OBJECTIVES: 1. To discuss common parasitic infections in man. 2.

. Discuss their morphology and characteristic features, epidemiology, mode of transmission, clinical manifestation, treatment and prevention.

COMMON PARASITIC INFECTIONS

Junie Dawn Decolongon- Reyno, MD, DPCP

INTESTINAL NEMATODES

NEMATODES

More than a billion worldwide are affected Common in regions with poor fecal sanitation Contribute to malnutrition and diminished work capacity Roundworms:

range from 1 mm to many cm when mature

complex and varied life cycle Person to person - E Vermicularis and S. stercoralis Require a soil phase A. lumbricoides andHookworm

NEMATODES
Species which parasitize the small intestines 1. Ascaris lumbricoides 2. Necator americanus 3. Ancylostoma duodenale 4. Strongyloides stercoralis 5. Capillaria philippinensis Species which parasitizes the large intestines 1. Enterobius vermicularis 2. Trichuris trichiura

LIFE CYCLES:

include egg stage 4 larval stages adult stage

Adult female may be: A. Oviparous- eggs are oviposited and embryo develops outside the maternal body e.g(A. lumbridoides)

B.Viviparous female gives birth to larvae (C.

Philippinensis)

C.Parthenogenetic can produce viable eggs without being fertlized by the male worms (S. stercoralis)

ASCARIS LUMBRICOIDES

Thrives in areas with lack of sanitation and poverty and ignorance Most common source of infection soil contaminated foods esp. in raw vegetables 2 separate populations and reservations 1. adult Ascaris parasitizing man 2. Ascaris eggs environment The most common intestinal roundworm of man Occurs most frequently in tropical and subtropical regions of Asia, Central and South America and Africa

ASCARIS LUMBRICOIDES (MORPHOLOGY)

Adult creamy white or pinkish yellow A. Female tapered at both ends; large; - measures 20 t0 35 cm by 5 mm ; may grow up to 45 cm long - reproductive potential : 240,000 eggs/day B. Male curved posteriorly - measures 15 to 25 cm by 3 mm

ASCARIS LUMBRICOIDES (MORPHOLOGY)

Fertilized eggs: mostly oval or spherical, golden brown : capable of further development in soil from single cell to embryonated eggs Shell contains: 1. inner non-permeable lipoidal vitelline membrane 2. thick transparent middle layer or glycogenlayer 3. outermost coarsely mammilated albuminoid layer Absent mamillated layer decorticated

ASCARIS LUMBRICOIDES (LIFE CYCLE)

ASCARIS LUMBRICOIDES
(PATHOLOGY & CLINICAL MANIFESTATIONS)

Migratory larvae hemorrhages and destruction of the lung parenchyma as the larvae breaks break through the capillaries - asthmatic type of respiration - cough with rales and chest pain - Ascaris pneumonitis - Loefflers syndrome ( allergic eosinophilic infiltration of the lungs) Larva bloodstream lodge in brain, spinal cord, the eyeball, kidneys adult worms pressure symptoms

ASCARIS LUMBRICOIDES

(PATHOLOGY & CLINICAL MANIFESTATIONS

-

Adult worms in small intestines: Decreased fat and nitrogen absorption Lactose intolerance Decreased growth rates in children Diarrhea, vague abdominal pain, loss of appetite

Vomited Ascaris pass larynx suffocation May enter Eustachian tube otitis media

ASCARIS LUMBRICOIDES

(PATHOLOGY & CLINICAL MANIFESTATIONS)

Due to erratic behavior May become entangled intestinal obstruction Appendix acute appendicitis Bile duct biliary ascariasis Liver multiple abscesses Perforate the bowel peritonitis Gallstones (Ascaris eggs)

ASCARIS LUMBRICOIDES

(DIAGNOSIS)
1. 2.

Direct Fecal Smear (DFS) 2 mg of stool used Kato-Katz technique 40-60mg of stool ADVANTAGES: a)quantitative: can count the number of eggs found measured stool sample b) can determine egg reduction rate after treatment c)determine intensity of infection

in a

Negative stool exam: a. When patients are actually free from infection b. During early larval migration via blood stream c. When worms are still sexually immature d. When only male worms are found in intestines

BILIARY ASCARIASIS

THE HOOKWORMS
1.

2.
3. 4.

