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HOOKWORM
Kingdom : Animalia
ANCYLOSTOMA DUODENALE Phylum : Nematoda
Class : Secernentea
NECATOR AMERICANUS Order : Strongiloidae
STRONGYLOIDES STERCORALIS Family : Ancylostomatidae
Genus : Necator/Ancylostoma
Species : Necator americanus (Charles W. Stiles, 1898)
Ancylostoma duodenale (Angelo Dubini, 1838)

§ Disease : Ancylostomiasis
ü Ancylostoma duodenale
Sukmawati Basuki ü Necator americanus
ü Attach to the small intestine è suck blood and protein è anaemia
ü A. duodenale : southern Europe, the north coast of Africa, nothern
Department of Parasitology, Faculty of Medicine India, northern China, Japan
Universitas Airlangga, Surabaya ü N. americanus : western, central, and southern Africa, southern
2020 Asia, Melanesia, Polynesia, Indonesia

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TYPE 3 : Penetration of the skin

HOOKWORMS

[WHO, 2010]
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Hookworm larvae
Hookworm egg

• Ovoid with thin, smooth eggshell

• Contain 2-16 cells (early in mitosis)
• Size : 55-75 μm x 35-40 μm

Sukmab,2017 Sukmab,2017
Hookworm larvae Hookworm larvae compared with others

Ad: Ancylostoma duodenale Na: Necator americanus

To: Trichostrongylus species Ss: Strongyloides stercoralis
Rh: Rhabditis species Td: Ternidens deminutus
Osp: Oesophagostomum species

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Hookworm adults
Hookworm adult
HOOKWORMS
A. duodenale N. americanus
ü A small cylindris white, grey or ü More slender [0.9-1.1 x 0.4 cm]
reddish worm
ü A buccal capsule containing two pairs ü Smaller containing cutting plates
of teeth instead of teeth
5-9 1 cm ü Male : 0.8-1.1 x 0.4-0.5 cm, a
mm copulatory bursa at the rear end, an
umbrella-like expansion of the cuticle
ü Female : 1-1.3 x 0.6 cm, occupied by ü The vulva in the anterior third of the
the ovary and coiled uterine tubes body
packed with eggs, the vulva in the
posterior third of the body
ü Max. egg output : 15-18 months after ü Slightly larger [64-75 x 36-40 um],
infection, 25-35,000 eggs/day, 50-60 x 6,000-20,000 eggs/day, life duration
35-40 um, elliptical shape, a on average of 5 years
transparent shell, 2-4 segmented
[blastomere], life duration on average
of 6 years

Sukmab,2017 Sukmab,2017
LIFE CYCLE

HOOKWORMS
Life cycle :

Eggs [2,4-8 blastomeres] in the lumen of the intestine è faeces è damp

shaded soil è hatch into rhabditiform [first stage/L1] larvae [free living, a
bulboesophagus, feed avidly on bacteria], moults on the third day, the
oesophagus disappears on the fifth day – elongated, fully developed at 20-
30°C [a simple muscular oesophagus, a protective sheath] : filariform –
move towards O2 [can not survive in water], numerous in the upper 2.5 cm
of soil, can live in warm damp soil for 2 years [fatal : direct sunlight,
drying, salt water] è a filariform larva [third stage/L3] contacts the skin,
penetrates, enters the bloodstream è lungs on the third day è alveoli –
bronchioles – trachea – oesophagus – the stomach – the small intestine on
the seventh day, a fourth moult [L4], attached by buccal capsule [during
migration : third moult – buccal capsule is formed] è mature in 3-5 weeks,
live for 1-9 years, produces eggs

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Sukmab,2017 Sukmab,2017
TYPE 3 : Penetration of the skin Pathology

HOOKWORMS HOOKWORMS
Life cycle :

v A. duodenale can infect by ingestion and via skin

v N. americanus infects only through the skin
v Migrating larvae of N. americanus grow and develop in the lungs, but A.
duodenale do not [for many months to be adult]

Transmission :
ü As above
ü Filariform larvae of A. duodenale are excreted in milk, and infect the child,
while larvae of N. americanus have been found in milk and the child has
not yet been found.

