trichiura
74
Symptoms
severe protein-losing enteropathy and hypoalbuminemia
malabsorption of fats and sugars
decreased excretion of xylose
low serum potassium, sodium and calcium
high levels of IgE
Serious cases may be fatal in 2 weeks to 2 months.
B. Capillaria philippinensis
75
Endemic
o Ilocos Norte, Ilocos Sur, Cagayan, La Union, Pangasinan, Zambales, Agusan del Norte, Leyte
o More: Zamboanga del Norte
o Few:
Zamboanga del Sur
Agusan del Sur
Misamis Occidental.
B. Capillaria philippinensis
76
Twice as many males as females become infected.
B. Capillaria philippinensis
77
Males are mostly fishermen who partake of the days catch.
B. Capillaria philippinensis
78
Definitive host/Reservoir: Fish-eating birds
Intermediate host
o fresh or brackish water fish
B. Capillaria philippinensis
79
Migratory birds
o parasite is widely distributed throughout Asia and elsewhere
B. Capillaria philippinensis
80
deposition of eggs in the liver parenchyma causes:
o granuloma formation and liver necrosis, which in heavy infections can lead to potentially fatal liver dysfunction
C. Capillaria hepatica
81
Cosmopolitan in wildlife
o Human cases have originated from all inhabited continents except for Australia, although it exists in wildlife
C. Capillaria hepatica
82
The prevalence in humans may be underestimated due to the nonspecific clinical presentation and difficulty of diagnosis
C. Capillaria hepatica
83
Typical host: rodents such as rats
o has a low host specificity
C. Capillaria hepatica
84
Infections have also been identified in:
o wild and domestic carnivores o humans
C. Capillaria hepatica
85
contaminated food is ingested
human feces are not the source of contamination
feces of carnivores or flesh-eating rodents are involved
C. Capillaria hepatica
86
Other symptoms vary depending on the location and number of larvae present
D. Trichinella spiralis
87
Cosmopolitan
o most common in Europe and America
o rarely reported in the tropics
D. Trichinella spiralis
88
It occurs particularly in members of the meat-eating population but the prevalence is low
D. Trichinella spiralis
89
pig
deer
bear
walrus
rat
D. Trichinella spiralis
90
ingestion of contaminated pork scraps by pigs
D. Trichinella spiralis
91
ingestion of contaminated infected rats by pigs – ubiquitous in pig farms
D. Trichinella spiralis
92
ingestion of contaminated meat by other animals
D. Trichinella spiralis
93
ingestion of contaminated pork meat by humans
o Cooking meat to 60ºC or freezing (20 days in a normal freezer or at - 20°C for 3 days) will kill larvae.
o Smoking, salting or drying the meat does not destroy the infective larvae.
D. Trichinella spiralis
94
The Trichinella cycle that is maintained in nature occurs among cannibalistic and carrion-feeding carnivores
D. Trichinella spiralis
95
Giant intestinal worm
A. Ascaris lumbricoides
96
Infection is caused by ingestion of embryonated eggs.
A. Ascaris lumbricoides
97
Larvae invade the intestinal mucosa, and are carried via the portal, then systemic circulation on to the heart, then into the lungs
A. Ascaris lumbricoides
98
The larvae break out of the capillaries into the alveoli.
A. Ascaris lumbricoides
99
The larvae (L4s) mature further in the lungs (10-14 days), after a molt, penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed.
A. Ascaris lumbricoides
100
Upon reaching the small intestine, they develop into adult worms.
A. Ascaris lumbricoides
101
Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female.
A. Ascaris lumbricoides
102
Adult worms can live 1 to 2 years.
A. Ascaris lumbricoides
103
Unfertilized eggs may be ingested but are not infective.
A. Ascaris lumbricoides
104
Larvae develop to infectivity within fertile eggs after 18 days to several weeks, depending on the environmental conditions (optimum: moist, warm, shaded soil).