Necator americanus* Ancylostoma duodenale* Ancylostoma braziliense Ancylostoma caninum

* soil-helminths that infect man

HOOKWORMS (EPIDEMIOLOGY)

Hookworm infections: 96% - N. americanus 2% - Ancyclostoma 2% - mixed Sandy loam type of soil with plenty of rain favorable for infection Chief sources of infection: Unsanitary disposal of feces Use of human feces as fertilizer

ANCYLOSTOMA DUODENALE

Copulatory bursa

NECATOR AMERICANUS

COPULATORY BURSA

HOOKWORM RHABDITIFORM LARVA

HOOKWORM FILARIFORM LARVA

HOOKWORM EGG
Eggs:

ovoidal, thin-shelled, colorless 4-8 cell stage in constipated stool embryo may develop inside shell

Differentiation of Necator and Ancylostoma difficult and impractical

HOOKWORMS: LIFE CYCLE

THE HOOKWORMS : PATHOLOGY AND CLINICAL MANIFESTATIONS

I. CAUSED BY LARVAL STAGE 1. Ground Itch / Coolie Itch - Intense localized itching, edema,
eruption
- Lasts up to 2 weeks - Site of entrance of filariform larvae dermatitis

erythema and papulovesicular

THE HOOKWORMS : PATHOLOGY AND CLINICAL MANIFESTATIONS

2. Creeping eruption or Cutaneous Larva Migrans
- Due to exposure of the skin to filariform larvae of A. braziliense/caninum;
- occasional N. americanus and A. duodenale - Serpiginous tunnel in stratum germinativum of skin - Larvae move at a rate of several mm to per day - Pruritus pyogenic infection

few cm

THE HOOKWORMS: PATHOLOGY AND CLINICAL MANIFESTATIONS

THE HOOKWORMS : PATHOLOGY AND CLINICAL MANIFESTATIONS

3. Pulmonary lesions - Petecchial hemorrhages - Eosinophilic and leucocytic infiltration

THE HOOKWORMS : PATHOLOGY AND CLINICAL MANIFESTATIONS

II. CAUSED BY ADULT WORM Hookworm anemia Due to continuous mechanical suction of blood from intestinal mucosa
Microcytic, hypochromic anemia Loss of RBC in gut 0.03-0.05 ml blood/ day (N. americanus) 0.16-0.34 ml blood/day (A. duodenale)

THE HOOKWORMS : PATHOLOGY AND CLINICAL MANIFESTATIONS

Hypoalbuminemia

Combined loss of blood and lymph

HOOKWORMS (DIAGNOSIS)

Ground itch and creeping eruption - character of lesion - history of contact with soil

recovery of eggs on stool ( DFS, Kato, Formalin Ether concentration)

STRONGYLOIDES STERCORALIS (EPIDEMIOLOGY)

-

Found throughout the world More of a fecally-transmitted worm that a soil-tansmitted helminth because it is infective shortly after passage with the feces Low local prevalence More frequently found among male children 7-14 years old than among females and adults

STRONGYLOIDES STERCORALIS

Disease : Strongyloides, Cochin-China diarrhea, Threaworm Epidemiology : infections runs parallel with hookworm infection Infective stage filariform larvae skin penetration

LIFE CYCLE OF STRONGYLOIDES

Adult parasite, Eggs Rhabditiform Female, in small in larva hatches Intestine of man mucosa from egg Esophagus 1.Autoinfection 2.Direct Cycle 3.Indirect in intestine (like hookworm) Swallowed Passed in feces into soil Pharynx Becomes filariform larva Free living adult (M & F) Trachea Penetrates intestinal mucosa Eggs Breaks out Into alveoli Larva in colon Rhabditiform larva Lungs Filariform larva on soil Heart Blood stream Penetrates the skin of man

STRONGYLOIDES (RHABDITIFORM LARVA)

-

free-living Smaller than the filariform larva Female: muscular double-bulbed esophagus and the intestine is a straight cylindrical tube Male: smaller than female; ventraly curved tail, 2 copulatory spicules, gubernaculum with no caudal alae

STRONGYLOIDES (FILARIFORM LARVA)

-

parasitic; semi-transparent, with fine striated cuticle Slender tapering anterior end and short conical pointed tail Buccal cavity has 4 distinct lips Uteri contain a single file of 8-12 thin-shelled transparent, segmented ova

