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Vector-borne zoonotic disease caused by genus
leishmania that is obligate intracellular protozoa
Vectors – Phlebotomus and Lutzomyia
Zoonotic form, dogs as main reservoir, occurs in
the Mediterranean basin, China, the Middle East,
and South-America; cause is L. infantum.
The anthroponotic form, humans as reservoir, is
caused by L. donovani ; prevalent in East Africa
and the Indian subcontinent.
 Major forms: Visceral, cutaneous and mucocutaneous
Anopheles
Risk of acquiring infection is determined by local
sand fly behavior and by the presence of an infected
animal or human reservoir
Transmission
Female sand flies (Phlebotomus and Lutzomiya
Spp.) get infected after sucking blood from infected
reservoir eg. human or other mammals
Amastigotes transform to promastigotes in sand fly
gut  Replicating and metacyclic promastigotes are
regurgitated and injected into the skin during
subsequent blood meal
Other route of transmission are via
 blood
 Shared needles
 Blood transmission
 Trans-placental spread
 Via organ transplantation
Population at risk – 350 million
Over all world prevalence – 12million
Annual new case reports – 2 million
About 90 countries affected
More than 20 spp of leishmania identified
VL in 70 countries,
 S. Asia 600,000 cases in 2006 – significantly
decreasing due to control measures
 East Africa 30,000 (mainly Sudan, Ethiopia)
 Brazil 4,000
E Diro Department of Internal Medicine
UoG
8
lowlands of Ethiopia with varying endemicity.
N West. - Metema and Humera, Wolkayit,
Libo/Fogera
N East – Ethio-Djibouti Awash Valley
S. West – Segen, Dawa, Genale, Woito, Konso,
Omo, Gambella Sudan border
40 localities and new foci are being reported.
Main risk factor - population migration
Estimated annual VL – 4500-5000 people
VL cause - by species of the Leshmania
donovani complex - L. donovani
The sand fly - Phlebotomus orientalis,
Phlebotomus martini and Phlebotomus celiae.
 Animal reservoirs are suspected, but not
documented yet.
11
VL- HIV co-infection rate at Humera
 1998/99 – 18.5%
 2006 – 40%
A Tigray retrospective review of 791 cases
showed >4x CFR in HIV + VL patients than VL
without HIV.
Libo – HIV –VL coinfection rate 15-18%.
More than 90% of the world's cases of
cutaneous leishmaniasis occur in Middle East
(Old World) and in Brazil and Peru (New
World).
The etiologic agents are L. tropica, L. major,
and L. aethiopica (Old World) and species of
the L. mexicana complex and the Viannia
subgenus (New World).
13
T cell Response
Th 1 pattern Response
Th 2 pattern Response
T lymphocyte release IL-2 and INF gamma
Ineffective humoral response
Effective cellular response
Activates macrophges to kill Leishmania
Leishmainin skin test positive, but no clinical VL
T lymphocyte release IL-4,IL-5,IL-10,
TNF - B
Inhibit macrophage from killing Leishmania
High Antibody level and Clinical VL
IL
4
&
10
-
Depends on – Parasitic properties (Infectivity,
pathogenicity and Virulence)
Host factors and host responses
Manifestation range from asymptomatic, self
healing cutaneous leishmaniasis to diffuse
cutaneous and visceral disease
Presentation
Kala-azar (Black fever in Hindu)
IP: Wks –Mo’s
Often remains asymptomatic
Symptomatic cases: acute, sub acute or chronic
course
Fever, night sweats, weakness ,weight loss
Cachexia, wasting, Pallor
Nontender, soft massive splenomegaly +
perisplenitis
Hepatomegaly + LAP
Darkening of face/ashen grey appearance
Bleeding 20 to thrombocytopenia
Susceptibility 20 infection
Pancytopenia (Anemia, Thrombocytopenia,
Leukopenia, Neutropenia)
Marked eosinopenia, Reactive lymphocytosis,
Monocytosis
Hypergammaglobulinemia
Hypoalbuminemia
Gold-standard: Demonstration of amastigotes
in tissue aspirates
Diagnostic sensitivity – Spleen - > 95%; Bone
marrow  70%, Lymph nodes  58%
DAT test: Anti-Leishmanial (titer) IgG sn >95%,
sp >90%
Detection of Anti-rK39-Abs Sn 72%, Sp 82%
Culture – NNN media
Isoenzyme and molecular techniques to
differentiate species
SSG + Paramomycin for 17 days
Sodium stibogluconate (SSG) 20mg/kg iv/im for
30 days
Alternative:
 AmBisome 4mg/kg for 5-7 doses: 1-5days, 10th, 14th.