A. Ascaris lumbricoides
105
Clinical manifestations of ascariasis are caused by the (?) of the:
o Larvae
o adult worms in the small intestine
o wandering adult worms
pulmonary migratory phase
106
The (?) causes allergic reaction.
larval migration
107
The initial exposure to larvae during the (?) is usually asymptomatic, except when the larval load is heavy.
lung migration phase
108
asthmatic respiration
cough with bronchial rales
chest pain
A. Ascaris lumbricoides
109
These symptoms may be due to the petechial hemorrhages and massive destruction of the lung parenchyma as the larvae break through the capillaries on their way to the alveolar sacs, in massive infection, the hemorrhage may give rise to Ascaris pneumonitis.
A. Ascaris lumbricoides
110
The pulmonary clinical features subside in 1 or 2 weeks after infection. Due to (?) in the blood stream, the larvae may lodge in vital organs such as the brain and spinal cord, the eyeball and the kidney.
larval migration
111
Clinical manifestations due to adult worm vary from asymptomatic infection to severe and even fatal consequences.
A. Ascaris lumbricoides
112
The (?), when present, are caused by spoliative action, toxic action, mechanical effects and wandering effects
pathological effects
113
The adult worms in the lumen of the small intestine feed on the liquid nutrient in the intestinal fluids.
A. Ascaris lumbricoides
114
The nutritional effects are usually seen when there is heavy worm burden.
A. Ascaris lumbricoides
115
The worms interfere with proper digestion and absorption of food.
A. Ascaris lumbricoides
116
Ascariasis may contribute to protein-energy malnutrition and vitamin A deficiency.
A. Ascaris lumbricoides
117
The (?) are due to hypersensitivity to the worm antigens and may be manifested as fever, urticaria and edema.
toxic effects
118
Ascariasis may cause complications due to (?). Masses of worms (Ascaris bolus) may cause intestinal obstruction.
mechanical effect
119
(?) is a complication of ascariasis due to a few factors, e.g. fever, use of anesthesia during surgery, and worms seeking mates.
Ectopic migration
120
The worm may migrate up or down along the intestine.
o It may block the biliary or pancreatic ducts causing acute biliary obstruction or pancreatitis.
A. Ascaris lumbricoides
121
It may enter the liver parenchyma causing liver abscesses.
A. Ascaris lumbricoides
122
The worm may go up the esophagus and come out through the mouth, nose, or ears.
o It may obstruct the appendix causing appendicitis. It may lead to peritonitis when it perforates the intestine.
A. Ascaris lumbricoides
123
This tendency makes preoperative deworming necessary before gastrointestinal surgery in endemic areas. The wandering worm may also reach kidneys.
A. Ascaris lumbricoides
124
most common human helminthic infection
A. Ascaris lumbricoides
125
↑ tropical and subtropical regions o embryonated eggs
can survive in moist shaded soil for a few months to about 2 years in tropical and subtropical areas, but for much longer in temperate regions
A. Ascaris lumbricoides
126
inadequate sanitation
A. Ascaris lumbricoides
127
rare to absent in developed countries
A. Ascaris lumbricoides
128
sporadic cases may occur in rural, impoverished regions of those countries
A. Ascaris lumbricoides
129
Some cases in these areas where human transmission is negligible have direct epidemiologic associations to pig farms.
A. Ascaris lumbricoides
130
Global
billion
↑ children
co-exists with Trichuris trichiura
A. Ascaris lumbricoides
131
Phlippines
80-90%
Risk group: public elementary school children
A. Ascaris lumbricoides
132
Ascaris lumbricoides – humans
A. Ascaris lumbricoides
133
Ascaris suum – humans and pigs
A. Ascaris lumbricoides
134
Fecal-oral route
↑ children
Night-soil
House-flies and cockroaches
A. Ascaris lumbricoides
135
Resistance of Ascaris eggs to chemicals – lipid layer of their eggshell
o 2%
Formalin
potassium dichromate
o 50%
Hydrochloric
Nitric
Acetic
Sulfuric acid
A. Ascaris lumbricoides
136
Pinworm, seatworm
Former name: Oxyuris vermicularis
B. Enterobius vermicularis
137
Infection occurs from ingestion of infective eggs
B. Enterobius vermicularis
138
These eggs hatch in the small intestine, and the adults establish themselves in the colon, usually in the cecum
B. Enterobius vermicularis
139
The time interval from ingestion of infective eggs to oviposition by the adult females is about one month.
