Intestinal strongyloidiasis

and hyperinfection
syndrome
 Introduction
Strongyloidiasis:an infection caused by
S.S .
First reported in the year 1876, 50 years
later life cycle discovered.
Endemic in developing country but is
sporadic and rare.
 Introduction

Chronic persistent infection, autoinfection,

hyperinfection, pulmonary and
gastrointestinal systems, disseminated
.infection
Fatal strongyloidiasis in immuno
suppression patients(HTLV-1 or HIV) and
.hematological malignancy
 Clinical manifestation
.symptomatic Asymptomatic disease
.Mild disease
.Chronic symptomatic disease
.Hyperinfection
.Dissemination infection
.Asymptomatic is common form
 Initial manifestations
.Serpurticaril rash
.iginous Mostly in legs
.Cough-tracheal irritation
.Abdonimal cramb-diarrhea-constipation
Most common complaint: abdominal
.bloating
 Chronic manifestation
Nausea-vomiting-epigastric pain-
intermittent vomitting-diarrhea-
constipation-weight loss-asthema-like
.symptoms-urticaria-larva currens rash
Hyperinfection syndrome
:Riskfactors
.Treatment by corticosteroids
.HTLV-1 and HIV infection
.Kala-azar
Prevalence: 1.5-2.5%
.Increas larvae in stool and sputum
 Hyperinfection syndrome
Enormouse multiplication and migration
.larvae in immunosappressed
Involving respiretory tranct and
.gastrointestinal
Extrintestinal manifestation: like asthema-
cough-wheezing-pneumonia-pulmonary
.hemorrhage
Hyperinfection syndroms
Itestinal manifestation: cramp-watery
.diarrhea-weight loss-nausea-vomiting
 Disseminated infection
.Involvment of multiple organ systems
Chronic infection and malnutrition
.predispose for it
Rate mortality: 87%
.Larval load increases
Cataneous manifestation: petechiae-
.purpurea-intensely-itching prurigo
Disseminated infection
.Gram negative bacteremia
Corticosteroid and strongyloidiasis
Increase fatal hyperinfection or
disseminated infection with corticosteroid
.therapy
Corticosteroid: increase apoptosis Th2-
reducing eosinophil-inhibiting mast cell
.response
Corticosteroid and strongyloidiasis
Increase ecdysteroid - molting signal –
increase autoinfection filariform – leading
to hyperinfection and disseminated
.infection
 Pathophysiological mechanisms
and host defense pathways
regulating strongyloidisis
T and B cell mediated immunity required
.in response to strongyloides stercoralis
Increase: IgE-eosinophilia in blood-mast
cell in intestine-hyperplasia of goblet cells
.in intestine
 serum-spesific IgA and IgE indicate
Increase Th2: IL4,5,6,9,10,13
Detection Tcell-dependent Tcell immunity
.in strongyloides stercoralis
Th2 stimulate eosinophils, mastcell, goblet
.cell-by IL4,5,9,10,13
In sever strongylodiasis no chang in Tcell
number compaird asymptomatic or mild
symptomatic disease that indicate other
.immune mechanisms
Masto cytosis without IL3 indicate other
.mechanisms
 IL4 in induction and maintenance of
.intestinal mast cells
.Role of IL4 being unknown
Humoral immunity with production
.immunoglobulins by plasma cells
Bcell no play a role in defence against
primary infection but play a role in
.subsequent infection
IgE mediated activation of accessory cells
.play a role in resistance to infection
IgE non-specific and block the
development defense mechanisms by
.saturating IgE receptors on effector cells
IgE and IgA have no effect on killing
.larvae
 .In humans,IgE is specific
Show no correlation exists between
quantities total IgE, specific IgE-IgG and
.clinical severity strongylodiasis
IgE-mediated anti-parasite immunity is
.controversial
IgA, IgG, IgM levels were lower compared
with asymptomatic or mildly symptomatic
.strongyloidiasis
IgM specific for primary infective filariform
.larvae is not effective autoinfective larvae
.ADCC is not required fo larval killing
ADCC in immunity to S.S, requring further
.research
.Eosinophil not sufficient for protection
A possibility of suppression eosinophil in
.disseminated infection
Local mucosal immunity along with
inflammatory changes a role in
.evadication
Mechanisms different: epulsion of worm-
decrease lenghth worm-reduction
fecundity female worm-failure infective
.larvae to establish
.Role goblet cells in expulsion worm
Goblet cells induced by IL13 secreted by
.Th2
 .Intestinal mastocytosis induced by IL13
.Mast cell haverole in defence to parasite
Architecture mucosa and absence
immune mediated diarrhea in S.S
.infection
Leucktrienes as immunostimulants to
.strongyloides
 Monitoring response to treatment be
difficult with detection S.S larvae in stool
.because inconsistent sheding of larvae
 Conclusions
Strongyloidiasis with tendency to chronic and
hyperinfection and disseminated infection
More chronic and asymptomatic
No specific ideal test to diagnosis
Non-endemic regions have endemic pockets for
it
Fatal strongyloidiasis happen in
immunocompromised especially those are
.taking steroid