STRONGYLOIDES STERCORALIS (PATHOLOGY & MANIFESTATIONS)

Filariform larva entry skin penetration petechial hemorrhage, congestion & edema, pruritus - lungs >>>pneumonitis (cough), pleural effusion Filariform & Adult intestines >>>GIT disturbances Stool water mucous diarrhea depends on

A. Intessity of infection B. Duration C. Host-tissue rxn = encapsulated the worms

Blood picture leukocytosis (WBC 25,000) Eosinophilia ( 40%)

STRONGYLOIDES STERCORALIS (DIAGNOSIS)

Finding the rhabditiform larvae feces or duodenal aspirate direct or concentration methods Eggs can only be obtained by drastic purge /NGT duodenal aspirates

CAPILLARIA PHILIPPINENSIS (EPIDEMIOLOGY)

Capillariasis first recorded in Northern Luzon Also reported in Thailand, Iran, Japan, Egypt, Korea, Taiwan and India Migratory fish-eating birds are considered natural hosts In the Philippines, this has been documented in the Northern Luzon provinces,Zambales, Southern Leyte, Compostela Valley and Zamboanga del Norte Mode of transmission: eating uncooked small freshwater/brackish water fish; Northern people like to eat bagsit and other fish found in lagoons

CAPILLARIA PHILIPPINENSIS (PARASITE BIOLOGY)

MALE

FEMALE

- 1.5-3.9mm
- spicule 230-300um long and has unspined sheath - thin filamentous anterior end and a slightly thicker and shorter posterior end - esophagus has rows of secretory cells - anus is subterminal

- 2.3-5.3mm - thin filamentous anterior end and a slightly thicker and shorter posterior end - esophagus has rows of secretory cells - anus is subterminal - vulva seen at the junction of anterior and middle thirds

CAPILLARIA PHILIPPINENSIS (PARASITE BIOLOGY)

EGG

- peanut-shaped with striated shells and flattened bipolar plugs

- 36-45um by 20um - embryonate in the soil or water

CAPILLARIA PHILIPPINENSIS (LIFE CYCLE)

CAPILLARIA PHILIPPINENSIS (CLINICAL MANIFESTATIONS)

Symptoms: abdominal pains, gurgling stomach (borborygmus), and diarrhea; weight loss, malaise, anorexia, vomiting, and edema Laboratory findings: severe protein-losing enteropathy, malabsorption of fats and sugars, decreased excretion of xylose, low electrolyte levels (esp. potassium), and high levels of immunoglobulin E Direct fecal smear finding the egg Stool concentration method Duodenal aspiration

ENTEROBIUS VERMICULARIS

Enterobiasis human pinworm - characterized by

perianal itching

ENTEROBIUS VERMICULARIS (MORPHOLOGY)

Adults: small, whitish or brownish in color anterior end pair of lateral cuticular expansion (LATERAL WINGS or CEPHALIC ALAE) posterior esophageal bulb male - 2-5 mm ; tail curves ventrad; single copulatory spicule female 8-13 mm ; long pointed tail

MALE

FEMALE

Eggs: measure 50-60 um by 2030 um elongated, ovoid, flattened on the ventral side similar to letter D egg shell two layers (outer thick hyaline albuminous shell and Inner embryonic lipoidal membrane) larva folded once within the shell (creating a line visible along the eggs long axis)

ENTEROBIUS VERMICULARIS LIFE CYCLE

ENTEROBIUS VERMICULARIS (PATHOLOGY AND MANIFESTATIONS)

1/3 asymptomatic 3 forms: I. Pathology at the site of attachment of the worm Minute ulcerations or abscesses in cecal mucosa II. Pathology due to egg deposition in the perineal area - intense itching or pruritus in the perianal region - scratching scarified - pruritus ani hemorrhage, eczema, bacterial perianal regions and perineum III.Pathology caused by migrating adults - migrating worms lay eggs in genital organs vulvovaginitis - worms enter fallopian tube salpingitis

infection of the anal and

ENTEROBIUS VERMICULARIS (DIAGNOSIS)

History and physical exam

Perianal cellulose tape swab D shaped ova - best time is soon after patient awaken and before bathing 5% only are demonstrable in feces worms may be seen migrating out of the childs anus at night

ENTEROBIUS VERMICULARIS (EPIDEMIOLOGY) 1. Infection may occur through:

a.Hand to mouth transmission most common transmission b. Inhalation of airborne eggs in dust c.Retroinfection through the anus - eggs hatch in the perianal region and larvae migrate back into large intestine 2. Only nematode that cannot be controlled through sanitary disposal of human feces because eggs are deposited in the perianal region.

