MEDICAL HELMINTHOLOGY

MEDICAL HELMINTHOLOGY
LECTURE NOTES ON MEDICAL HELMINTHOLOGY Dept. of Parasitology FK Unpad

Introduction to Medical Helminthology
Medical helminthology : the study of parasitic worms (helminthes/ vermes/cacing) affecting man, which : Spend part or the entire life cycle in a human host or Animal parasite causing disease in human

CLASSIFICATION HELMINTHES NEMATHELMINTHES PLATYHELMINTHES NEMATODES
TREMATODES CESTODES

General characteristics of Nematodes
The species parasitic in man range in length from 2 mm (Strongyloides stercoralis) to over a meter (Dracunculus medinensis) The adult is an elongate cylindrical worm, bilaterally symmetrical like a thread; also known as roundworm Unsegmented Body covered by fine and smooth cuticle, sometimes striated Has inner body cavity (pseudocoelom)

Nematodes Life cycle Transmission to a new host :
Ingestion the mature infectious egg or larva Penetration of the skin or mucous membranes by the larva Some species have an intermediate host – usually an arthropod The same animal both the definitive and intermediate host of Trichinella spiralis Nematodes, do not multiply in man

Nematodes Pathogenicity
The effect of parasitic nematodes upon the host depends upon : species, the intensity of the infection and the location of the parasite Simultaneous infection with several species of intestinal nematodes is common in tropical and subtropical countries Injury may be produced by adult and larval parasites Intestinal parasites produce less local and systemic effect than tissue parasites

Nematodes Pathogenicity
The local reaction from intestinal parasites result from irritation, invasion of the intestinal wall and occasionally penertation to extraneous site The local reaction in the liver, lungs (and other) – may destroy or encapsulate the larvae The degree of local reaction – depend upon the sensitivity of the host to the proteic product of the parasite Intestinal mucosa is damaged by biting and bloodsucking, by lytic ferment secreted by the parasite and by mechanical irritation

Pathogenicity The general reaction are produced by loss of blood, absorption of toxin, nervous reflexes and proteic sensitization The larvae of certain species, produce local and general reaction In unatural host the larvae may be pass through their invasive stages, never become established as adult parasite – paratenic host Immunity is acquired through the invasion of the tissues by the parasite and its larvae or through the absorption of its products Immunity is both humoral and cellular

Classification based on Habitat
NEMATODES Classification based on Habitat HABITAT INTESTINAL NEMATODES BLOOD AND TISSUE NEMATODES SOIL TRANSMITTED HELMINTHS (STH) OTHER (NON-STH) FILARIA and DRACUNCULUS

NEMATODES Soil Transmitted Helminthes Ascaris lumbricoides
Trichuris trichiura Hookworm (Necator americanus, Ancylostoma duodenale) Strongyloides stercoralis Important Non-Soil Transmitted Helminthes Enterobius vermicularis Trichinella spiralis Filaria and Dracunculus Wuchereria bancrofti Brugia malayi Brugia timori Important

Disease caused by Soil transmitted helminthes
DEFINITION Soil transmittedhelminth : NEMATODE WORMS WHICH REQUIRE PERIOD OF DEVELOPMENT AND MATURATION DURING ITS LIFE CYCLE ON SOIL IMMATURE INFECTIVE INTO

SOIL TRANSMITTED HELMINTHS
GENERAL CHARACTERISTICS OF STH INFECTION Non-acute and not fatal Occurs primarily in slum areas Children are commonly infected with : Ascaris lumbricoides Trichuris trichiura Young adults mostly infected with hookworms (in the plantations and mining area) : Necator americanus Ancylostoma duodenale

Ascaris lumbricoides Cosmopolitan Prevalence 70-90 %
DISTRIBUTION Cosmopolitan Prevalence % Primarily affects underfives and school children HABITAT Lumen of the intestine : Jejunum Media ileum

