ascariasis, strongyloidiasis, ancylostomiasis, loeffler syndr, clm.pptx
TRANSCRIPT
Soil Transmitted Helminthiasis
Refference
1. Roberts L, Janovy Jr J. Gerald D. Schmidt & Larry S. Roberts’ Foundations of Parasitology. 7th ed. McGraw Hill. New York. 2005 : 397-99, 417-24, 431-5
2. Brooker S, Bundy DAP, Soil Transmitted Helminths (Geohelminths). In : Cook GC, Zumla AI (ed). Manson’s Tropical Disease. 22nd ed. Saunders Elsevier. 2009 : 1517-40
3. World Health Organization. Preventive Chemotherapy in Human Helminthiasis : Coordinated Use of Anthelminthic Drugs in Control Intervensions : A Manual for Health Professionals and Programme Managers. Geneva, Switzerland : World Health Organization; 2006
4. World Health Organization. Weekly Epidemiological Record : Soil- Transmitted Helminthiasis : Estimates of The Number of Children Needing Preventive Chemotherapy and Number Treated . Geneva, Switzerland : World Health Organization; 2011
5. Hotez PJ, Brooker S, Bethony JM, et al. Hookworm Infection. The New England Journal of Medicine. 2004; 351 : 799-807
References
Soil Transmitted HelminthiasisLearning ObjectiveAgents of the diseasePathologyDiagnosis Prevention
Soil Transmitted HelminthiasisGeneral
o Nematode infectionso Transmitted via soil medium either :
1. Ingestion of embryonated eggs
2. Skin penetration by infective larvae
Soil Transmitted HelminthiasisGeneral o Etiology :
• Ascaris lumbricoides• Trichuris trichiura• Hookworms• Strongyloides stercoralis• Toxocara spp.
Common STH agents
Soil Transmitted HelminthiasisGeneral
o Infections STH associated with: Poverty and poor
condition Crowded living
conditions, combined with lack of access to health care and low levels of education (poor personal and health awareness)
Soil quality and climate Inadequate water supply
and poor environmental sanitation
Soil Transmitted HelminthiasisGlobal Estimation
AscariasisGeneral
o Etiology : Ascaris lumbricoides (roundworm)o Habitat : small intestine, especially jejunum
and upper ileumo One of the most common & widespread human
infection, about 1 billion people worldwide
Ascaris lumbricoidesMorfology
Adult Ascaris lumbricoides
Ascaris lumbricoidesMorfology
corticated
decorticated
Egg of A. lumbricoides
Fertilized Unfertilized
Ascaris lumbricoidesMorfology
Infectious corticated
Egg of A. lumbricoides
AscariasisLife Cycle
Infective stage : fertilized eggDiagnostic stage : egg & adult in fecesRoute of infection : ingestion
AscariasisPathology
o Majority symptomlesso May caused by migrating larva or adult
worm
AscariasisPathology
Migrating Larvae
• When juveniles break out of lung cappilaries into the resp. system → small hemorrhage
• Segments of 4th stage larvae can be seen in the bronchioles associated with infiltration with PMN and eosinophil with scattered Charcot-Leyden crystals and radiological pulmonary infiltration → Ascaris pneumonitis (Löffler’s pneumonia)
AscariasisPathologyAscaris pneumonitis (Löffler’s
pneumonia) : fever, cough, sputum, wheeze, skin rash, eosinophilia, and radiological pulmonary infiltration
Larvae may wander into the brain, eye, causing granulomas
AscariasisPathology
Adult can cause physiological abnormalities in the small intestine → malabsorbtion of nutrients and micronutrients, malnutrition, growth failure and cognitive impairments
Intestinal ascariasis → GI discomfort, colic and vomiting are quite common
Adult worms
AscariasisPathology
The commonest complication of ascariasis among children below 10 years is small-bowel obstruction
Heavy infection can cause intestinal colic, fatal intestinal blockage
AscariasisPathology
Wandering worms :– may reach liver, billiary tract,
appendix and oesophagus – acute and chronic
inflammation with infiltrations by eosinophils, histiocytes and mononuclear cells at sites of ectopic ascariasis
– granuloma formation around ova in tissues
AscariasisDiagnostico Adult worm out of body openingso Larvae std 4th in sputumo Eggs in feces – fertilized / unfertilizedo Eosinophilia o Serology (?)