ENTEROBIUS VERMICULARIS (EPIDEMIOLOGY)

3.

4. 5. 6.

Local prevalence - 29% among schoolchildren from exlcusive private schools - 56% among those from public schools Local prevalence higher in females compared to males Have been collected from fingertips and fingernails of schoolchildren Adult female worms migrate to the perianal area even during daytime but more migration occurs at night time.

TRICHURIS TRICHIURA

Whipworm Soil-transmitted Frequently occurs together with Ascaris Children from 5 15 years old are more frequently infected In the Philippines, prevalence is from 80-84% Factors affecting transmission: a. Indiscriminate defecation of children around yards b. Poor health education c. Poor personal, family and community hygiene.

TRICHURIS TRICHIURA (PARASITE BIOLOGY)

Male worm - 30 45mm

Female worm
- 35-50 mm - bluntly rounded posterior - attenuated anterior 3/5 traversed by a narrow esophagus; posterior 2/5 contains the intestine and a single set of reproductive organs - lays 3,000-10,000 eggs/day

- shorter than female - coiled posterior end with a single spicule and retractile sheath - attenuated anterior 3/5 traversed by a narrow esophagus; posterior 2/5 contains the intestine and a single set of reproductive organs

TRICHURIS TRICHIURA (PARASITE BIOLOGY)

EGG - 50-54um by 23 um - lemon shaped with pluglike translucent polar prominences - yellowish outer and a transparent inner shell - embryonic development takes place in the environment when eggs are deposited in clayish soil

TRICHURIS TRICHIURA (PARASITE BIOLOGY) Inhabit the large intestine Entire whip-like portion embedded into the intestinal wall of the cecum Eggs become embryonated within 2-3 weeks No heart-lung migration

TRICHURIS TRICHIURA (LIFE CYCLE)

TRICHURIS TRICHIURA (CLINICAL MANIFESTATIONS)

Worms embedded in the mucosa can cause petechial hemorrhages Rectal prolapse Appendicitis >20,000 eggs/gm of feces: severe diarrhea or dysenteric syndrome Light infections: asymptomatic In heavy parasitism: blood-streaked stools, abdominal pain, anemia, weight loss

TRICHURIS TRICHIURA (LABORATORY DIAGNOSIS)

In heavy infections, clinical symptoms may be relied upon to make a diagnosis

In light infections: 1. direct fecal smear 2. Kato thick smear method

TREATMENT, PREVENTION,

AND CONTROL

TREATMENT SCHEME

Mass treatment Selective treatment treating only those found positive for eggs on stool * Targeted group treating children alone

TREATMENT FOR NEMATODES

Broad Spectrum antihelminthics

worms

neuromuscular blocking effect on parasites paralysis of

1. albendazole

- 400 mg single dose

- give for 3 days for SS - give for 10 days for CP

*preferred over mebendazole inCPbecause itkils larvae more readily

2. mebendazole

- 500 mg single dose

- 200mg BID x 20 days for CP

3. pyrantel pamoate - 10 mg/kg single dose

* drug ofchoice forenterobius with2nd dose after2-4 weeks

*drug ofchoice fortrichuris, 3days inmoderate tosevere infections

4. thiabendazole - 50 mg/kg in 2 divided doses

Ascariasis Community based chemotherapy interval of 4 months or 3 times a year for 3 years

Among schoolchildren treatment at least twice a year at an interval of 4-6 months

Hookworm infections Severe anemia increase Hgb to 7-8 g/dL before dealing with worm infection

Severe hypoalbuminemia deworm quickly

Capillariasis Correction of electrolyte imbalance and protein malnutrition

PREVENTION & CONTROL FOR NEMATODES

Proper disposal of feces Proper treatment of human excreta used as fertilizer Personal hygiene use of shoes/slipper Avoiding ingestion of raw vegetables not washed properly Thorough cooking of food