B. Enterobius vermicularis
140
At full maturity adult females measure 8-13 mm, and adult males 2-5 mm; the adult life span is about two months.
B. Enterobius vermicularis
141
Gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area.
B. Enterobius vermicularis
142
The larvae contained inside the eggs develop (the eggs become infective) in 4 to 6 hours under optimal conditions
B. Enterobius vermicularis
143
? – infected individuals may reinfect themselves
infective eggs are ingested via hand-to-mouth contamination due to scratching of perianal area with fingers → deposition of eggs under the nails.
o ↑ children
Autoinfection
144
eggs laid on the perianal skin immediately hatch into the infective stage larva and migrate through the anus → develop into worms in the cecum
Retroinfection
145
one-third are asymptomatic
Enterobiasis or oxyuriasis
146
worm produces intense itching of the perianal area (pruritus ani) and also the perineal area, when it crawls out of the anus to lay eggs
o scratching and irritation of the skin around the anus
o may give rise to secondary bacterial infection
o Children infected – insomnia due to the pruritus
Enterobiasis or oxyuriasis
147
poor appetite
weight loss
irritability
nocturnal enuresis (involuntary urination)
grinding of teeth
abdominal pain
B. Enterobius vermicularis
148
not associated with eosinophilia or with elevate lgE
B. Enterobius vermicularis
149
In female patients
worms may cause (?) when they crawl into the vulva and vagina causing irritation
ectopic migration
150
It may migrate up to the uterus and fallopian tubes
B. Enterobius vermicularis
151
This may cause symptoms of:
o Cervicitis o chronic salpingitis o peritonitis o recurrent urinary tract infections
B. Enterobius vermicularis
152
The worm is sometimes found in surgically removed appendix and has been claimed to be responsible for appendicitis.
B. Enterobius vermicularis
153
Cosmopolitan
o both temperate and tropical areas
B. Enterobius vermicularis
154
Global
↑ temperate regions and urban areas
Enterobiasis – most common helminth infection in the United States
B. Enterobius vermicularis
155
Phlippines
29% - schoolchildren from exclusive private schools
56% - public schools
16% - females
9% - males
B. Enterobius vermicularis
156
Natural host: Humans
B. Enterobius vermicularis
157
Rare: airborne – inhaled and swallowed
B. Enterobius vermicularis
158
anus-to-mouth
o contaminated fingers or other objects in the mouth
o inhalation of dust containing Enterobius eggs
B. Enterobius vermicularis
159
cool moist conditions – eggs remains viable for about 2 weeks
B. Enterobius vermicularis
160
warm, dry conditions – eggs begin to lose their infectivity within 2 days
B. Enterobius vermicularis
161
Factors:
Overcrowding
wearing soiled clothing
lack of adequate bathing and poor personal hygiene
o especially among young school-aged children
Finger sucking and nail biting
o may be sources of recurrent infection in children
sexual activity o oral and anal sex
extremely contagious and can easily spread among members of a family or in institutions o familial or a group disease
B. Enterobius vermicularis
162
Two (2) species of hookworms are human parasites:
Necator americanus - New world hookworm
Ancylostoma duodenale - Old world hookworm
C. Hookworms
163
Infection occurs from penetration of filariform larvae (L3) larvae
C. Hookworms
164
Infective stage are filariform larvae (L3) that penetrate the skin and are carried through the blood vessels to the heart and then to the lungs.
o penetrate into the pulmonary alveoli
o ascend the bronchial tree to the pharynx
o are swallowed o reach the jejunum of the small intestine
reside and mature into adults
C. Hookworms
165
Adult worms live in the lumen of the small intestine, typically the distal jejunum, where they attach to the intestinal wall by means of well-developed mouth parts (cutting plates in N. americanus and teeth in A. duodenale)
C. Hookworms
166
Eggs are passed in the stool, and under favorable conditions
C. Hookworms
167
Larvae hatch in 1 to 2 days and become free-living in contaminated soil.