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TYPE 3 : Penetration of the skin TYPE 3 : Penetration of the skin

HOOKWORMS HOOKWORMS
Pathology : Pathological anatomy :

Three stages [the first two caused by larval hookworms]
1.Vesiculation and pustulation at the site of entry [ground itch]
2.Asthma and bronchitis, with small haemorrhages, eosinophilic and
leucocytic infiltration
3.Established infection è hookworm anaemia and hookworm disease
Hookworm anaemia è hypochromic anaemia [blood loss = 0.03 ml/worm
N. americanus, and 0.15 ml/worm A. duodenale, worm loads of 500-1000,
depletion of iron stores, deficiency of iron intake, a folate deficiency ±]
Hypoproteinaemia è protein-losing enteropathy [excess of the red cell loss,
limited capacity for albumin synthesis]
Hookworm enteropathy è hypoalbuminaemia
A minute wound in the centre of of each extravasation – worm attachment
[anticoagulant è move spot to spot, damage é, blood loss]
Immunity :
üNo evidence of protective immunity against N. americanus infection
üPrimary infection : fever, eosinophilia, moderate anaemia
Clinical features :
üNatural history – anaemia
ü Incubation period : in larval symptoms appear 1-2 weeks after primary
infection, in established infection eggs appear from the 42 day onwards
üSymptoms and signs : ground itch, vesicular rash, 1-2 weeks – pulmonary
symptoms [a dry cough, asthmatic wheezing], fever, eosinophilia é,
gradually disappear, ova can be seen [42-day infection] : self-limiting

Sukmab,2016 Sukmab,2017
TYPE 3 : Penetration of the skin TYPE 3 : Penetration of the skin

HOOKWORMS HOOKWORMS
Differential diagnosis:
ØLight infection [moderate eosonophilia, mild anaemia] : Schistosoma, F. Geohelminths Control :
hepatica, other liver flukes, Strongyloides ü Chemotherapy
ØSevere hookworm anaemia : anasarca kwashiorkor, nephrotic syndrome ü Sanitation
ü Health education
Diagnosis : ü Community participation
§ Eggs in stool ü Monitoring and evaluation
§ Rhabditiform larvae in stale stool

Therapy :
§Albendazole [the drug of choice] : 400 mg, a single dose – against the adult
worms, or N. americanus larva [80% reduction in egg], 200 mg/day for 3
days [100% cure]
§Mebendazole : 500 mg, a single dose – A. duodenale + N. americanus
§Levamisole : 2.5 mg/kg, 150 mg [a single dose] – N. americanus
§Pyrantel palmoate : 10 mg/kg, a single dose
§Ferrous sulphate or gluconate : 200 mg. 3 times in a day – 3 months
§Parenteral iron

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STRONGYLOIDES STERCORALIS STRONGYLOIDES STERCORALIS

(Bavay, 1876; Stiles et Hassall, 1902) ü The genus Strongyloides contains 53 species.

ü Strongyloidiasis is caused by 2 species of the intestinal nematode

ü S. stercoralis
Kingdom : Animalia ü S. fuelleborni, is found sporadically in Africa and Papua New Guinea
Phylum : Nematoda
ü S. stercoralis was first reported in 1876 in the stools of French soldiers on
Class : Secernentea duty in Vietnam who had severe diarrhea, and the disease the organism
Order : Rhabditida produces was known for many years as Cochin-China diarrhea
Family : Strongyloididae
Genus : Strongyloides ü Strongyloidiasis affects anywhere from 30 to 100 million people
Species : Strongyloides Worldwide, and is endemic in Southeast Asia, Latin America, sub-
Saharan Africa, and parts of the southeastern United States
stercoralis
ü S. stercoralis has a complex life cycle in which parthenogenetic females
Disease : Strongyloidiasis (i.e., capable of reproducing without males) embedded in the intestinal
mucosa lay embryonated eggs that hatch internally