Enterobius
allmembersofhouseholdwho arepositive shouldbetreated
at least7 consecutivepost-treatment perianalsmearsusingscotch-tapeswabmethodshouldbenegative- declarenegativeinfection personalhygiene cut fingernailsshort bed linensandclothingof infected persons sterilizedby boiling

Trichuris
mass tx if infection rate is more than 50%

CESTODES

TREMATODES(FLUKES) Intestinal Flukes:

Heterophyes heterophyes Metagonimus yokogawi

Lung Flukes:
Paragonimus westermani

Blood Flukes:
Schistosoma mansoni Schistosoma japonicum Schistosoma hematobium

TREMATODE

Flatworms
Major Human Trematode Infections:
1. Blood Flukes 2. Biliary Flukes 3. Intestinal Flukes 4. Lung Flukes Common Morphologic Features: a. macroscopic size b. Flattened bilaterally symmetric bodies

TREMATODE

C. prominence of 2 suckers d. hermaphroditic Definitive Host ( mammalian/Human) Intermediate Host ( Snails) Transmission direct penetration of intact skin/ ingestion Infection with trematodes that migrate through or reside in host tissues are associated with moderate to high degree of peripheral blood EOSINOPHILIA, a useful clinical indicator of infection.

HETEROPHYES HETEROPHYES

Common name: None. Habitat: Intestinal tract. Definitive host: Human,dogs,cats,canines. First intermediate host: Water snail. Second intermediate host: Water fish. Infective stage: Encysted metacercariae. Diagnostic stage: Eggs in feces. Disease: Heterophyiasis.

HETEROPHYES HETEROPHYES LIFE CYCLE1

HETEROPHYES HETEROPHYES ADULT

Very small; 1 1.7 x 0.3 - 0.4 mm Oral & Ventral Suckers Anterior scales. Unbranched caecum. Pharynx. Coiled Uterus Round ovary Round Testes ( side by side) Vitellariae in posterior third.

HETEROPHYES HETEROPHYES EGGS

Small, ovoid; 25-30 x 15-17 um. Yellow-brown color. Thick egg shell. Inconspicuous operculum. Embyonated (miracidium inside). No shoulders. No posterior knob.

HETEROPHYES HETEROPHYES: CLINICAL MANIFESTATION

Assymptomatic Symptoms occur in heavily infected or immunocompromised patient Onset of signs and symptoms: 9 days after ingestion of contaminated fish Anorexia, nausea, abdominal pain, weight loss, dyspepsia and mucous diarrhea Eggs are ocassionally hematogenously distributed to ectopic sites, such as the heart or central nervous system

HETEROPHYES HETEROPHYES: DIAGNOSIS AND TREATMENT

Finding the characteristic eggs in the stool

Confirmatory Test: recovery of adult worms following helminthic therapy Peripheral eosinophilia is present Treatment: Praziquantel ( 75mg/kg in 3 divided doses)

PARAGONIMUS WESTERMANI

Common name: The Lung Fluke. Habitat: Encapsulated in Lungs. Definitive host: Human, also other mammals. First intermediate host: Water snail. Second intermediate host: Crustaceans,Crabs. Infective stage: Encysted metacercariae. Diagnostic stage: Eggs in sputum or feces. Disease: Paragonimiasis.

PARAGONIMUS WESTERMANI: EPEDEMIOLOGY

Several parts of Central and South America and the Far east (including the Philippines) Prevalence of infection increase with numerous human and animal reservoir host and abundance of the 1st and 2nd intermediate host Prevailing social custom of eating raw undercooked seafood

PARAGONIMUS WESTERMANI MORPHOLOGY

7 12 x 4 6 mm. Oral & Ventral Suckers Unbranched caecum. Pharynx. Coiled Uterus ( black color) Lobed ovary Lobed Testes ( side by side) Vitellariae; branched extensively.