o These released rhabditiform (L1) larvae grow in the feces and/or the soil, and after 5 to 10 days (and two molts) they become filariform (third-stage) larvae that are infective
C. Hookworms
168
Hookworm disease (?) manifests three main phases of pathogenesis
necatoriasis or ancylostomiasis
169
filariform larvae penetrate skin
the invasion or cutaneous period
170
do little damage to superficial layers, since they seem to slip unbroken skin through hair follicles, or pores
the invasion or cutaneous period
171
usual sites of infection:
o the dorsum of the feet or between the toe
o the hands, especially interdigital spaces
the invasion or cutaneous period
172
Once in the dermis, however, their attack on blood vessels initiates a tissue reaction.
the invasion or cutaneous period
173
If, as it usually happens, pyogenic bacteria are introduced into skin with the invading larva, a severe local itching known as ground itch, dew itch, or coolie itch will result
the invasion or cutaneous period
174
Erythematous papular rash develops when a large number of larvae penetrate the skin.
o This is a self-limiting condition, lasting for 2 to 4 weeks
the invasion or cutaneous period
175
larvae break out of the lung capillary bed into alveoli and progress up bronchi to the throat.
the migration or pulmonary phase
176
Each site hemorrhages slightly, with serious consequences in massive infections; however, very large numbers of larvae migrating through the lungs simultaneously are rare
the migration or pulmonary phase
177
The phase is usually asymptomatic, although there may be some dry coughing and sore throat.
the migration or pulmonary phase
178
A pneumonitis and Loeffler’s syndrome may occur in heavy larvae infection
the migration or pulmonary phase
179
Asymptomatic
the intestinal phase
180
Attachment of the worms to the mucosa with their strong buccal capsule and teeth or cutting plates may stimulate:
o Abdominal pain
o Nausea
o Anorexia
the intestinal phase
181
Adult worms suck blood aided by the anticoagulant that they secrete.
the intestinal phase
182
The worms change feeding sites and the old biting sites will continue to bleed.
the intestinal phase
183
Blood loss per worm is about 0.03 ml per day for N. americanus and about 0.15-0.25 ml per day for A. duodenale.
the intestinal phase
184
Thus, in heavy infection, a substantial amount of blood can be lost, and a severe iron-deficiency (microcytic, hypochromic) anemia may develop in a short time.
the intestinal phase
185
Nevertheless, a moderate hookworm infection will gradually produce an iron-deficiency anemia as body reserves of iron are used up
the intestinal phase
186
Patients have reported vague gastrointestinal disturbances and eosinophilia (sometimes referred to as Wakana syndrome) following peroral infection
the intestinal phase
187
Cosmopolitan
C. Hookworms
188
N. americanus – tropical Africa and the Americas
C. Hookworms
189
A. duodenale – Europe and Southwestern Asia
C. Hookworms
190
But now, both species have become widely distributed throughout the tropics and subtropics, and rigid demarcations are no longer present
C. Hookworms
191
Global
25%
C. Hookworms
192
Phlippines
5-45%
C. Hookworms
193
N. americanus – 97%
A. duodenale – 1%
mixed infections – 2%
C. Hookworms
194
Principal host: Humans
C. Hookworms
195
percutaneous transmission of filariform larvae from the soil
necatoriasis and ancylostomiasis
196
oral route
o eating raw vegetables contaminated with infective filariform larvae
o A. duodenale may remain dormant in the intestines or in the muscles, resulting in a prolonged incubation period and creating problems in treatment.