 Amphotericin B 1mg/kg every other day for 30
days/total 15 doses.
 Single dose AmBisome not effective in N Ethiopia
Other drugs but less effective:
 Paramomycin, Pentamidine, Miltefosine (oral prep)
Secondary prophylaxis (in HIV)- ?? Pentamidine
Clinical improvement after 7-10 days in majority
Apparent cure response (Afebrile,  splenic size,
no visible amastigotes on repeat splenic aspirate
within 2 weeks of Rx in > 90% of cases
Hematologic abnormality improvement by 4th
weeks of Rx
Splenomegaly disappear < 6 months after Rx
Reactive skin test + ve < 1 yr after Rx
No response or death : 5-10%
Relapses after apparent cure: 5-10% (often < 6
months after Rx)
Cure documented after 6 months of Rx
completion (-ve splenic aspirate for leishmania
i.e. test of cure)
New infection or Reactivation (>95% of co-
infection reports are of VL)
Less virulent leishmania spp cause VL.
Most patients with CD+
4 count <200/l
Widespread atypical organ involvement eg GIT
Frequent parasitemia, high yield from buffy coat
 Peripheral blood 50%, buffy-coat culture 70%
Sub optimal specific IgG production
Lower diagnostic sensitivity to serologic tests
(50% Vs >90%)
High rate of relapse / drug toxicity
Reduced responsiveness to tx (comparable
initial response)
HAART-  incidence of clinical leishmaniasis
Demonstration of amastigote forms on geimsa
or wright stain
method VL with out HIV VL with HIV
spleen 93-99%
Bone marrow 53-86% 67-94%
Lymph node 53-65%
Buffy coat / BF ~ 30% 50- 53%
DAT 95-97%* 95% in Ethiopia; 89-90%
rK39 93-100%* 22-62%
IP =Weeks - Months
Start as a papule at the site of insect bite and
evolve to nodules, ulcer, plaque
It may complicate with regional adenopathy,
sporotrichoid subcutaneous nodules, lesion
pain or pruritis, 20 bacterial infection
The infecting spp, the location of lesion and
the host immune response determine the
manifestation and chronicity of the lesion
Visualization of amastigote in Giemsa-Stained
thin smear from dermal scraping /biopsy
specimen.
Serology tests – insensitive
Indication for treatment
Persistent lesion ( > 6 months)
Lesions that are located over joints
Multiple lesions (> 5 to10 in number)
Large lesions (> 4-5cm)
IV/IM SSG therapy, Pentamidine,
Ketoconazole, dapson
Local/Topical therapy - Intralesional SSG
therapy, Heat therapy, Cryo therapy
Presentation: - Erythema and ulceration of the
nares  Nasal septal perforation and
destructive inflammatory lesion 
obstruction of pharynx/larynx and remarkable
disfigurement.
Treatment
IV/IM SSG therapy, Amphotericin B
Etiology:- Entamoeba histolytica
Epidemiology: Transmission and cycle
E. histolytica acquired by the ingestion of infectious
viable cysts from feces contaminated water, food or
hands  Release of motile trophozoite from cysts in
small intestine 
Large bowel mucosa invasion with sub mucosal
extension  Inoculation of amoebas in to the portal
system distant metastatic abscess in liver
/lung/brain  Encystation of trophozoites and/or
motile trophozoites passage in stool.
1. Intestinal amoebiasis
Mostly asymptomatic cyst passage (90%)
Symptomatic cases (10%):
IP = 2 - 6weeks
Lower abdominal pain, Bloody mucoid diarrhea,
Fever (<40%), malaise
Toxic megacolon :- Bowel dilation with intra-
mural air
 predisposing factor: - Glucocorticoid treatment
Chronic amoebic colitis - DDX: IBDs
? Post amoebic colitis
Bowel perforation
GI bleeding
Acute presentation in young pts with prominent
symptoms <10 days
Chronic /sub acute presentation in older pts with
hepatomegaly /Wt loss/anorexia > 6 months
Pathology : “ Anchovy paste”
Fever – possible cause of FUO (10-15%)
RUQ pain + Hepatic point tenderness
Rt. Sided pleural effusion
Preceding active diarrhea (<30%)
Pleuropulmonary amoebiasis (20-30%)
Hepato-bronchial fistula
Rupture into the peritoneal space
Rupture into the pericardium (left lobe site)
1. Stool examination
 Microscopic fecal findings: Wet mount
 +ve test for heme
 Paucity of neutrophils
 Amoebic cysts or hematophagous trophozoites of
E.histolytica
2. Serologic test for invasive amoebiasis
 ELISA
 Agar-Gel diffusion assay
 +ve in >90% of pts with colitis /Amoebomas/liver
abscess
3. Liver imaging - US/CT scan/MRI for oval /round
hypoechoic cyst
>80% who had Sxs >10 days –single abscess in rt.