PARAGONIMUS WESTERMANI

Encysted in the muscles of Crabs. 250-500 um

PARAGONIMUS WESTERMANI: CLINICAL MANIFESTATION

assymptomatic, depending on the intensity of infection and the organs affected

Incubation Period: 2- 20 days following ingestion Initially: local inflammation and necrosis leading to diarrhea and abdominal pain, followed by fever, malaise, chest pain, dyspnea and cough as the fluke reach the lungs Can also affect other extrapulmonary sites such as the brain, and subcutaneous tissues

PARAGONIMUS WESTERMANI: DIAGNOSIS

Microscopy: detection of eggs in sputum or stools CSF: bloody with numerous eosinophils Skin Test: 80-90% sensitive, use for epidemiologic screening Elisa test: 92% sensitive 90 % specific

PARAGONIMUS WESTERMANI: TREATMENT

1. Praziquantel: 75mg/kg in 3 divided doses for 2 days Cure rate: 100% 2. Triclabendazole- alternative to those who cant tolerate Praziquantel

PARAGONIMUS WESTERMANI: PREVENTION

1. Avoid eating raw crabs and crayfish in endemic area 2. educate about the potential of contamination of utensils 3. Strict hygiene measure

SCHISTOSOMA

SCHISTOSOMA

Bilharziasis, after Theodore Bilharz, who identify the parasite in 1852 Associated with serious morbidity and mortality Chronic complication are generally seen in those with high parasite load which usually occurs in individuals who live in endemic areas Can also cause complication even with people with brief exposure, such as travellers

SCHISTOSOMA: EPIDEMIOLOGY

More than 200 million 200,000 deaths annually On a global scale, 1 in every 30 individuals has schistosomiasis Infection is acquire in childhood Prevalence and intensity of infection rises with age and peaks at approximately 15-20 years Transmission is higher in rural than urban Risk of infection are higher among those who live near lakes and rivers.

LIFE CYCLE

A. Humans as Definitive Host Mesenteric venule of the Small intestine S. japonicum Mesenteric venule of the colon S. Mansoni Vesical venous plexus C. haematobium

B. Snails as intermediate host: S mansoni Biomphalaria sp S. japonicum Oncomelania sp S. haematobium Bulinus sp

PATHOGENESIS

Adult worms: unless adult worms migrate to an unusual location( spinal cord or brain), do little damage Schistosoma eggs: 1. Inflammation and granuloma formation leading to fibrosis Liver: eggs lodge in the presinusoidal areas of the portal vein eliciting granulomatous fibrosis leading to blockade Symmers pipestem fibrosis Vesical and ureteral wall: fibrosis due to egg of S. haematobium leading to hydroureter and hydronephrosis, leading to renal failure

CLINICAL FEATURES

Acute Infections: A. Swimmers itch pruritic papular or urticarial rash at the site of entry typically on the lower extremities B. Katayama fever systemic hypersensitivity reaction against the migrating parasite - 2 -8 weeks after exposure - seen more on S. mansoni and japonicum - sudden onset of fever, chills, myalgia, arthralgia and dry cough, diarrhea and headache

CLINICAL FEATURES
Chronic Infection 1. Intestinal Schistosomiasis - chronic or intermittent abdominal pain, poor appetite and diarrhea - bloody stool leading to IDA 2. Hepatic Schistosomiasis - main cause of hepatosplenomegaly, develop in young and middle age adults with a long duration of intense infection -diffuse collagen deposit in the periportal spaces is the pathognomonic signs of SYMMERS pipestem fibrosis

CLINICAL FEATURES

3. Urinary Schistosomiasis cause by S. heamatobium - macroscopic and microscopic hematuria, dysuria and urinary frequency - can lead to Renal failure - risk in developing squamous cell CA of the bladder 4. Neurologic Complication a. spinal cord neuroschistosomiasis b. Localized cerebral and cerebellar neuroschistosomiasis

SCHISTOSOMA MANSONI
Common name: Blood Fluke. Habitat: Intestinal blood vessels ( veins) Definitive host: Human. First intermediate host: Water snail. Infective stage: Cercariae Diagnostic stage: Eggs in feces. Disease: Intestinal Schistosomiasis ( Intestinal Bilharziasis). Occurrence: Africa, Arabian area, South America

SCHISTOSOMA MANSONI ADULT

Separate sex; unisexual ( Diaceous) Male: 6.4 12.0 mm Female: 7.2 17.0 mm

SCHISTOSOMA MANSONI EGGS

140-180 x 45-70 um Has lateral spine. Embryonated ( with miracidium). Thin egg shell

SCHISTOSOMA JAPONICUM EGGS

70-105 x 50-80 um Smaller than S. mansoni and S. hematobium. Ovoid, thin clear shell. Embryonated. Non-operculated. Has lateral knob. Habitat of Adult: Intestinal blood vessels( veins). Disease: Oriental Schistosomiasis ( Katayama disease). Occurrence: China,Philippines,Far east.

