CESTODES TRANSMISSSION PATHOGENISIS CLINICAL DIAGNOSIS TREATMENT

FEATURES

ECHINOCOCCUS The embryo of E granulosus Lung cysts can extend into bronchus -In definitive host is difficult -Surgery: with the goal of
GRANULOSIS Contamination of forms one large fluid filled causing hemoptysis by ordinary microscopy leaving the cyst intact so
-Geographic hands food with feces (unilocular) “hydatid” cyst, Brain cysts cause headache and focal because it will look like new cysts do not form
Distribution: of infected dog which consist of neurologic signs Taenia and Echinococcus -Mebendazole can be taken
Worldwide 1-Outer thick laminated cyst Rupture of cyst can result a fatal eggs over a long period of time
-Higher prevalence wall anaphylactic reaction -Eosinophilia at low dosages
in South America 2-Inner thin nucleated germinal -Intradermal (Casoni) test -Praziquantel
(Argentia,Uruguay), layer with hydatid fluid PREVENTION
Europe(Mediterrane -Detection of antigens in -Keep dogs from being
an bassin), Northern 1-Brood capsules are from the feces by ELISA - best ifected by prevent them
Africa, Middle East, germinal layer available technique from eating infected feaces
South Central and 2-Prtoscoleces are formed -Polymerase chain reaction or contaiminated meat.
East Asia inside the brood capsule (PCR) is also used to - to avoid human infection
--Three species 3-The outer thick and fibrous identify the parasite from by avoidingingestion of
-Echinococcus layer. DNA isolated from eggs or food or other substances
granulosus: causing -Free brood capsule and feces. contaminated with dog
hydatid disease individual protoscoleces feaces.
-Echinococcus released from the capsule form -Best method is to disrut
multilocularis: the hydatid sand. the life cycle
causing alveolar .BASIC HYGIENE practices
hydatid disease Daughter cysts are formed .Avoid raw offal to dog.
-Echinococcus within the main cyst when part
vogeli: causing of germinal layer become
hydatid disease detached
Because cyst fluid can sensitize
the host, the rupture of the
cyst can cause fatal
anaphylaxis; can also
disseminate protoscoleces.
 TRANSMISSION PATHOGENESIS
TREMATODES
Life cycle :
SCHISTOSOMA to man by free -Definitive host: human beings,
SCHISTOSOMA swimming fork tailed Teen age/ children effected.
HEMATOBIUM cercariae, penetrate hematobium in vesical plexus,
skin by while bathing mansoni & japonicum in
Distribution: Africa, or washing and hemorrhoidal plexus.
Middle east. fishing, agricultural -Intermediate host: fresh water
Dams and irrigation work or contact with snail.
schemes led to infected water. -Cercariae → larvae
increased incidence schistosomula → enter blood
in veins → arterial circulation
→ superior mesenteric →
portal circulation → liver →
mature to adult worm → pair
up. Female resides in
gynecophoric canal in male →
venous plexus between rectum
and bladder
-Female lays eggs in venules
20-200/day, pale yellow oval
145x55um, spine at one end,
contain fully developed
miracidium
-Eggs penetrate endothelium
→ bladder → passed in urine.
Flame cell movement
-Hatch infresh water → ciliated
larvae miracidium → penetrate
snail → develop into sporocyst
→ multiply → many cercariae
→ enter water → penetrate
CLINICAL FEATURES DIAGNOSIS TREATMENT
-Asymptomatic. -Urine Microscopic exam:
-Early stage: Swimmers itch - RBC, protein, eosinophils, Praziquantel, Niridazole
dermatitis and itch at site of cercarial bacteria, eggs or
penetration. miracidium. No of PREVENTION:
-Acute stage: .Occurs 1-2 months after egg/10ml more than 50 → proper disposal of human
entrance , last for 3 months, due to heavy infection wast
growing schistosomule in systemic & -Blood test: Eosinophillia - Safe water supply
portal circulation. fever, cough, -Skin (fairley’s) test: chlorinated, 48 hr storage, -
abdominal pain, chills diarhoea, cercarial antigen Safe bathing sites.
lymphadenopathy, Hepatomegaly & intradermally àdelayed Swimming in endemic
splenomegaly, hematuria, dysuria, hypersensitivity. areas should be avoided
frequency UTI, Rise of salmonella -Avoid contamination.
infection, arthralgia. Migratory larvae Destroy snails
→ eosinophilia -Specimens: urine, feces,
- Chronic stage: blood, biopsies from
.Within 3-9 months of infection, due bladder & rectal wall, &
to eggs. painless hematuria, liver.
frequency of micturition, fibrosis &
calcification, stones leading to renal
failure and uremia. Ectopic lesions to
lungs, spinal cord. impaired growth,
anemia
skin

URINARY SCHISTOSOMIASIS
-Cercariae causes immediate
hypersensitivity response.
-Egg eggs erode blood vessels
& bladder wall, resulting in
hemorrhage, induce
granulomatous inflammation
→ fibrosis in liver and bladder.
Eggs Produce proteolytic
enzymes. Eggs die → calcified
→ sand patches in bladder
-Worm coat themselves with
host antigens → inability to
recognize as foreign
-Heavy infection → other parts
of body
- long standing untreated
infection → immune response
→ thickening of wall → bladder
obstruction →UTI →obstructive
renal disease → renal damage
-Chronic → associated with
squamous cell carcinoma
INTESTINAL
SCHISTOSOMIASIS
-Schistosoma japonicum egg
small spine) and mansoni
(eggs lateral spine →
mesenteric venules → large
intestine → feces → GIT
hemorhage → death from
ruptured esophageal verices
-Early & acute stage similar to
hematobium
-Chronic stage: abdominal pain
and distention, dysentery,
hepatomegaly, splenomegaly,
rectal prolapse