Ascaris lumbricoides LIFE CYCLE Ingestion of mature eggs
Source : Medical Parasitology in Plates Piekarski G. Larva Ingested Adults Infertile eggs Mature eggs Migration of larva inside the circulatory system Ingestion of mature eggs Hatched in the gaster, larva penetrates the wall of the intestine and enter into blood circulation To the right heart chamber, into the lungs Alveoli – bronchioles - bronchus - trachea - swallowed Arrived in the intestine and becomes mature adult

PATHOGENESIS AND CLINICAL SYMPTOMS Complaints due to direct effect by
Ascaris lumbricoides PATHOGENESIS AND CLINICAL SYMPTOMS Disease ; Ascariasis Complaints due to direct effect by (1). Larva Allergic manifestation : urticaria, swollen lips, asthma attack Loffler Syndromes : Ascaris pneumonia (coughing) Hyper-eosinophilia Thorax X-ray : temporary white spots Larva migration

Ascaris lumbricoides DISTRIBUTION HABITAT Cosmopolitan
Prevalence % Primarily affects underfives and school children Source : Dept. of Parasitologi FKUP, 1999 Source : Color Atlas of Medicine and Parasitology. 1977 Peters W. & Gillers H.M. Adult worms expelled after deworming HABITAT Lumen of the intestine : Jejunum Media ileum

PATHOGENESIS AND CLINICAL SYMPTOMS Complaints due to direct effect by
Ascaris lumbricoides PATHOGENESIS AND CLINICAL SYMPTOMS Complaints due to direct effect by (2). Adult worm Irritations of the mucosal folds Blocking of the intestine - ileus Erratic migration Competes in the absorption of food and vitamins Release of toxic metabolic products

Ascaris lumbricoides Diagnosis Laboratory diagnosis
Identify the eggs found in feces using following methods : Direct smear method Concentration method Identify larva found in sputum Identify adult worm found expelled from anus, mouth, nostril Do quantitative lab method to measure level of infection Additional : chest X-ray

A. lumbricoides in one area :
Ascaris lumbricoides Mass treatment Treatment Based on prevalence of A. lumbricoides in one area : Drug available Pyrantel pamoate Mebendazol Oxantel pamoate Piperazine Albendazole ? prevalence > 30 %, treatment 3x/year prevalence (20-30) %, treatment 2x /year prevalence (10-20) %, treatment 1x /year prevalence < 10 %, individual treatment in positive cases only

Ascaris lumbricoides PREVENTION treatment of individual case
Provision of sanitary public bath, wash and toilet facilities Media information and health education Routine health check up of children

Infection by Trichuris trichiura
Distribution Trichuriasis - cosmopolitan Primarily in hot and humid areas prevalence %, especially among underfives and school children Habitat Caecum, appendix, colon (proximal end) Mode of infection  oral Infective eggs embedded under fingernail (hand to mouth infection) Ingested with contaminated food/drinks (carried by insect vector: cockroach, flies)

Trichuris trichiura LIFE CYCLE

PATHOLOGY AND CLINICAL SYMPTOMS
Trichuris trichiura PATHOLOGY AND CLINICAL SYMPTOMS Disease : Trichuriasis Heavy infection worm migrate to colon, rectum Prolapsus recti, worm found in mucosal lining (due to frequent defecation)

Trichuris trichiura PATHOLOGY AND CLINICAL SYMPTOMS Chronic and heavy infection Heavy anemia (Hb = 3 gr%) (1 worm absorb 0,005 cc blood/day) Abdominal pain, nausea, weight loss, vomiting Prolapsus recti Headache, fever Mixed infection may occur with Ascaris lumbricoides, hookworm and Entamoeba histolytica

Trichuris trichiura Diagnosis Identify egg worm found in fecal sample
Identify adult worm from prolapsed anus and rectum (by proctoscopy) Measure level of infection by counting : Number of eggs per gram feces Number of female worm expelled through deworming