SCHISTOSOMA HEMATOBIUM EGGS

112-170 x 40-70 um Larger than S. japonicum. Non-operculated. Has terminal spine. Embryonated. Transparent shell. Habitat of adult: Vesicle blood vessels ( Bladder, Rectum). Disease: Urinary Bilharziasis. Occurrence: Africa,

DIAGNOSIS

1. CBC 2. Microscopy demonstartion of the characteristic parasite eggs in stool and urine 3. Tissue biopsy rectal, intestinal or bladder biopsy 4. Radiology : USD liver involvement, periportal fibrosis around the portal vein tributaries CT Scan periportal fibrosis

TREATMENT

All patients with evidence of infection should be treated regardless of symptoms since adult worm can live for years Praziquantel treatment of choice Mechanism of action: induces ultrasructural changes in the teguments of adult worms Dose: S. heamatobium and mansoni 40mg/kg in 1 to 2 doses S. japonicum 60 mg/kg in 2 to 3 doses at least 3 hour apart

PREVENTION Water sanitation Mass treatment in endemic areas

CESTODES Diphyllobothrium latum Taenia saginata Taenia solium Echinococcus granulosus Echinococcus multilocularis

CESTODES

Consist of a head, neck and a segmental body Proglottid segmented body; complete set of repro organs Scolex head, equipped with suckers, hookers or grooves by which worm attaches itself to the intestine of the lumen

TAENIA SAGINATA
Common name: The Beef Tapeworm. Habitat: Small intestine. Route of infection: Eating of unwell cooked cow meat. Definitive host : Human. Intermediate host: Cows also other herbivores. Infective stage: Cysticercus larvae. Diagnostic stage: Eggs in Feces. Disease: Adults cause: Taeniasis.

TAENIA SAGINATA infection of man with the adult beef tapeworm Mode of transmission: eating raw or insufficiently cooked beef containing the cysticercus] Longest human parasite capable of growing to 7.5 m therefore most individuals harbor only one adult worm

TAENIA SAGINATA SCOLEX

1-2 mm in diameter. Four suckers. No hooklets. No rostellum ----------------------Adult: 5 10 meters. 1000-2000 segments

TAENIA SAGINATA

MATURE PROGLOTTID
Common genital pore (lateral). Uterus ( simple tube) Ovary ( Bilobed). Testes ( lateral, small). Vitellariae ( Scattered, dorsal).

TAENIA SAGINATA GRAVID PROGLOTTID

16-20 mm in length x 5-7 mm in width. Uterus with 15-30 lateral branch. Lateral genital opening. This segment is infective for Herbivores.

TAENIA SAGINATA GRAVID PROGLOTTID

This segment is stained with Iodine by injection of it through genital opening. You can count the number of Uterine Branchs. ( 15-30 Branch).

TAENIA SPP., EGGS

31-43 um ( Round to Oval) - Hexacanth embryo inside - Radially striated egg shell.

TAENIA SOLIUM

Common name: The Pork Tapeworm. Habitat: Small intestine. Route of infection: Eating of unwell cooked Pork meat. Definitive host : Human. Intermediate host: Pork or Swine. Human (occasional). Infective stage: Cysticercus larvae. Diagnostic stage: Eggs in Feces. Disease: Adults cause: Taeniasis. Larvae cause: Cysticercosis( presences of Cysticercus larvae in brain and muscles.

TAENIA SOLIUM
Taeniasis solium - refers to infection of humans with

adult pork tapeworm Human cysticercosis - refers to infection of humans with larval stage of parasites Diseases produced by infection with larval taenia solium is not uncommon in regions where Taenia solium adult infection exist In human cysticercosis: Man becomes the intermediate host

EPIDEMIOLOGY
T. solium infection

- prevalence of infection is directly related to eating habit of people (raw or insufficient cooked pork) - Man is the only known definitive host and the pig appears to be the only intermediate host a. Man become the intermediate host b. Can be caused by: ingestion of eggs from contaminated food or water contamination from dirty fingers by internal autoinfection when the eggs are carried by reverse peristalsis back to the doudenum

LIFE CYCLE

PATHOLOGY
1. Pathology brought about by adult taenia solium in lumen of the small intestines maybe negligible a. Mild transitory intestinal obstruction b. Vague abdominal pain similar to hunger pain which is due to heavy cysticercosis resulting to regurgitation of gravid segments in to the stomach of patients suffering from taeniasis solium 2. pathology brought about by larval stage (cysticercus cellulosae)

TAENIA SOLIUM, SCOLEX,NECK, IMMATURE,

MATURE PROGLOTTIDS

TAENIA SOLIUM MATURE PROGLOTTID

Common genital pore (lateral). Uterus ( simple tube) Ovary ( Bilobed). Testes ( lateral, small). Vitellariae ( Scattered, dorsal).