Strongyloides stercoralis General
Family StrongyloididaeFacultative parasiteWidely distributed on earth,
most densely in those areas characterized by high temperature and humidity and poor hygienic conditions
Strongyloides stercoralis MorphologyThe egg is 70 x 40 m with an
extremely thin eggshellFemale adult of parasitic generation:
thin and long, about 2 mm long, two sets of genital organs, with lack of seminal receptacles (because no sperm is required for parthenogenesis)
Female adult of free living generation: thicker and shorter, seminal receptacles (+)
Male adult: smaller, about 0.7-1 mm long, the tail end curls on the ventral side
Strongyloides stercoralis Morphology
Rhabditiform larva: only can be differentiated with those of Ancylostomatidae through electron microscopy
Filariform larva: 0.4-0.7 mm in length, a half is occupied with esophagus, forked tail
Life Cycle & Transmission
Infective stage: filariform larvaeDiagnostic stage : rhabditiform larvae in feces
Strongyloides stercoralis Life Cycle
Direct Cycle: filariform larva invades human skin, proceed in the blood stream to the heart and lung, then return to the small intestine via tracheal migration
Indirect cycle: when outside conditions are favorable, rhabditiform larvae grow become male and female free living form, and after copulation and lying eggs, adults die, and the eggs give rise rhabditiform larvae, and become infective form after two molts
Strongyloides stercoralis Route of Infection
Internal autoreinfection: if a host has constipation or immune deficiency
External autoreinfection: in poor hygienic host, whose perianal is contaminated by rhabditiform, the larvae grow become infected larvae and then invade the perianal skin or mucosa, proceed to the lung, etc.
StrongyloidiasisClinical manifestation:
Immunocompetent (Intestinal):
Acute: diarrhoea abdominal pain, nausea, vomitting, constipation, weight loss, GI-bleeding, pruritus ani.
Chronic: protein losing enteropathy, malabsorbtion, paralytic ileus.
Pulmonary: - Cough & wheezing.- Loeffler’s syndrome- Haemoptysis- Bronchopneumonia- Hypereosinophilia.
Cutaneous- Rash- Pruritus- Larva currens
Neurological:- Infection of brain & meninges
Strongyloidiasis :
Immunocompromised (Extra – Intestinal):
Diagnosis
Non-specific; increased eosinophilia and IgE.Stool FEME: larvae form more often seen than
eggs.Concentration of larva by Baermann’s method.Stool culture by either Harada mori or Sand&
charcoal culture; wait for larva to emerge within 5-7 days.
Duodenal aspirateUrine, sputum, cerebrospinal fluidSpecimen biopsy and autopsy.
AncylostomiasisGeneral o Etiology : Ancylostoma
duodenale Necator americanus
o Habitat : small intestine o Recent estimate suggest that
hookworms infect 740 million people worldwide
AncylostomiasisMorfology
Adult Ancylostoma duodenale
AncylostomiasisMorfology
Adult Necator americanus
AncylostomiasisMorfology
Hookworm larvae
Rhabditiform larvae Filariform larvae
AncylostomiasisMorfology
Egg of Hookworm
AncylostomiasisLife Cycle
Infective stage : Filariform larvaeDiagnostic stage : Eggs in fecesRoute of infection : normally aquired by skin penetration A.duodenale
Uncommon, A. duodenale can be transmitted through undercooked meat incl. rabbit, lamb, beef and pork (Wakana’s disease) and lactogenic during breast-feeding (infantile hookworm)
AncylostomiasisPathology
Hookworm disease manifests three main phases of pathogenesis :
o The cutaneous or invasion period
o The migration or pulmonary phase
o Intestinal phase
AncylostomiasisPathology
Begins when larva penetrates the skin
Pruritic , erythematous, papular rash at the site entry (ground itch)
Cutaneous Phase
AncylostomiasisPathology
Occurs when juveniles break out of the lung capillary into alveoli and progress up bronchi to the throat
Each sites hemorrhage slightlyUsually asimptomatic, although there may be cough
and sore throatPulmonary hookworm infection resembles Löffler’s
syndrome because of its association with eosinophilia in the lung.