Trichuris trichiura PREVENTION Treatment Drugs available:
Elimination of source of infection Improved personal hygiene (hand washing, toilet training) Through washing of sold vegetables Health education Provision of sanitary public toilet Treatment Drugs available: Oxantel pamoate Mebendazol (drug of choice)

Infection by Hookworm Ideal soil for egg development :
PREFERENTIAL HABITAT Small intestine (jejunum) In heavy infection : duodenum, colon GEOGRAPHIC DISTRIBUTION Cosmopolitan, especially : Tropical equator Coal/tin mines, coffee/rubber plantations Ideal soil for egg development : Sandy soil Clay soil Muddy soil hindered from excessive dryness or wetness

HOOKWORM LIFE CYCLE

HOOKWORM PATHOLOGY AND CLINICAL SYMPTOMS Disease: Ancylostomiasis Synonym: Uncinariasis, necatoriasis infection by A. duodenale are more serious than N. americanus Chronic infection rarely produce acute manifestation Tissue damage and symptoms are caused by : Larva stage Adult worm

PATHOLOGY CAUSED BY LARVA STAGE
HOOKWORM PATHOLOGY CAUSED BY LARVA STAGE Larva penetrates the skin - maculopapules - erythema - heavy itching : ground itch/dew itch In sensitive patient, larva carried in the circulation, may cause: Bronchitis / Pneumonitis

PATHOLOGY CAUSED BY ADULT WORM
HOOKWORM PATHOLOGY CAUSED BY ADULT WORM Hooked to the intestinal mucosal wall : abdominal pain, nausea, diarrhea Absorbing 0,2-0,3 ml of blood/day/worm : progressive anemia, hypo chrome, microcytic type of Fe deficiency anemia Heavy anemia (Hb may reach 2 gr %) : Dyspnea, physical weakness, headache Rapid pulse beat, cardiac weakness Children : physical growth retardation, mental

HOOKWORM PATHOLOGY CAUSED BY ADULT WORM (Anemia by HOOKWORM) Source : Color Atlas of Medicine and Parasitology Peters W. & Gillers H.M. Blood smear of patient with heavy infection caused by hookworm indicating Fe deficiency anemia with low MCHC and low serum Fe concentration

HOOKWORM PATHOLOGY CAUSED BY ADULT WORM (Anemia by hookworm) Atrophic glossitis found with hypo chromic microcytic anemia, caused by heavy infection of hookworm Tongue surface become smooth and lacking of papillae

HOOKWORM PATHOLOGY CAUSED BY ADULT WORM (Anemia by hookworm) Glositis atrofik pada anemi hipokrom mikrositer yang disebabkan infection berat HOOKWORM Tampak lidah halus dan kurang papila source : Atlas Parasitologi Kedokteran, Zaman P. Alih Bahasa : Anwar C.; Mursal Y. Patient with atrophic glossitis also show fingernail deformity (koilonichia) Fingernail becomes thin and concave with elevated ridge

HOOKWORM Diagnosis Identify eggs from feces sample
Identify larva from : Fecal culture Old feces sample

HOOKWORM ANTIHELMINTHICS Tetrachlorethylen Mebendazole Albendazole
Pyrantel pamoate Bitoskanate Bephenium hidroxynaphtoate PREVENTION Same as with Ascariasis but with the addition of : wearing shoes during work in plantation or mine area

Infection by Strongyloides stercoralis
HOST, HABITAT AND DISTRIBUTION Man is the definitive Host Habitat of female worm, mucosal lining of : Duodenum Jejunum (proximal end) Found very cosmopolitan, especially in the tropical and subtropical region

Strongyloides stercoralis
LIFE CYCLE

CLINICAL FEATURES Disease : Strongyloidiasis, Strongyloidosis, Cochin China diarrhea Level of infection : Mild - asymptomatic Moderate Heavy and chronic

In moderate infection Female worm embedded in the mucosal wall of duodenum Burning sensation and stinging pain in the epigastrium Nausea, vomiting, diarrhea and constipation