Sukmab,2017 Sukmab,2017
TYPE 3 : Penetration of the skin
Geographic distribution of Strongyloidiasis

STRONGYLOIDES STERCORALIS

[WGO, 2004]
[Afzal A. Siddiqui and Steven L. Berk, 2001]

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STRONGYLOIDES STERCORALIS STRONGYLOIDES STERCORALIS

Rhabditiform larvae Filariform larvae posterior part
Filariform larva with notched tail.
• 220 x 15 um.
• Short buccal cavity. Infective stage
Size 600 x 20 um.
• Diagnostic stage
• appear in stools within 4 weeks of infection.

Sukmab,2017 Sukmab,2017

STRONGYLOIDES STERCORALIS

a)

b)

Parasitic female:
- 2.2 mm in length
c) - Cylindrical oesophagus (1/3 body length)
- Posterior end straight

Free living female:

a) parasitic female - 1 mm in length
- rhabditiform oesophagus
b) free-living male - posterior end straight
c) free-living female

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Rhabditiform
larvae

Hookworm and Strongyloides Larvae [ Adapted from Melvin, Brooke, and Sadun,1959]

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STRONGYLOIDES STERCORALIS

[James B. Lok, 2007]

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Pathology TYPE 3 : Penetration of the skin

STRONGYLOIDES STERCORALIS STRONGYLOIDES STERCORALIS

Clinical pathology
Ø Chronic infections with S. stercoralis can be clinically inapparent or can lead to
cutaneous, gastrointestinal, or pulmonary symptoms

Ø Skin involvement is characterized by a migratory, serpiginous, urticarial rash,

termed larva currens.
Ø Gastrointestinal symptoms of strongyloidiasis include diarrhea, abdominal
discomfort, nausea, and anorexia
Ø The symptoms of pulmonary strongyloidiasis (hyperinfection) include cough
and shortness of breath

Ø In hyperinfection and dissemination, complete disruption of the mucosal patterns,

ulcerations, and paralytic ileus have been observed. In the presence of
dissemination, pulmonary involvement may be heralded by bilateral edema and
patchy, often rapidly changing infiltrates

Ø Massive secondary bacterial infections are frequently the immediate cause of death
in patients with the hyperinfection syndrome

Sukmab,2017 Sukmab,2017

Clinical pathology

• Larva currens (most characteristic sign)

TERMINOLOGY • Itch (usually on feet)
Acute • Wheezing/cough/low grade fever
• Epigastric tenderness
“Autoinfection": the process that enables the parasite to survive very long in the • Diarrhea/nausea/vomiting
human host; mostly asymptomatically. The intestinal mucosa (internal • Larva currens (most characteristic sign)
autoinfection) or the skin of the perianal area (external autoinfection) • Epigastric tenderness
• Asymptomatic/vague abdominal complaints
Chronic (usually the result of auto-
"Hyper-infection": the process of intense auto-infection; the phase in which third • Intermittent diarrhea (alternating with constipation)
infection)
• Occasional nausea and vomiting
stage larvae can be found in fresh stools
• Weight loss (if heavier infestation)
• Recurrent skin rashes (chronic urticaria)
"Disseminated infection”: the outcome of hyperinfection: larvae can be found
anywhere, particularly in sputum and skin • Insidious onset
• Diarrhea (occasionally bloody)
• Severe abdominal pain, nausea and vomiting
Severe(usually as a result of hyper or
• Cough, wheezing, respiratory distress
disseminated infection)
• Stiff neck, headache,confusion (meningismus)
• Skin rash (petechiae, purpura)
• Fever, chills

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STRONGYLOIDES STERCORALIS STRONGYLOIDES STERCORALIS

Ø The term “hyperinfection” is often used to denote autoinfection, a phenomenon in DIAGNOSIS
which the number of worms increases tremendously and the worms are detectable in
extraintestinal regions, especially the lungs. ü A number of techniques have been used to discern larvae in stool samples, including direct
Ø HIV/AIDS smear of feces in saline–Lugol iodine stain, Baermann concentration, formalin-ethyl acetate
Ø Immunosuppressive drugs / disease concentration, Harada-Mori filter paper culture, and nutrient agar plate cultures.