lobe
50% who had Sxs <10 days –multiple abscesses
Findings favoring complications
 Large abscess (>10cm)
 Abscess in superior part of rt. lobe
 Multiple abscesses
 Abscess in left lobe
1. Intestinal amoebiasis
Asymptomatic carriers: Luminal agents – Iodoquinol
650mg tid/20 days, or paromomycin 500mg tid
/10days
2. Acute Colitis
Metronidazole 750mg po/iv for 5-10days + luminal
agent
3. Amoebic liver abscess
Metronidazole 750mgtid/5-10days or Tinidazole
2gmpo or Ornidazole 2gmpo plus luminal agent
Need to R/O Pyogenic abscess (in multiple
hepatic abscess)
Failure to respond clinically within 3-5 days of Rx
The threat of imminent rupture
Prevention of left lobe abscess rupture into
pericardium
Surgery
Bowel perforation
Abscess rupture into the pericardium
/peritoneum/ pleural space
Adequate sanitation + Eradication of cyst
carriage
Avoid unpeeled fruits/vegetables
Use of bottled water
Water disinfection by iodination
A trematode/flat worm blood fluke
Five spp. Intestinal (mansoni, japonicum,
mekongi, intercalatum) and urinary
(haematobium)
Intermediate host – snails; definitive host –
humans
Infected snails in fresh water release infective
cercariae
Cercaria penetrate intact skin (they have
anterior and ventral sucker) – in the skin form
schistosomula (morphologic, membrane and
immunologic transformation) from trilaminar to
hepatolaminar membrane adaptive mechanism
for survival in humans.
Mature forms migrate to specific sites –
intestine, vesicle – mate and gravid females
travel retrogradely in veins and deposit their
eggs in small veins
Eggs reach intestinal lumen aided by enzymes
and are voided in stool and urine - miracidum
About 50% are retained in host tissue and
flow to liver and other tissues
Prevalence starts from age 3-4 yrs and peaks at 15-
20 yrs and decline with older age
Infect 200–300 million individuals in South America,
the Caribbean, Africa, the Middle East, and
Southeast Asia
HIV and schistosomiasis - fewer eggs in their stools
than those infected with S. mansoni alone for
unknown reasons
Treatment with praziquantel may result in reduced
HIV replication and increased CD4+ T lymphocyte
counts
Ethiopia – prevalent around Lake Tana,
tributaries of Blue Nile, Awash; Adwa area
Associated with the water use
Dermatitis/swimmer’s itch – popular pruritic
rash at skin penetration site in 24-48hrs
Katayama fever – serum sickness like illness
associated with excess antigenemia and
formation of soluble immune complexes
Eggs retained in host tissues – presinosoidal in
the liver
Cell-mediated granulomatous response around
the ova regulated both positively and negatively
by a cascade of cytokine, cellular and humoral
responses
Granuloma formation begins with recruitment of
a host of inflammatory cells in response to
antigens secreted by the living organism within
the ova
Granuloma formation results in
organomegally, obstruction and fibrosis
Fibrosis of the portal veins can occur and result
in periportal (Symmers' clay pipe–stem) fibrosis;
local or diffuse
Portal HTN results in ascitis, splenomegally and
esophageal varices
Similar pathologic changes occur in the bladder
and results in granuloma formation,
polypomatous growth that can ulcerate and
bleed, obstructive uropathy, urosepsis, risk of
bladder ca
Lung – pulmonary HTN and corpulmonale
Brain and spinal cord affection by granuloma
and neurologic manifestation is possible eg
transverse myelitis
GIT – bloody diarrhea and abdominal pain
With concomitant HBV and/or HCV infection
can lead to significant deterioration and
cirrhosis of the liver
Swimmer’s itch – typical history contact hx, several
DDx.
Katayama fever - peripheral blood eosinophilia, and
a positive serologic assay for schistosomal
antibodies: the Falcon assay screening test/enzyme-
linked immunosorbent assay (FAST-ELISA) and the
confirmatory enzyme-linked immunoelectrotransfer
blot (EITB). Some have ova in stool.
Chronic cases – detection of ova in the stool, urine.
Kato thick smear or other concentration method.
Antipruritic agents for local lesions
Supportive care and glucocorticoids for acute
severe illnesses
Praziquantal (20mg/kg in 2 divided doses)
effectiveness - 85% parasitological cure and
90% egg reduction.
