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THE TRAVEL OF THE WORM
Míriam J. Álvarez-Martínez, M. D., Ph. D.
Hospital Clinic, Barcelona (Spain)
CRESIB (Barcelona Center for International Health Research)
University of Barcelona
[email protected] ESCMID Online Lecture Library
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CLINICAL CASE • 69y/ Spanish male, had lived in Dominican Republic (2000-2002) • Hypertension treated with enalapril
• DM-2 years of evolution without treatment and without known
chronic complications
• Bronchial asthma treated with salmeterol, ipratropium bromide and chronic oral glucocorticoids
• Vocal cord carcinoma intervened in 2003 (free from disease)
• Prostate adenocarcinoma treated with radical prostatectomy in 2003 (disease-free)
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February 1st, 2008 (Hospital 1):
• Left hemiparesis with partial remission
• MRI brain acute cerebral ischemic injury
CURRENT DISEASE
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15 days later (hospital 1): • Vomiting, headache and fever 38 º C • Physical exploration moderate neck stiffness without source
NRL standard ENT examination
• LP purulent CSF, 26000 Leukocyte (PMN 95%), Gram and cultures negative
• Cerebral CT not added lesions to the objectified in MRI performed during previous admission
• Broad spectrum ATB treatment good clinical outcome and normalization of CSF
CURRENT DISEASE
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• Blood cultures & urine culture (+) for Escherichia coli
• Discharge 1 month later (March 1st)
Since discharge: • Wife of patient reported a progressive malaise,
anorexia, weight loss and episodes of disorientation
CURRENT DISEASE
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March 15th, 2008 (Hospital 2, HC-BCN) • Suddenly worsening decreased level of consiousness, without
fever • Physical exploration cachectic appearance • LP 900 leukocytes (PMN 100%), Prot 320, Glu 0, ADA 13, CSF
cytocentrifuge abundant cellularity (PMN only), Gram- stain, no microorganism
• CT Brain unchanged from previous studies
CURRENT DISEASE
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• Diagnosis of Bacterial meningitis treatment meropenem 1g/12h, vancomycin 1 g/12h & ampiciline 1g/6h
• Due to reduced consiousness level ICU • At 48h of ATB treatment Control LP • CSF culture Gram negative rods
CURRENT DISEASE
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• ATB change to meropenem & ciprofloxacin • Urine culture Mixed bacteria • CSF culture E. coli susceptible to
amoxicilin-clavulanic, ampicilin, cefazoline, cefuroxime & gentamicine, & resistent to ciprofloxacine & cotrimoxazole
• Negative blood cultures
CURRENT DISEASE
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• ATB change to Ceftriaxone • Normal Abdominal Eco • TT Ecocardio none valvular vegetations
“…at that time a test was performed showing the diagnosis…”
CURRENT DISEASE
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Microbiology results • 28 April 2008 • 29 April • 30 April
• 8 May
• 9 May
• CSF: E. coli • BAS: E.coli
• CSF: E. coli • Traqueal aspirate :
larvaeStrongyloides stercoralis; Candida sp.
• Urine: Candida sp. • CSF: NO parasites or bacterias • Duodenal Aspirate : larvae
Strongyloides stercoralis • Negative faecal sample
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Rhadbitiforme Larva (L1) & Strongyloides stercoralis eggs in duodenal aspirate.
Larva: 250 x 20 µm. Egg: 50 µm . 40X
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Strongyloides
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Cestodostape worms
Trematodosflukes
Platyhelmintosgusanos planos
Nematodosround worms
Nematohelmintosgusanos redondos
Metazoa
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Nematodes characteristics
• Round worms • No segmented • Mouth, esophagus & anus • Separated sex (female > male) • Reproduction - oviparus - larviparus • Infection - ingestion eggs/ larvae
- penetration - larvae
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Strongyloides stercoralis
• Round worm • S. fülleborni chimpancees & limited
human infections. • World distribution • Tropical & subtropical areas • Microhabitats in rural areas in the
Mediterranean basin of Spain (La Safor)-rice fields
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Larva rhabditiforme
Larva filariforme
Rhabditiforme larva (L1)
Filariform larva (L3)
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Strongyloides’ travels
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Life cycle of Strongyloides
Chiodini et al., Atlas of helminthology,2006.