In heavy and chronic infection
Loss of body weight; Anemia Dysentery (chronic); Slight fever May be accompanied by secondary bacterial infection where worm inhabits the entire intestinal epithelium up to the distal colon)

Diagnosis Find and identify Rhabditiform larva : From fresh feces Gastric (duodenal) juice *Eggs : In heavy diarrhea After administration of laxative

TREATMENT AND PREVENTION Drugs given Thiabendazole Mebendazole Pyrvinium pamoate

Similar to the prevention of hookworm
Autoinfection is prevented by means of : Avoid constipation Anal hygiene

NON-SOIL TRANSMITTED HELMINTHS
= Members of intestinal nematode that have transmissions are not via soil. = It happens because egg or larva of non-soil transmitted helminths don’t do maturation process (to become infectious) in the soil.

NON-SOIL TRANSMITTED HELMINTHS
1. Enterobius vermicularis 2. Trichinella spiralis

Enterobius vermicularis
A. MORPHOLOGY > Enterobius vermicularis = Oxyuris vermicularis = pinworm. > In its life, this worm (ovipar) develops from: egg larva worm. > Its egg is oval, assymetry, that contains embrio. > This worm has lateral ala cephalic in anterior tip. > One female worm can produce eggs in one day. > The female worm will die after producing eggs. > The male worm will die after copulation.

B. LIFE CYCLE of Enterobius vermicularis
Female & male worms do copulation in cecum & around (appendix, ascending colon & ileum) Pregnant female worms migrate at night & produce eggs in anus & around (anal area) After several hours, eggs become mature & infectious, then come to host, via: air (person inhalates) food (person eats food with infectious hand after scartching anal area) Eggs crack in duodenum & larvas appear Larvas become mature (be worm) in ileum

C. SPREADING > Cosmopolite (spread around the world), especially in children. D. PATHOLOGY & CLINIC > The worm causes disease, called enterobiasis. > This disease has clinical symptoms: - Ithcing in anal area (pruritus ani) at night. - In girl, this disease can make inflammation in fallopian tube (salpingitis). - Intestine is seldom disturbed, etc.

E. DIAGNOSIS > Scotch adhesive tape swab method, is done before taking a bath or defecating. F. TREATMENT > Mebendazole, thiabendazole, etc. G. PREVENTION > Washing hand before eating > Cutting long fingernail, etc.

Trichinella spiralis A. MORPHOLOGY
> Trichinella spiralis = porkworm. > In its life, this worn (vivipar) develops from larva worm. > Its larva can become cyst (circular larva which is covered by hyaline capsule). > This worm has stylet mouth to invade intestine or muscle tissue. > One female worm can produce about larvas. > The male worm will die after copulation.

B. LIFE CYCLE of Trichinella spiralis
Female & male worms do copulation in mouse/pig/person duodenum to cecum Pregnant female worms enter to intestinal villi and then lymphatic sinus Pregnant female worms bear larvas in lymphatic sinus Larva is brought by lymphatic flow, to thorachic duct, right heart, lung, left heart, and then to around body Host (person/pig/etc) can die Larva enter to mouse/pig/person muscle tissue & make cysts (larva can live until 30 years in muscle) Health person eats meat (pig muscle) before cooked perfectly Cyst wall rupture & larva release & larva become mature (be worm) in health person duodenum The worm can also pass placenta & mammary

Trichinella spiralis C. SPREADING
> Cosmopolite (spread around the world). D. PATHOLOGY & CLINIC > The worm causes disease, called trichinosis. > There are 3 clinical stadium: - Intestinal invasion that is done by worm (1-2 days after eating infectious muscle). - Larva migration (7-28 days after eating infectious muscle). It results cerebral disturbing, cardiac distrubing, fever, even die. -Forming cyst & healing process (90 days after eating infectious muscle).

BLOOD AND TISSUE NEMATODE
THERE ARE THREE GROUPS : Filaria dan Dracunculus Larva Migrans (TROPICAL MEDICINE) Rarely found nematode (LESS IMPORTANT !)