Transmammary
o larvae are able to pass into the mammary glands of the mother, so that the newborn baby can receive a large dose of infective larvae through its mother’s milk
o cases of heavy and sometimes fatal hookworm infections in children a month or so of age
ancylostomiasis
197
Ancylostoma caninum (dog hookworm)
Ancylostoma braziliense (cat hookworm)
D. Zoonotic hookworms
198
The larvae produce itching papules, which develop into serpigenous tracks in the epidermis called (?) or creeping eruption.
o These tracts can elongate by several centimeters a day; larvae can migrate for upto one year until they die, but the lesions usually heal spontaneously within weeks to months.
o Secondary pyogenic infection may occur at these sites.
cutaneous larva migrans (CLM)
199
Definitive host: dogs and cats
D. Zoonotic hookworms
200
Threadworm
o UK and Australia – pinworm or seatworm (Enterobius vermicularis)
E. Strongyloides stercoralis
201
Free-living cycle - Heterogonic cycle
Parasitic cycle - Homogonic
E. Strongyloides stercoralis
202
Rhabditiform larvae in the gut become infective filariform larvae that can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal and perineal area (external autoinfection).
Autoinfection
203
They ultimately enter the lymphatics or venules and are carried to the right heart and the lungs to complete the life cycle as earlier, or disseminate throughout the body
Autoinfection
204
benign and asymptomatic
Strongyloidiasis
205
only indications of infection
o Eosinophilia and larvae in stool
Strongyloidiasis
206
In immunocompromised individuals, it may cause clinical manifestations which may be severe and even fatal
Strongyloidiasis
207
filariform larvae may enter blood circulation and lodge in various organs, e.g. heart, lungs, brain, kidneys, pancreas, liver and lymph nodes
Disseminated strongyloidiasis
208
- dermatitis, with erythema and itching at the site of penetration of the filariform larva, particularly when large numbers of larvae enter the skin
Cutaneous manifestations
209
- larva currens (meaning racing larvae) has been applied to the rapidly progressing linear or serpiginous urticarial tracks caused by migrating filariform larvae
Cutaneous manifestations
210
- often follow autoinfection and start perianally
Cutaneous manifestations
211
- This rash usually advances very rapidly (up to 10 cm/hr)
Cutaneous manifestations
212
- When the larva escape from the pulmonary capillaries into the alveoli, small hemorrhages may occur in the alveoli and bronchioles.
Pneumonia and Loeffler's syndrome may be present in some patients.
Pulmonary manifestations
213
- This may present as malabsorption syndrome.
Diarrhea is often present.
Intestinal manifestations
214
- In heavy infection, there may be extensive sloughing of the intestinal mucosa.
Intestinal manifestations
215
internal autoinfection in immunocompromised
Hyperinfection
216
large number of worms in the intestine and lungs
individuals
217
Other manifestations include:
o protein losing enteropathy
o paralytic ileus
E. Strongyloides stercoralis
218
Clinical manifestations depend on the sites affected:
o Brain abscess
o meningitis and peritonitis
E. Strongyloides stercoralis
219
Cosmopolitan
o tropics and subtropics
o Europe and the USA
o follows a distribution pattern similar to hookworm
E. Strongyloides stercoralis
220
Global
Unknown
Estimate: 30–100 million
E. Strongyloides stercoralis
221
Phlippines
relatively rare
E. Strongyloides stercoralis
222
Host
Humans
E. Strongyloides stercoralis
223
Rarer human-infecting species of Strongyloides zoonotics:
o S. fuelleborni (fülleborni) subsp. fuelleborni
o S. fuelleborni subsp. kellyi
E. Strongyloides stercoralis
224
direct contact with soil contaminated by Strongyloides larvae
E. Strongyloides stercoralis
225
area: poor sanitation
o feces are disposed in the warm moist soil
o provide an optimal atmosphere for the organism to exist
E. Strongyloides stercoralis
226
allows for maintenance of the parasite within the host for years following the initial exposure
Autoinfection
227
Toxocara canis - dog ascarid
Toxocara cati - cat ascarid
F. Toxocara spp.
228
Ingesting infective eggs or undercooked meat/viscera of infected paratenic hosts
F. Toxocara spp.
229
Humans are accidental hosts
F. Toxocara spp.
230
eggs hatch
F. Toxocara spp.
231
larvae penetrate the intestinal wall and are carried by the circulation to a variety of tissues (liver, heart, lungs, brain, muscle, eyes)
F. Toxocara spp.
232
Toxocara spp. can follow a [?] (one host) or [?] (multiple host) life cycle.
direct
indirect
233
Unembryonated eggs are shed in the feces of the definitive host.