ü The Baermann method and the Harada-Mori filter paper capitalize on the ability of S. stercoralis
Ø The term “disseminated” is usually restricted to infections in which worms are found to enter a free-living cycle of development. These methods are much more sensitive than single
in ectopic sites (e.g., the brain) stool-smears, but they are rarely standard procedures in clinical parasitology laboratories

DIAGNOSIS ü Microscopic examination of a single specimen of duodenal fluid was found to be more sensitive
than wet mount analysis of stools samples for the detection of larvae
Ø The diagnosis of strongyloidiasis should be suspected if there are clinical signs and
ü Also, in some cases, histological examination of duodenal or jejunal biopsy specimens may
symptoms, eosinophilia, or suggestive serologic findings
reveal S. stercoralis embedded in the mucosa
Ø Definitive diagnosis of strongyloidiasis is usually made on the basis of detection of
ü The larvae can be identified in wet preparations of sputum, bronchoalveolar lavage fluid,
larvae in the stool. In more than two-thirds of cases, there are 25 larvae per gram of bronchial washings and brushings, lung biopsies, or examination of pleural fluid by means of
stool. a single stool examination fails to detect larvae in up to 70% of cases. Gram, Papanicolaou, or acid-fast (auramine O and Kinyoun) staining procedures.
diagnostic sensitivity increases to 50% with 3 stool examinations and can approach
100% if 7 serial stool samples are examined.

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TYPE 3 : Penetration of the skin TYPE 3 : Penetration of the skin

STRONGYLOIDES STERCORALIS STRONGYLOIDES STERCORALIS

Figure 2. Different diagnostic staining and culture
procedures for the detection of S. stercoralis larvae.
DIFFERENTIAL DIAGNOSIS
[A] Lugol iodine staining of the rhabditiform larva in stool. This is
the most commonly used procedure in clinical microbiology
laboratories. A single stool examination detects larvae in only 30%
of cases of infection. Scale barp25 mm. [B] Human fecal smear There are many conditions producing similar symptoms - Consider:
stained with auramine O, showing orange-yellow fluorescence
of the rhabditiform larva under ultraviolet light. Routine acid-fast
staining of sputum, other respiratory tract secretions (e.g., bronchial
• Intestinal Infections (amebiasis, bacterial colitis, shigella,
washings), and stool may also serve as a useful screening campylobacter, yersinia, clostridium difficile)
procedure. Scale barp25 mm. [C] Agar plate culture method.
• Inflammatory bowel disease
Motile rhabditiform larvae and characteristic tracks or furrows,
which are made by larvae on the agar around the stool sample. This • Irritable bowel syndrome
diagnostic method is laborious and time-consuming (2–3 days) but • Functional abdominal disorders
is more sensitive than other procedures (e.g., wet mount analysis)
for the detection of larvae in feces. Tracks are marked (arrows and • Drugs (NSAIDS, gold)
T). S, stool sample on agar plate; L, larva or larvae. Scale barp250
mm. [D] Gram stain demonstrating S. stercoralis filariform larvae
(FL). Gram staining of a sputum sample is an excellent tool for
diagnosing pulmonary strongyloidiasis. Scale barp250 mm.