Hepatomegally and bladder lesions also
regress with early treatment but established
fibrosis persists.
Avoid contact with fresh water sources in
endemic areas be it fast or slow flowing
Skin topical agents
Molluscicides – eg. Lemma toxin (Aklilu
Lemma from “endod”)
Safe water supply
Follow up of exposed individuals.
History is important for dx
Epidemiology, occupation, travel
Life cycle of major parasites
Specimen collection
Helminths & protozoa
Excreted by feces - Collection on clean card
board
Avoid water contamination
Take before contrast medium or anti diarrhea
agent intake
3 specimens on alternative days
Polyvinyl alcohol preservation for transport
(for protozoa trophozoits)
Macroscopy - nature of stool
- segments of Taenia / motility
- Ascaris worm
Microscopy - with wet mount (saline, dilute
iodine)
Concentration methods:
 formalin ether sedimentation (all sediment -
preference
 zinc sulfate flotation ( not all float )
Stains
 Iron hematoxylin, Trichrome
Amoebic liver abscess - trophozoites in the abscess
wall
 S. haematobium - in urine sediments
Malaria; leishmania; Trypanosoma - in blood and
lymphoid tissues
Pneumocystis carinii - silver stain of bronchial
aspirate
Onchocerciasis - skin snips
Schistosoma mansoni - rectal snips
Cutaneous and muco-cutaneous leishmania - punch
biopsy
Eosinophilia - in trichinosis & Migratory phase
filariasis
 Pulmonary migration of larva's of intestinal round worms
 Not common in protozoal infections except isospora &
Dientamoebe fragilis
HCMC anemia - in hook work infection
Portal HTN - in Schistosomiasis
Anemia, thrombocytopenia in Malaria, VL
 cysts, mass lesion, ring enhancement ......on radiologic
examination (CT, US) in hydatid cyst, toxoplasmosis of CNS....
Limitations - for individual pt use
- cross rxn
- not distinguish current & past infection
Negative result rules out infection
Molecular Teachnology PCR - for T. vaginalis
(in USA)
Cestodes /flat worms
Intestinal Parasite stage Specimen Remark
T. Saginata ova/segment feces Motile segments
H. Nana Ova "
D. Latum Ova/ segmenta " Megaloblastic
T. solium ova/segment " non motile
cysticercus muscle/CNS CT/MRI
Treatment
-Niclosamide
-Praziquantal
-Albendazole
somatic
Echinococcus hydatid cyst liver/lung US/X-ray/CT
liver flukes/F. hepatica ova feces/bile cirrhosis/portal hpt
Blood flukes
schistosoma mansoni ova/adult feces rectal snip, liver bx
S heamatobium ova/adult urine bladder biopsy
Treatment
Echinococcus - long term Albendazole, surgery
Schistosomia _ praziquantel
Round worms
E. vermicularis/pin worm ova perianal skin scotch tape test
T. trichiuria/wipe worm ova feces rectal prolapse
Ascaris lumbricoids ova " pulm. migration
Hook worm ova " " "
S. stercolaris larva feces/sputum diss. in HIV
Hookworm
ova
Ascaris ova
Treatment
-Mebendazole, Albendazole –
hoodworm, ascaris
-Piperazine citrate – ascaris
-Thiabendazole for strongyloids
Tissue round worms
Trichinella spiralis larva muscle muscle biopsy
W. bancrofti filaria microfilariablood, L.nd nocturnally active
O. Volvulus/river blindness adult/larva skin/eye nodules,skin snip
D. Medinensis (guinea worm) " “ skin in the lesion
Visceral larva migrans larva viscera/CNS ?other worms
Protozoa
E. histolytica trophozoit/cyst feces/liver US/CT liver
G. lamblia " feces
isospora belli oocyst " Acid fast
Cryptosporidium Oocyst " AFS, biopsy, PCR
Microsporidia(? fungi) spore " Modif. trichrome,
biopsy, PCR
Treatments
•Amoeba and giardia – metronidazole, tinidazole
•Isospora belli – cotrimexazole 960mg QID for 10 days; for HIV pts
additional 960mg TID for 3 weeks
•Cryptosporidium – no effective tx, trial with paramomycin,
Nitazoxanide
•Microsporidia – albendazole 400 mg po BID for 2 - 4 weeks
Blood and tissue protozoa
Plasmodium asexual forms blood
Trypa rhodesiense trypomastigoteblood, CSF chancre, L.node
Leishmania amastigote RES biopsy, culture
Toxoplasma gondi cyst, trophozoite CNS, eye, muscle ?HIV
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leish,lvbhhjķllkbvvv jjjjjjjjjjjjjjjjjjjjjjjj

  • 1. Vector-borne zoonotic disease caused by genus leishmania that is obligate intracellular protozoa Vectors – Phlebotomus and Lutzomyia Zoonotic form, dogs as main reservoir, occurs in the Mediterranean basin, China, the Middle East, and South-America; cause is L. infantum. The anthroponotic form, humans as reservoir, is caused by L. donovani ; prevalent in East Africa and the Indian subcontinent.  Major forms: Visceral, cutaneous and mucocutaneous
  • 2.