F. Toxocara spp.
234
Eggs embryonate over a period of 1 to 4 weeks in the environment and become infective, containing thirdstage (L3) larvae.
F. Toxocara spp.
235
Following ingestion by a definitive host, the infective eggs hatch and larvae penetrate the gut wall
F. Toxocara spp.
236
In younger dogs (T. canis) and in cats (T. cati):
the larvae migrate through the lungs, bronchial tree, and esophagus, where they are coughed up swallowed into the gastrointestinal tract
adult worms develop and oviposit in the small intestine
direct (one host)
237
In older dogs, patent (egg-producing) infections can also occur
larvae more commonly become arrested in tissues
Arrested larvae are reactivated in female dogs during late gestation and may infect pups by the transplacental (major) and transmammary (minor) routes in whose small intestine adult worms become established
direct (one host)
238
In cats, T. cati:
larvae can be transmitted via the transmammary route to kittens if the dam is infected during gestation
somatic larval arrest and reactivation does not appear to be important as in T. canis
direct (one host)
239
ingestion of paratenic hosts
indirect (multiple host)
240
Eggs ingested by suitable paratenic hosts hatch and larvae penetrate the gut wall and migrate into various tissues where they encyst
indirect (multiple host)
241
The life cycle is completed when definitive hosts consume larvae within paratenic host tissue, and the larvae develop into adult worms in the small intestine
indirect (multiple host)
242
preschool children
visceral larva migrans (VLM)
243
larvae invade multiple tissues
o commonly liver
o lung
o skeletal muscle
o occasionally heart
visceral larva migrans (VLM)
244
cause various nonspecific symptoms
o fever
o myalgia
o weight los
o cough
o rashes
o hepatosplenomegaly
usually accompanied by hypereosinophilia
visceral larva migrans (VLM)
245
Migration to the central nervous system
neurotoxocariasis or neural larva migrans
246
Uncommon
neurotoxocariasis or neural larva migrans
247
eosinophilic meningoencephalitis
neurotoxocariasis or neural larva migrans
248
Death
o severe cardiac
o pulmonary
o neurologic involvement
neurotoxocariasis or neural larva migrans
249
larvae produce various ophthalmologic lesions
(OLM)
250
may cause diffuse unilateral subacute neuroretinitis (DUSN)
o unilateral (affecting one eye) involvement
(OLM)
251
associated visual impairment usually presents with
uveitis, retinitis, or endophthalmitis
permanent visual damage or blindness
F. Toxocara spp.
252
associated larval granulomas
misdiagnosed as retinoblastoma
F. Toxocara spp.
253
Cosmopolitan
o among domestic dogs and cats
F. Toxocara spp.
254
both animals and people
o ↑ developing countries
F. Toxocara spp.
255
people of lower socioeconomic strata
o ↑ developed countries
F. Toxocara spp.
256
Public places: 10-30%
F. Toxocara spp.
257
western countries: 25% to 30 to 60% (dogs)
F. Toxocara spp.
258
Accidental hosts: Humans
F. Toxocara spp.
259
all wild and domestic canids
puppies
o patent infections
Toxocara canis
260
wild and domestic felids of all ages
kittens
o patent infections
Toxocara cati
261
Paratenic hosts: mammals and birds; livestock
Paratenic or transport hosts: Cockroaches and earthworms
F. Toxocara spp.
262
soil-transmitted zoonosis
Human toxocariasis
263
↑ children living in homes and in neighborhoods where dogs and puppies are not dewormed o tendency to play in soil o geophagia or soil eating
Human toxocariasis
264
Poor personal hygiene
Human toxocariasis
265
consumption of inadequately washed vegetables chronic low-dose infections
Human toxocariasis
266
consumption of undercooked beef, lamb, chicken, and duck meat (particularly liver)
Human toxocariasis