[Afzal A. Siddiqui and Steven L. Berk, 2001]

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STRONGYLOIDES STERCORALIS STRONGYLOIDES STERCORALIS

THERAPY PREVENTION

ü In S. stercoralis, however, only complete eradication of parasites removes the
danger of potentially serious disease—that is, any truly effective anthelmintic
must kill every autoinfective L3 larvae, which are relatively resistant to chemical
agents.
ü Thiabendazole has been the drug of choice for the treatment of strongyloidiasis.
ü Ivermectin is the best drug for the treatment of uncomplicated S. stercoralis
infection. Ivermectin has been found to be the most effective drug in treating
disseminated strongyloidiasis in patients with chronic intestinal disease,
including children and adults. Recently, ivermectin has also been registered as
the drug of choice in the World Health Organization’s list of essential drugs for
the treatment of S. stercoralis.
• The ideal method would be prevention by improved sanitation
(proper disposal of feces), practicing good hygiene (washing of
hands), etc..
• Stay away from moist soil, do not work or play with
contaminated water/soil.
• Avoid direct skin contact with soil containing infective larvae.
People at risk - especially children - should wear footwear
when walking on areas with infected soil.
• No accepted prophylactic regimen exists and no vaccine is
available

ü Other drugs, such as mebendazole and albendazole, have had variable

therapeutic efficacy.

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PARATENESIS (Beaver, 1969)

ü When the effective stages of the parasite accidently enter

hosts other than natural definitive hosts.
ü In these non natural hosts, the larvae migrate through the
tissues without undergoing development and eventually
encapsulate, remaining indefinitely as infective larvae in the
tissues.
ü No transformation of the larvae occurs
ü Paratenic host CUTANEOUS LARVA MIGRANS

INTERMEDIATE HOST Sukmawati Basuki

ü Obligatory hosts in which the larvae change and grow into

the infective stage for the definitive hosts Department of Parasitology, Faculty of Medicine
Universitas Airlangga, Surabaya
2020

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CUTANEOUS LARVA MIGRANS

[creeping eruption, sandworm, plumbers itch, duckhunter’s itch]

A syndrome, while creeping eruption is a clinical sign è a linear or serpiginous, slightly

elevated, erythematous track that moves forward in the skin in an irregular pattern

A cutaneous eruption resulting from exposure of the skin to the effective filariform larvae
of non-human hookworm : A. braziliense, A. caninum

Distribution : in most warm, humid, tropical and sub-tropical area

A. braziliense :
ü Dogs and cats
ü Smaller than A. duodenale [female: 1 cm, male: 8.5 mm]
ü Ventral teeth are smaller
ü The dorsal rays in the copulatory bursa are distinctive
ü Life cycle is similar to A. duodenale
ü The third-stage larva does not enter the bloodstream

A. caninum : dog hookworm, similar to A. duodenale

DD : filariform larva of S. stercoralis – autoinfection [larva currens]

[Byron Blagburn, 2010]

Sukmab,2017 Sukmab,2017

CUTANEOUS LARVA MIGRANS CUTANEOUS LARVA MIGRANS

[creeping eruption, sandworm, plumbers itch, duckhunter’s itch] [creeping eruption, sandworm, plumbers itch, duckhunter’s itch]

Biology :
Ø Adult hookworms live in the intestine of dogs and cats.
Ø Eggs are shed in feces, hatch in the superficial layer of the soil
within one day, and develop into third-stage larvae after about
one week.
Ø In favorable environmental conditions, larvae can survive and
remain infective for several months.
Ø After having located a host, larvae creep across the skin and
probe sites suitable for penetration into the epidermis.
Ø Animal hookworm larvae can not penetrate the basal membrane
of human skin è they are unable to develop and complete their
lifecycle, as they would do in an appropriate animal host è
human beings are a dead end for the parasite è a self-limiting
disease
Pathology :
Ø unable to penetrate below the stratum greminativum, the stratum
granolusum as a roof, local eosinophilia, cell infiltration – for
months
Ø rarely reach the lungs
Ø does not mature in the intestine
Ø Incubation period : immediately [a few hours]
Ø Symptoms and signs : a red itchy papule – elevated – vesicular,
move several mm to a few cm / day, intense pruritus, skin is
scratched – secondary infection è hand and feet
Therapy :
ü Albendazole : 400 mg, a single dose [46-100% cure]
ü Ivermectin : 12 mg, a single dose [81-100% cure]- drug of choice
ü Topical thiabendazole