FILARIA LIFE CYCLE Insect as a vector : Anopheles, Aedes, Mansoni, Culex juga Simulium, Chrysops atau Culicoides Habitat : blood, lymph, muscle, conective tissue, serous cavity

BLOOD AND TISSUES NEMATODE Filaria – caused Filariasis
TOPICS (As problem of Public Health in Indonesia) Wuchereria bancrofti Brugia malayi Brugia timori All species above – nocturnal periodicity

LIFE CYCLE OF FILARIA In the human body, found stages :
Adult filaria – lymph node and vessel, difficult to find – not important Microfilariae – pralarvae stage – in the peripheral blood – important for diagnostic Microfilariae, must be attention about : Morphology for identified species of filaria Periodicity for chose right time for take blood Periodicity – when microfilariae found in most number : Nocturnal Periodicity – only in the night Subperiodic nocturnal – in the night more number than in the daytime Diurnal Periodicity – only in the daytime Subperiodic diurnal – in the daytime more number than in the night Nonperiodic – same number in the daytime and in the night

MORPHOLOGY OF MICROFILARIAE
Appearance graceful or stiff Sheathed, its clear in part of the head or the tail (the three of them are sheathed) “Nuclei” in the body : spread in average or in groups, show in the part of : Head – without nuclei, named cephalic space, compare its length with its wide Tail, contain the nuclei or not

PRIMARY CAUSE Wuchereria bancrofti Brugia malayi Brugia timori

Life Cycle of B. malayi

Mansonia, Anopheles, Culex, Aedes

MAIN MOSQUITO VECTORS W. bancrofti  Anopheles sp
B. malayi  Mansonia sp B. timori  An. barbirostris

Habitat and Distribution
Wuchereria bancrofti Habitat and Distribution HABITAT Vessel and lymph node (bellow the diaphragm) Can live years Microfilaria in blood, penetrate placenta 3 times metamorfosa

DISTRIBUTION : Urban bancroftian filariasis, vektor Culex fatigans Rural bancroftian filariasis, vektor Aedes, Anopheles dan Mansoni

Wuchereria bancrofti Periodicity PERIODICITY (WHO, 1967)
Commonly nocturna, also in Indonesia In Polynesia, subperiodic diurna, vector Aedes polynisiensis

Wuchereria bancrofti Clinical
DIVIDED IN : Biologic incubation periode Asymptomatic periode Acute stage Chronic stage Biologic incubation periode - asymptomatic, amicrofilaremi larva - microfilaremi (± 1 year) Asymptomatic Periode - asymptomatic, microfilaremi symptom (-), microfilaria (+), especially in endemic area

Wuchereria bancrofti Clinical Acute stage - symptomatic, microfilaremi
Acute alergic filarial lymphangitis Lymphangitis, limphadenitis (±) Filaria fever, alergic symptom (±) Chronic stage - symptomatic, microfilaremi Elephantoid tissue formation at lower extremity and scrotum Adult worm die : microfilaria reduce

PERIODICITY Nocturnal Periodicity Sub periodic nocturnal
Diurnal Periodicity Sub periodic diurnal Non periodic All 3 species have nocturnal periodicity

Grading of lymphoedema
Grade 1 Reversible pitting oedema

Clinical manifestation
Acute filariasis Chronic filariasis Atypical presentation Asymptomatic carrier

Acute manifestations Characterised by recurrent attacks of fever associated with inflammation of lymph nodes (adenitis) and /or lymph vessels (adenolymphangitis, ADL) Involvement of genitalia lymphatic in male – funiculitis, epididymitis or orchitis Lasting for 4-5 days Repeated episode important in the progression of disease

Acute manifestation: ADL
Acute Filarial Lymphangitis Cord-like structure with retrograde lymphangitis: painful, red and tenderness Systemic reaction mild, distal oedema rare Recurrent at same site common ADL with secondary bacterial infection Most common form of ADL Associated with fever, chills, myalgia and headache Cellulitis and oedematous, subside after each attack