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Larva Dermatitis in site of penetration
L3
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L1 intestinal lumen --- faeces ESCMID Online Lectu
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Free life cycle
Direct
L1 in faeces
L3 infects again
Rhabditiform larva
Filariform Larva L3
L3 L1
L1 ESCMID Online Lecture Library
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male-female adults
Filariform larva Rhabditiform
L3 L1
L1
L3
Free Life Cycle Indirect L3—Adults—eggs—L1—L3
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Direct cycle to other person External Autoinfection Internal Autoinfection
L1 L3
L3
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Diagnosis of Strongyloides • Identification of larvae (rhabditiforms-L1 & rarely
filariform larvae) in faeces or duodenal fluid. – Wet preparation – Hot water emergence technique – Faecal Concentration (formol-ether) – Culture (Charcoal, Agar) – Harada Mori – Enterotest o string test
• Detection of larvae in sputum (diseminated form) ESCMID Online Lectu
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Rhabditiform larva of Strogyloides stercolaris wet prep. Size 200-250 µm.
L1
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Detail esophagus Rhabditiform larva of Strongyloides
L1
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Rare worm’s travel
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Recurrent meningitis by E. coli caused by severe disseminated
Strongyloidosis
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• Acute Strongyloidiasis • Chronic Strongyloidiasis • Hyperinfection syndrome
– High acceleration autoinfection process within the life cycle.
– Larvae are confined to locations own cycle: intestines, lungs and skin.
– Motivated by alteration of the immune status of the host.
Igual Adell et al. Estrongiloidiasis. EIMC, 2007
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Genta et al., Disregulation of Strongyloidiasis: a new hipothesis. Clin Microb Rev, 1982.
Molting rate of lavae in the instestinal lumen
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Corticoids & Hiperinfection • Main factor in triggering hyperinfection.
– < 10 days after corticosteroids hiperinfection produced. – No hiperinfection after inmunosupression by non-
steroids drugs. – Even with subconjuntival/parenteral corticosteroids – VIH + Corticosteroids: Hiperinfection, but not in other
OI – HIPERINFECTION SYNDROME IS NOT associated
to the LEVEL of immunosuppression, but to the used IMMUNOSUPRESSED AGENT
Genta et al., Disregulation of Strongyloidiasis: a new hipothesis. Clin Microb Rev, 1982.
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Vadlamudi et al. Intestinal strongyloidiasis and hyperinfection syndrome. Clin Mol Allerg 2006, 4(8); 1-13.
1
2
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• Acute Strongyloidiasis • Chronic Strongyloidiasis • Hyperinfection syndrome • Disseminated Strongyloidosis
– In the context or not of hiperinfection – Larvae afecting different organs: Brain, liver, lymphatic, urinary & others.
• Severe Disseminated Strongyloidosis – Complicated with bacterial infection from intestine.
High Mortality. – Frequency 1,5 -2,5% – Due to alteration of intestinal wall because high
penetration of larvae from the intestinal lumen. Igual Adell et al. Estrongiloidiasis. EIMC, 2007
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Recurrent Meningitis by E. coli Form of Severe Disseminated Strongyloidosis
– Rare recurrence (5% of disseminated forms) – Theories of bacterial transportation (to brain)
• Disrruption of intestinal wall and pass fecal flora into the circulation.
• Bacteria adhered to the outer surface of the larvae are transported during migration .
• Excreted bacterial to circulation from the intestinal tract of the larva.
• Favored by a defect in the cranial valve system.
Smallman et al. Strongyloides stercoralis hyperinfestation syndrome with E.coli meningitis. J Clin Pathol, 1986. Somin et al. Fatal recurrent bacterial meningitis- A complication of chronic Strongyloides infection. Eur J Int Med, 2008.
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CHAGAS & STRONGYLOIDES COINFECTION
Screening S. stercoralis
218 patients
79 (36,2%)
S. stercoralis positive
39 (49%)
coinfected
S. stercoralis & T.cruzi
• High prevalence of co-infection
of St and CD in patients from Latin-America.
• Bolivian patients the most important group.
• At the presence of eosinophilia, the screening
for St and CD is strongly recommended.
• Taking into account the nature of these NTDs,
their burden could be underestimated
in non-endemic areas.
Bolivia
RD Congo
Ecuador
Guinea Ecualtorial
Honduras
India
Sierra Leona
Alvarez et al., Communication, SEIMC, 2012
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ACKNOWLEDGEMENTS
THANK YOU FOR YOUR ATTENTION
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