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CUTANEOUS LARVA MIGRANS

[creeping eruption, sandworm, plumbers itch, duckhunter’s itch]

Epidemiology and Control :

Ø Soil contaminated with dog and cat faeces, wearing sandals and
gloves
Ø The risk of infestation may be 15 times higher in the rainy season
compared to the dry season
Ø Agricultural occupations may increase the risk for infestation
Ø Larvae may be transmitted through fomites VISCERAL LARVA MIGRANS
Differential diagnosis :

Scabies, loiasis, myiasis, cercarial dermatitis (schistosomiasis), tinea Sukmawati Basuki

corporis, and contact dermatitis
Department of Parasitology, Faculty of Medicine
Universitas Airlangga, Surabaya
2020

Sukmab,2017 Sukmab,2017
TOXOCARA CANIS, TOXOCARA CATI
CLASSIFICATION
ü Disease : Toxocariasis
ü Prevalence of infection in dogs – 25% : western countries (Barriga,
Kingdom : Animalia
Phylum : Nematoda 1988), in cats – 30-60% : France (Petithory et al, 1996)
Class : Secernentea ü Human acquire the infection by ingesting infective eggs in soil [STH]
Order : Ascaridida
ü Tropical and subtropical countries
Family : Toxocaridae
Genus : Toxocara ü Risk factors : urban children - geophagia - having a litter of puppies
Species : T. canis (Werner, 1782) at home [more dogs per square mile and less space
T. cati (Schrank, 1788)
for them to defecate]
ü Zoonosis : consumption of raw meat from potential paratenic hosts
(chickens, lambs, rabbits), of raw vegetables
ü Seroprevalence of human toxocariasis : 2-5% in healthy persons in
Western countries, 63.2% in Bali, 86% in children in West Indies,
92.8% in adults in La Reunion

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MORPHOLOGY
DISTRIBUTION OF TOXOCARIASIS
EGG
• oval or spherical shapes with
granulated surfaces,
• thick-walled,
• T. canis : 85µm by 75µm
• T. cati : 65µm by 70µm

ADULT WORM

• Yellow cuticula.
• Two lateral alae (length 2–3.5
mm, width 0.1 mm)
• Male worms measure 9–13 by
0.2–0.25 cm, spicules : 1.7 to
1.9 mm in length (posterior)
• Female worms 10–18 by 0.25–
0.3 cm

Sukmab,2017 Sukmab,2017
MORPHOLOGY

[Byron Blagburn, 2010]

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(Dickson Despommier, 2003)

Sukmab,2017 Sukmab,2017

PATHOGENESIS
ü The hatched larvae have been found in the liver, lungs, heart, eye,
brain, and muscles - migratory tracks characterized by hemorrhage,
necrosis, and inflammation, with eosinophils predominating
ü Larvae è encapsulated within granulomas where they are either
destroyed or persist in aviable state for many years
ü Eye è the migration of a single larva – be observed è
inflammatory response è partial or total retinal detachment with
visual loss
ü The larval excretory-secretory antigens (TES-Ag) : released by larvae
from their epicuticle
CLINICAL FEATURES
1. Acute signs (hepatic and pulmonary larval migration) : abdominal pain,
decreased appetite, restlessness, fever, coughing, wheezing, asthma, and
hepatomegaly
A marked eosinophilia (>2,000 cells/mm3), leukocytosis, and
hypergammaglobulinemia
2. Ocular larva migrans : unilateral in children and young adults è visual loss
Funduscopy and biomicroscopic examination : uveitis, endophthalmitis,
papillitis (Gass and Braunstein, 1983), retinal granulomatous lesions
(Gillespie et al., 1993), or inflammatory masses (snow-banks) in the
peripheral vitreous
ü routine eye examination
ü endemic disease : estimated incidence of 1 per 100,000 persons in
Alabama, USA
3. Neurological toxocariasis : the finding of Toxocara larvae in cerebral spinal
fluid (CSF), in brain tissue, in the meninges, and/or by immunodiagnosis
on CSF