  • 3.
  • 5. Risk of acquiring infection is determined by local sand fly behavior and by the presence of an infected animal or human reservoir Transmission Female sand flies (Phlebotomus and Lutzomiya Spp.) get infected after sucking blood from infected reservoir eg. human or other mammals Amastigotes transform to promastigotes in sand fly gut  Replicating and metacyclic promastigotes are regurgitated and injected into the skin during subsequent blood meal
  • 6. Other route of transmission are via  blood  Shared needles  Blood transmission  Trans-placental spread  Via organ transplantation
  • 7. Population at risk – 350 million Over all world prevalence – 12million Annual new case reports – 2 million About 90 countries affected More than 20 spp of leishmania identified VL in 70 countries,  S. Asia 600,000 cases in 2006 – significantly decreasing due to control measures  East Africa 30,000 (mainly Sudan, Ethiopia)  Brazil 4,000
  • 8. E Diro Department of Internal Medicine UoG 8
  • 9. lowlands of Ethiopia with varying endemicity. N West. - Metema and Humera, Wolkayit, Libo/Fogera N East – Ethio-Djibouti Awash Valley S. West – Segen, Dawa, Genale, Woito, Konso, Omo, Gambella Sudan border 40 localities and new foci are being reported. Main risk factor - population migration Estimated annual VL – 4500-5000 people
  • 10. VL cause - by species of the Leshmania donovani complex - L. donovani The sand fly - Phlebotomus orientalis, Phlebotomus martini and Phlebotomus celiae.  Animal reservoirs are suspected, but not documented yet.
  • 11. 11 VL- HIV co-infection rate at Humera  1998/99 – 18.5%  2006 – 40% A Tigray retrospective review of 791 cases showed >4x CFR in HIV + VL patients than VL without HIV. Libo – HIV –VL coinfection rate 15-18%.
  • 12. More than 90% of the world's cases of cutaneous leishmaniasis occur in Middle East (Old World) and in Brazil and Peru (New World). The etiologic agents are L. tropica, L. major, and L. aethiopica (Old World) and species of the L. mexicana complex and the Viannia subgenus (New World).
  • 13. 13 T cell Response Th 1 pattern Response Th 2 pattern Response T lymphocyte release IL-2 and INF gamma Ineffective humoral response Effective cellular response Activates macrophges to kill Leishmania Leishmainin skin test positive, but no clinical VL T lymphocyte release IL-4,IL-5,IL-10, TNF - B Inhibit macrophage from killing Leishmania High Antibody level and Clinical VL IL 4 & 10 -
  • 14. Depends on – Parasitic properties (Infectivity, pathogenicity and Virulence) Host factors and host responses Manifestation range from asymptomatic, self healing cutaneous leishmaniasis to diffuse cutaneous and visceral disease
  • 15. Presentation Kala-azar (Black fever in Hindu) IP: Wks –Mo’s Often remains asymptomatic Symptomatic cases: acute, sub acute or chronic course Fever, night sweats, weakness ,weight loss Cachexia, wasting, Pallor Nontender, soft massive splenomegaly + perisplenitis
  • 16. Hepatomegaly + LAP Darkening of face/ashen grey appearance Bleeding 20 to thrombocytopenia Susceptibility 20 infection Pancytopenia (Anemia, Thrombocytopenia, Leukopenia, Neutropenia) Marked eosinopenia, Reactive lymphocytosis, Monocytosis Hypergammaglobulinemia Hypoalbuminemia
  • 17.
  • 18. Gold-standard: Demonstration of amastigotes in tissue aspirates Diagnostic sensitivity – Spleen - > 95%; Bone marrow  70%, Lymph nodes  58% DAT test: Anti-Leishmanial (titer) IgG sn >95%, sp >90% Detection of Anti-rK39-Abs Sn 72%, Sp 82% Culture – NNN media Isoenzyme and molecular techniques to differentiate species
  • 19.