Acute adenolymphangitis (ADL)

Subcutaneous abscess may form and rupture releasing chylous fluid

Chronic manifestation
Major signs Hydrocoele Chyluria Rupture of lymphatic lining the bladder leading to passage of lymph in the urine May resolve spontaneously Lymphocytes in urine Lymphoedema elephantiasis

Major signs Hydrocoele Chyluria Lymphoedema Swelling due to collection of lymph fluid in soft tissue Pitting oedema, may or may not be reversible Thickened skin elephantiasis

Major signs Hydrocoele Chyluria Lymphoedema Elephantiasis Irreversible, non-pitting oedema with fibrotic and verrucous skin changes (thickening, folding, hyperkeratosis, pigmentation, ulceration) Skin & soft tissue infection common

Grade 2 Irreversible oedema No skin changes

Grade 3 Irreversible oedema Skin thickened

Grade 4 (5,6 & 7) Irreversible oedema Skin thickened, fibrotic & verrucous changes (elephanthiasis)

Only a small proportion of filarial-infected population affected Immigrants tend to develop chronic manifestation more often and sooner than indigenous people Occurrence of major signs differ between places

Chronic manifestations: Pathology
Adult worm Host response Reticular cells hyperplasia Worm factors? Thrombosis & inflammatory reaction Dilatation of lymph vessel Granulomatous reaction with giant cells, histocytes, epitheloid cells Dysfunctional valve Retrograde lymph flow Healing with re-canalization Transient oedema Dying worms Intense inflammatory reaction with granuloma formation Healing with fibrosis Secondary bacterial infection Loss of architecture & complete obliteration Elephantiasis & other chronic manifestations

Lymphatic vessel dilatation, valve incompetency, lymphatic back flow, pooling & oedema

Asymptomatic Microfilaraemic
Microfilaraemic carrier No sign and symptom of infection Source of infection to others Evidence of sub-clinical infections:- 40% with sub-clinical hematuria/proteinuria: low grade renal damage. Complete reversal after clearing Mf Lymphoscintigraphy: markedly dilated, tortuous lymphatics and abnormal lymph flow

Secondary bacterial infection of chronic lymphoedema
Commonest cause of morbidity in lymphatic filariasis Recurrent attack of lymphadenitis, lymphangitis and cellulitis May last for more than 1 weeks, 5-6 times a year Unable to work, going to school

Alleviating morbidity
An important strategy Those already suffering the disease must be given necessary help Unfortunately, neglected in our National Programme We do not even know the magnitude of the disease

Cause Chronic swelling, lost of skin architecture
Crack and fissures, point of entry of bacterial Poor hygiene aggravate the situation

In elimination programme
Prevention of morbidity Personal hygiene Protecting from injury Provision of appropriate treatment at every level of health care

LIFE CYCLE AND PERIODICITY
Brugia malayi LIFE CYCLE AND PERIODICITY Definitive host : human, monkey, dog, cat In vector 6-8,5 days, 2 times metamorf Nocturna, vector Anopheles barbirostris (farm) Subperiodic nocturna, vector Mansonia uniformis, M. indiana (swamp)

CLINICAL, THERAPY AND PREVENTION
Brugia malayi CLINICAL, THERAPY AND PREVENTION CLINICAL: Main symptom : fever, limphangytis, limphadenitis Elephantiasis : lower extremity bellow knee, elbow,inguinal, rarely scrotum THERAPY : Hetrazan, po 0,1 gr, 3-4 x/day, as long as 10 days PREVENTION : Pentachlorophenol (dowicide G), kill water plant Pistia stratioides, Eichornia, Salvinia

ELEPHANTIASIS by B. malayi
Example from Thailand ELEPHANTIASIS by B. malayi Not involving external genitalia Courtesy Prof. Radomyos P. Mahidol U.

