ascariasis, strongyloidiasis, ancylostomiasis, loeffler syndr, clm.pptx

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


corticated

decorticated

Egg of A. lumbricoides

Fertilized Unfertilized


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


Adult Necator americanus


Hookworm larvae

Rhabditiform larvae Filariform larvae


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


Begins when larva penetrates the skin

Pruritic , erythematous, papular rash at the site entry (ground itch)

Cutaneous Phase


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


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



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/.

Documents

ascariasis, strongyloidiasis, ancylostomiasis, loeffler syndr, clm.pptx