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DIAGNOSIS

ü The gold standard for diagnosing infections caused by

protozoa or helminths is microscopic or macroscopic
observation of the parasite
ü Radiologis/Imaging techniques : CT, MRI, USG
ü Laboratory : Blood eosinophilia, serology test : ELISA, CSF
ü A mobile larva can be directly observed under the retina Liver tissue

ü Pathology examination : liver, brain, lung, enucleated eye

ü Molecular analysis : PCR

Sukmab,2017 Sukmab,2017

TREATMENT TREATMENT

Ø Benzimidazole derivatives : thiabendazole (TBZ), mebendazole (MBZ),

and albendazole (ABZ), as classified by seniority

Ø TBZ : orally every day in doses of 25 mg/kg b/w for 3-7 days

Ø MBZ, the best therapeutic schedule was 20-25 mg/kg b/w daily
for 3 weeks

Ø ABZ given at 10 mg/kg b/w daily for 5 days

Ø Cryopexy, Photocoagulation of the parasite when visible : 200 to 500

µm, 0.2 to 0.5 second of thermal laser application è ocular granuloma

Ø Diethylcarbamazin (DEC) + corticosteroid, TBZ, MBZ : neurological

toxocariasis

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EPIDEMIOLOGY PREVENTION

ü Puppies should be routinely treated starting at 2 to 3 weeks of age

ü Home-gardens should be fenced to prevent fecal contamination by
dogs and cats
ü Vegetables and salads gathered from possibly contaminated
gardens should be thoroughly washed
ü Avoid the consumption of raw or undercooked meat
ü the attention of an appropriate health provider for treatment.
ü Personal hygiene also should be upgraded by encouraging
handwashing, especially prior to eating and discouraging hand to
mouth activity at all times

Sukmab,2017

REFERENCES
Ø Cook G.C. and Zumla A. Manson’s Tropical Diseases. New York, ELST. 2003
Ø Markell and Voge. Medical Parasitology. 9 th. ed. Saunders elsevier, St. Louis, Missouri, 2006
Ø Roberts LS and Schmidt GD. Foundations of Parasitology. 7 th. ed. Mc Graw Hill, Singapore,
2006
Ø Craig and Faust, Clinical Parasitology. 8 th. Ed. Lea&Febiger, Philadelphia. 1970.
Ø Garcia L.S. and Bruckner D.A.. Diagnostic Medical Parasitology. 3 rd Ed. ASM Press.
Washington D.C. 1997.
Ø Neva F.A. and Brown H.W. Basic Clinical Parasitology. 6 th.ed. Appleton&Lange. Connecticut.
1994.
Ø WHO, Helminth Control in School-Age Children, 2 nd ed.,WHO, Geneve, 2011
Ø Magnaval J-F, Glickman LT, et.al. 2001. Highlights of Human toxocariasis. The Korean J. of
Parasitology. 39(1):1-11
Ø Hotez PJ., Wilkins PP. 2009. Toxocariasis: America’s Most Common Neglected Infection of Poverty
and a Helminthiasis of Global Importance?. PLOS Neglected Tropical Diseases. 3(3):e400
Ø Farthing M, Fedail S, Saviolo L, et al. 2004. World Gastroenterology Organization:
Management of Strongyloidiasis.
Ø Siddiqui AA, Berk SL. 2001. Diagnosis of Strongyloides stercoralis. Clin. Infect. Dis. 33:1040-7
Ø Lok JB. 2007. Strongyloides stercoralis: a model for translational research on parasitic nematode
biology. WormBook.org.
Ø Byron Blagburn. 2010. Internal Parasites of Dogs and Cats : Diagnostic Manual. Novartis
Animal Health US. Inc

TERIMAKASIH

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