  • 20. SSG + Paramomycin for 17 days Sodium stibogluconate (SSG) 20mg/kg iv/im for 30 days Alternative:  AmBisome 4mg/kg for 5-7 doses: 1-5days, 10th, 14th.  Amphotericin B 1mg/kg every other day for 30 days/total 15 doses.  Single dose AmBisome not effective in N Ethiopia Other drugs but less effective:  Paramomycin, Pentamidine, Miltefosine (oral prep) Secondary prophylaxis (in HIV)- ?? Pentamidine
  • 21. Clinical improvement after 7-10 days in majority Apparent cure response (Afebrile,  splenic size, no visible amastigotes on repeat splenic aspirate within 2 weeks of Rx in > 90% of cases Hematologic abnormality improvement by 4th weeks of Rx Splenomegaly disappear < 6 months after Rx
  • 22. Reactive skin test + ve < 1 yr after Rx No response or death : 5-10% Relapses after apparent cure: 5-10% (often < 6 months after Rx) Cure documented after 6 months of Rx completion (-ve splenic aspirate for leishmania i.e. test of cure)
  • 23. New infection or Reactivation (>95% of co- infection reports are of VL) Less virulent leishmania spp cause VL. Most patients with CD+ 4 count <200/l Widespread atypical organ involvement eg GIT Frequent parasitemia, high yield from buffy coat  Peripheral blood 50%, buffy-coat culture 70%
  • 24. Sub optimal specific IgG production Lower diagnostic sensitivity to serologic tests (50% Vs >90%) High rate of relapse / drug toxicity Reduced responsiveness to tx (comparable initial response) HAART-  incidence of clinical leishmaniasis
  • 25. Demonstration of amastigote forms on geimsa or wright stain method VL with out HIV VL with HIV spleen 93-99% Bone marrow 53-86% 67-94% Lymph node 53-65% Buffy coat / BF ~ 30% 50- 53% DAT 95-97%* 95% in Ethiopia; 89-90% rK39 93-100%* 22-62%
  • 26. IP =Weeks - Months Start as a papule at the site of insect bite and evolve to nodules, ulcer, plaque It may complicate with regional adenopathy, sporotrichoid subcutaneous nodules, lesion pain or pruritis, 20 bacterial infection The infecting spp, the location of lesion and the host immune response determine the manifestation and chronicity of the lesion
  • 27.
  • 28.
  • 29. Visualization of amastigote in Giemsa-Stained thin smear from dermal scraping /biopsy specimen. Serology tests – insensitive Indication for treatment Persistent lesion ( > 6 months) Lesions that are located over joints Multiple lesions (> 5 to10 in number) Large lesions (> 4-5cm)
  • 30. IV/IM SSG therapy, Pentamidine, Ketoconazole, dapson Local/Topical therapy - Intralesional SSG therapy, Heat therapy, Cryo therapy
  • 31. Presentation: - Erythema and ulceration of the nares  Nasal septal perforation and destructive inflammatory lesion  obstruction of pharynx/larynx and remarkable disfigurement. Treatment IV/IM SSG therapy, Amphotericin B
  • 32.
  • 33. Etiology:- Entamoeba histolytica Epidemiology: Transmission and cycle E. histolytica acquired by the ingestion of infectious viable cysts from feces contaminated water, food or hands  Release of motile trophozoite from cysts in small intestine  Large bowel mucosa invasion with sub mucosal extension  Inoculation of amoebas in to the portal system distant metastatic abscess in liver /lung/brain  Encystation of trophozoites and/or motile trophozoites passage in stool.
  • 34. 1. Intestinal amoebiasis Mostly asymptomatic cyst passage (90%) Symptomatic cases (10%): IP = 2 - 6weeks Lower abdominal pain, Bloody mucoid diarrhea, Fever (<40%), malaise
  • 35. Toxic megacolon :- Bowel dilation with intra- mural air  predisposing factor: - Glucocorticoid treatment Chronic amoebic colitis - DDX: IBDs ? Post amoebic colitis Bowel perforation GI bleeding
  • 36. Acute presentation in young pts with prominent symptoms <10 days Chronic /sub acute presentation in older pts with hepatomegaly /Wt loss/anorexia > 6 months Pathology : “ Anchovy paste” Fever – possible cause of FUO (10-15%) RUQ pain + Hepatic point tenderness Rt. Sided pleural effusion Preceding active diarrhea (<30%)
  • 37.