TAENIA SOLIUM GRAVID PROGLOTTID

This segment is stained with Iodine by injection of it through genital opening. You can count the number of Uterine Branch. ( 7-12 Branch).

TAENIA SP
CYSTICERCUS LARVAE (C.S

Most are assymptomatic Cysticerci in the brain is initially viable but do not cause much inflammation If symptoms are present, these are mainly due to mass effect, an inflammatory response or obstruction of the foramina and ventricular system of the brain Most common symptoms: seizure, focal neurologic sign and intracranial hypertension.

CLINICAL MANIFESTATION

CLINICAL MANIFESTATION

NCC can be classified into parenchymal or extraparenchymal infections: Parenchymal cyst: most common form : severe headache, nausea and vomiting Calcific cyst: granuloma formation and calcification Cystecercal encephalitis: due to massive number of cyst, result in encephalitis and diffuse brain edema Subarachnoid cyst: lodge in the subarachnoid space resulting to meningeal inflammation Spinal cystecercosis: involvement of the spinal cord, a distinct clinical entity which can have a devastating consequence

CLINICAL MANIFESTATION AND DIAGNOSIS

Extracranial Cystecercosis: - Ocular cystecercosis; cause chorioretinitis - Subcutaneous and intramuscular; muscle and tissues

Diagnosis: 1. Demonstration of eggs in stool

2. Imaging : Radiography calcified cystecercal lesion in muscle and subcutaneous tissue may be seen in Xrays Brain imaging visible cyst are seen as non enhancing hypodense lesion 2. Serology 3. CSF examination

DIAGNOSTIC CRITERIA FOR HUMAN CYSTICERCOSIS

Absolute Criteria a. demonstration of cystecerci by histologic or microscopic exam of biopsy material b. Visualization of the Parasite in the eye by fundoscopy c. Neuroradiologic demonstration of cystic lesion Major Criteria: a. neuroradiologic lesion suggestive of neurocysticercosis b. Demonstration of antibodies to cysticerci by enzyme linked immuno electrotransfer blot c. Resolution of intracranial cystic lesion spontaneously

DIAGNOSTIC CRITERIA FOR HUMAN CYSTICERCOSIS

Minor Criteria a. lesion compatible with neurocystecercosis detected by neuro imaging study B. Clinical manifestation suggestive of NCC c. Demo of antibodies to cystecerci or cysticerci antigen in CSF fluid by ELISA d. Evidence of cysticercosis outside the CNS Epidemiologic Criteria a. Residence in an endemic area B. Frequent traveller to an endemic area c. Household infarct with an individual infected with T. solium

DIAGNOSTIC CRITERIA FOR HUMAN CYSTICERCOSIS

Diagnosis is confirmed by either 1 absolute criterion or a combination of 2 major criteria, 1 minor criteria and 1 epidemiologic criteria. A probable diagnosis is supported by the fulfillment of 1. major criterion plus 2 minor criteria, (2). 1 major plus 1 minor plus 1 epidemiologic or (3) 3 minor criteria plus 1 epidemiologic criterion.

DIAGNOSIS

Immune diagnosis Coproantigen assay

76% sensitivity, 99% specificity

Parasitology Journal, 2002 April Dept of Parasitology, Liverpool School of Tropical Medicine, UK

TREATMENT

a. Praziquantel : Dose 10-20mg/kg single dose b. Niclosamide c. Paramomycin disadvantage: - cause proglottids to rupture and release numerous eggs in the bowel that can increase the risk of cystecercosis

PREVENTION

Taenia solium: avoid eating raw or insuficiently cooked pork proper excreta disposal Human Cystecercosis: good personal hygiene avoidance of drugs which causes disintegration of the gravid segments

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