Hookworm pneumonitis may indicate severe infection
Pulmonary Phase
AncylostomiasisPathology
The attachment of hookworm’s cutting organ to the intestinal mucosa and submucosa and the subsequent rupture of intestinal capillaries and arterioles → blood loss
Hookworm produce active suction impulses 120-200 times per minute
The secretion of anticoagulation by parasite help to maintain continous oozing of blood at the attachment site
Intestinal Phase
AncylostomiasisPathologyThe major clinical manifestations of
hookworm disease : chronic intestinal blood loss.
Infection with A. duodenale causes greater blood loss than does infection with N. americanus
The blood loss has been estimated as : 0,15 ml/ day per worm in A. duodenale inf. 0,03 ml/ day per worm in N. americanus inf.
AncylostomiasisPathologyIn very heavy infection → iron
deficiency anemia, hypoproteinemia, edema, potbelly in children, delayed puberty, mental dullness, impair cognitive ability, heart failure and death
AncylostomiasisDiagnostic
o Hookworm eggs or adult worm in
feceso Rhabditiform larva cultured from
eggs by the Harada-Mori methodo Serologi
Soil Transmitted Helminthiasis Treatment and Control
WHO has recommended three interventions to control morbidity due to STH infections:
1. Regular drug treatment of high-risk groups for reduction of the worm burden over time
2. Health education 3. Sanitation supported by personal
hygiene aimed to reducing soil contamination
The recommended drugs : 1.Albendazole (400mg) tablets given in a
single dose, 2. Levamisole (40mg) tablets given in a
single dose by weight (2.5mg/kg)3.Mebendazole (500mg) tablets given in a
single dose;4. Pyrantel pamoate tablets given in a
single dose by weight (10mg/kg)
Regular drug treatment of high-risk groups
Soil Transmitted Helminthiasis Treatment and Control
Soil Transmitted Helminthiasis Treatment and Control
CUTANEOUS LARVA MIGRANS
Cutaneous larva migransSynonim: creeping eruption, ground itchCausativa agents: nematodes (zoonotic
hookworms): Ancylostoma braziliense, Ancylostoma caninum, Ancylostoma ceylanicum, Strongyloides stercoralis
Filariform larvae penetrate human skin, usually feet and hands invade epithellium aimless wandering through the skin red, itchy wound usually infected by pyogenic bacteria
PathogenesisContact with soil containing infective larvae
(filariform larvae) that are capable of penetrating the skin.
This can’t occur after first exposure but follows reinfection only after several weeks, this infection suggests that the disease is due to hypersensitivity to larval secretions (Provic and Croese, 1996)
The larva produces a number of enzymes which may assist in dermal invasion; such as metaloprotease, minor protease and hyluronidase (Hotez, Hawdon and Capello,1995)
PathologyLesions may also become vesiculated,
encrusted, or secondarily infected.The larvae eventually die and become
absorbed without treatment.The cutaneous symptoms typically last for
days to months.Only 29% of patients had lesions that
persisted for 1 month, but in occasional patients had lesions in follicles and cause disease for as long as 2 years.
Slightly increase of eosinophilia and normal IgE
49
50
TreatmentApplication of 15% thiabendazole
ointment for 5 days.Systemic treatment with
albendazole or ivermectin may also be used, especially in severe cases.
If applicable : 2nd bacterial infection th/.