  • 38. Pleuropulmonary amoebiasis (20-30%) Hepato-bronchial fistula Rupture into the peritoneal space Rupture into the pericardium (left lobe site)
  • 39. 1. Stool examination  Microscopic fecal findings: Wet mount  +ve test for heme  Paucity of neutrophils  Amoebic cysts or hematophagous trophozoites of E.histolytica 2. Serologic test for invasive amoebiasis  ELISA  Agar-Gel diffusion assay  +ve in >90% of pts with colitis /Amoebomas/liver abscess
  • 40. 3. Liver imaging - US/CT scan/MRI for oval /round hypoechoic cyst >80% who had Sxs >10 days –single abscess in rt. lobe 50% who had Sxs <10 days –multiple abscesses Findings favoring complications  Large abscess (>10cm)  Abscess in superior part of rt. lobe  Multiple abscesses  Abscess in left lobe
  • 41. 1. Intestinal amoebiasis Asymptomatic carriers: Luminal agents – Iodoquinol 650mg tid/20 days, or paromomycin 500mg tid /10days 2. Acute Colitis Metronidazole 750mg po/iv for 5-10days + luminal agent 3. Amoebic liver abscess Metronidazole 750mgtid/5-10days or Tinidazole 2gmpo or Ornidazole 2gmpo plus luminal agent
  • 42. Need to R/O Pyogenic abscess (in multiple hepatic abscess) Failure to respond clinically within 3-5 days of Rx The threat of imminent rupture Prevention of left lobe abscess rupture into pericardium Surgery Bowel perforation Abscess rupture into the pericardium /peritoneum/ pleural space
  • 43. Adequate sanitation + Eradication of cyst carriage Avoid unpeeled fruits/vegetables Use of bottled water Water disinfection by iodination
  • 44. A trematode/flat worm blood fluke Five spp. Intestinal (mansoni, japonicum, mekongi, intercalatum) and urinary (haematobium) Intermediate host – snails; definitive host – humans
  • 45.
  • 46.
  • 47. Infected snails in fresh water release infective cercariae Cercaria penetrate intact skin (they have anterior and ventral sucker) – in the skin form schistosomula (morphologic, membrane and immunologic transformation) from trilaminar to hepatolaminar membrane adaptive mechanism for survival in humans.
  • 48. Mature forms migrate to specific sites – intestine, vesicle – mate and gravid females travel retrogradely in veins and deposit their eggs in small veins Eggs reach intestinal lumen aided by enzymes and are voided in stool and urine - miracidum About 50% are retained in host tissue and flow to liver and other tissues
  • 49. Prevalence starts from age 3-4 yrs and peaks at 15- 20 yrs and decline with older age Infect 200–300 million individuals in South America, the Caribbean, Africa, the Middle East, and Southeast Asia HIV and schistosomiasis - fewer eggs in their stools than those infected with S. mansoni alone for unknown reasons Treatment with praziquantel may result in reduced HIV replication and increased CD4+ T lymphocyte counts
  • 50. Ethiopia – prevalent around Lake Tana, tributaries of Blue Nile, Awash; Adwa area Associated with the water use
  • 51. Dermatitis/swimmer’s itch – popular pruritic rash at skin penetration site in 24-48hrs Katayama fever – serum sickness like illness associated with excess antigenemia and formation of soluble immune complexes
  • 52. Eggs retained in host tissues – presinosoidal in the liver Cell-mediated granulomatous response around the ova regulated both positively and negatively by a cascade of cytokine, cellular and humoral responses Granuloma formation begins with recruitment of a host of inflammatory cells in response to antigens secreted by the living organism within the ova
  • 53. Granuloma formation results in organomegally, obstruction and fibrosis
  • 54. Fibrosis of the portal veins can occur and result in periportal (Symmers' clay pipe–stem) fibrosis; local or diffuse Portal HTN results in ascitis, splenomegally and esophageal varices Similar pathologic changes occur in the bladder and results in granuloma formation, polypomatous growth that can ulcerate and bleed, obstructive uropathy, urosepsis, risk of bladder ca
  • 55. Lung – pulmonary HTN and corpulmonale Brain and spinal cord affection by granuloma and neurologic manifestation is possible eg transverse myelitis GIT – bloody diarrhea and abdominal pain With concomitant HBV and/or HCV infection can lead to significant deterioration and cirrhosis of the liver
  • 56. Swimmer’s itch – typical history contact hx, several DDx. Katayama fever - peripheral blood eosinophilia, and a positive serologic assay for schistosomal antibodies: the Falcon assay screening test/enzyme- linked immunosorbent assay (FAST-ELISA) and the confirmatory enzyme-linked immunoelectrotransfer blot (EITB). Some have ova in stool. Chronic cases – detection of ova in the stool, urine. Kato thick smear or other concentration method.
  • 57. Antipruritic agents for local lesions Supportive care and glucocorticoids for acute severe illnesses Praziquantal (20mg/kg in 2 divided doses) effectiveness - 85% parasitological cure and 90% egg reduction. Hepatomegally and bladder lesions also regress with early treatment but established fibrosis persists.
  • 58. Avoid contact with fresh water sources in endemic areas be it fast or slow flowing Skin topical agents Molluscicides – eg. Lemma toxin (Aklilu Lemma from “endod”) Safe water supply Follow up of exposed individuals.
  • 59. History is important for dx Epidemiology, occupation, travel Life cycle of major parasites Specimen collection
  • 60. Helminths & protozoa Excreted by feces - Collection on clean card board Avoid water contamination Take before contrast medium or anti diarrhea agent intake 3 specimens on alternative days Polyvinyl alcohol preservation for transport (for protozoa trophozoits)
  • 61. Macroscopy - nature of stool - segments of Taenia / motility - Ascaris worm Microscopy - with wet mount (saline, dilute iodine) Concentration methods:  formalin ether sedimentation (all sediment - preference  zinc sulfate flotation ( not all float ) Stains  Iron hematoxylin, Trichrome
  • 62. Amoebic liver abscess - trophozoites in the abscess wall  S. haematobium - in urine sediments Malaria; leishmania; Trypanosoma - in blood and lymphoid tissues Pneumocystis carinii - silver stain of bronchial aspirate Onchocerciasis - skin snips Schistosoma mansoni - rectal snips Cutaneous and muco-cutaneous leishmania - punch biopsy
  • 63. Eosinophilia - in trichinosis & Migratory phase filariasis  Pulmonary migration of larva's of intestinal round worms  Not common in protozoal infections except isospora & Dientamoebe fragilis HCMC anemia - in hook work infection Portal HTN - in Schistosomiasis Anemia, thrombocytopenia in Malaria, VL  cysts, mass lesion, ring enhancement ......on radiologic examination (CT, US) in hydatid cyst, toxoplasmosis of CNS....
  • 64. Limitations - for individual pt use - cross rxn - not distinguish current & past infection Negative result rules out infection Molecular Teachnology PCR - for T. vaginalis (in USA)
  • 65. Cestodes /flat worms Intestinal Parasite stage Specimen Remark T. Saginata ova/segment feces Motile segments H. Nana Ova " D. Latum Ova/ segmenta " Megaloblastic T. solium ova/segment " non motile cysticercus muscle/CNS CT/MRI Treatment -Niclosamide -Praziquantal -Albendazole
  • 66.
  • 67. somatic Echinococcus hydatid cyst liver/lung US/X-ray/CT liver flukes/F. hepatica ova feces/bile cirrhosis/portal hpt Blood flukes schistosoma mansoni ova/adult feces rectal snip, liver bx S heamatobium ova/adult urine bladder biopsy Treatment Echinococcus - long term Albendazole, surgery Schistosomia _ praziquantel
  • 68. Round worms E. vermicularis/pin worm ova perianal skin scotch tape test T. trichiuria/wipe worm ova feces rectal prolapse Ascaris lumbricoids ova " pulm. migration Hook worm ova " " " S. stercolaris larva feces/sputum diss. in HIV Hookworm ova Ascaris ova
  • 69. Treatment -Mebendazole, Albendazole – hoodworm, ascaris -Piperazine citrate – ascaris -Thiabendazole for strongyloids
  • 70. Tissue round worms Trichinella spiralis larva muscle muscle biopsy W. bancrofti filaria microfilariablood, L.nd nocturnally active O. Volvulus/river blindness adult/larva skin/eye nodules,skin snip D. Medinensis (guinea worm) " “ skin in the lesion Visceral larva migrans larva viscera/CNS ?other worms
  • 71. Protozoa E. histolytica trophozoit/cyst feces/liver US/CT liver G. lamblia " feces isospora belli oocyst " Acid fast Cryptosporidium Oocyst " AFS, biopsy, PCR Microsporidia(? fungi) spore " Modif. trichrome, biopsy, PCR Treatments •Amoeba and giardia – metronidazole, tinidazole •Isospora belli – cotrimexazole 960mg QID for 10 days; for HIV pts additional 960mg TID for 3 weeks •Cryptosporidium – no effective tx, trial with paramomycin, Nitazoxanide •Microsporidia – albendazole 400 mg po BID for 2 - 4 weeks
  • 72. Blood and tissue protozoa Plasmodium asexual forms blood Trypa rhodesiense trypomastigoteblood, CSF chancre, L.node Leishmania amastigote RES biopsy, culture Toxoplasma gondi cyst, trophozoite CNS, eye, muscle ?HIV