Example of filariasis from Malaysia

Filariasis Case at Pusat Pencegah Penyakit Untut – Kepala Batas

Filariasis research - IMR

Brugia timori With giemsa, sheath not clear Size longer than B. malayi
Vector : Anopheles barbirostris Lesion mild/moderate at lower extremity bellow the knee No reservoir host

Blood Trematoda (Schistosoma sp.)

There are four species of schistosome which are infective to humans:
Schistosoma mansoni, found in Africa, Brazil, Venezuela, Suriname , Puerto Rico, and the Dominican Republic. Freshwater snails of the Biomphalaria genus are an important host for this trematode.

S. japonicum whose common name is simply blood fluke is found widely spread in Eastern Asia and the southwestern Pacific region. In Taiwan this species only affects animals, not humans. Freshwater snails of the Oncomelania genus are an important host for S. japonicum.

S. mekongi is related to S
S. mekongi is related to S. japonicum and affects both superior and inferior mesenteric veins. S. mekongi differs in that it has smaller eggs, a different intermediate host, and longer prepatent period in the mammalian host.

S. haematobium, commonly referred to as the bladder fluke, originally found in Africa, the Near East, and the Mediterranean basin, was introduced into India during World War II. Freshwater snails of the Bulinus genus are an important host for this parasite

Schistosoma mansoni causes intestinal schistosomiasis
Schistosoma haematobium causes urinary schistosomiasis Schistosoma japonicum and Schistosoma mekongi cause Asian intestinal schistosomiasis

HABITAT S. Haematobium  Venous vessel (Vv) of urinary bladder, colon; Hepar S. Japonicum  Vv. of intestine; Hepar S. Mekongi  Vv. of intestine; Hepar S. Mansoni  Vv. of Colon, Rectum; Hepar

Group of age hit by between 5-50 year. Mass treatment every 6 month.
EPIDEMIOLOGY Disease of schistomiasis or bilharzasis in Indonesia only schistomiasis japonica found in middle sulawesi, relate to agriculture getting water from irrigation. Group of age hit by between 5-50 year. Mass treatment every 6 month.

S. japonicum The S. japonicum worms are yellow or yellow-brown. The males of this species are slightly larger than the other Schistosomes and they measure ~ 1.2cm by 0.5 mm. The females measure 2cm by 0.4 mm. The adult worms are longer and narrower than the related S. mansoni worms.

S. japonicum This Parasite at human being cause oriental of schistosomiasis, schistosomiasis japonica, katayama fever or Snail Fever disease

Katayama Fever Acute schistosomiasis (Katayama's fever) may occur weeks after the initial infection, especially by S. mansoni and S. japonicum. Manifestations include: Abdominal pain Cough Diarrhea Eosinophilia Fever Fatigue Hepatosplenomegaly

Faeces with egg of s. JAponicum have contact with water
Those egg will hatch and release free-swimming larva called Miracidia Miracidia will infect Oncomelaria hupensis by penetrating their skin Inside the snail they will undergo asexual reproduction, and will become sporocysts Further reproduction will produce large number of Cercaria, which is free-swimming larva Cercaria can infect us by penetrating our skin After penetration, they will loose their tail and become Schistosomule Enter circulation, and end at the mesenteric veins There, they will undergo sexual reproduction and produce egg Egg will penetrate the tissue and are passed with the faeces

S. mansoni The male S. mansoni is approximately 1 cm long (0.6 to 1.4 cm) and is 0.11 cm wide. It is white and it has a funnel-shaped oral sucker at its anterior end The female has a cilindric body, longer and thinner than the male (1.2 to 1.6 cm long by cm wide). The female parasite is darker and it looks gray. The darker color is due to the presence of a pigment (hemozoin) in its digestive tube

CLINICAL SYMPTOM AND PATHOLOGY
Similar with S. japonicum, but it is lighter

MORPHOLOGY AND LIFE CYCLE
Adult Worm of fairish male about 1,3 cm and female about 2,0 cm. its life in small vena flank. Egg found in urine, and rectum genitals

Pathology It can break the wall of the urinary bladder
The most characteristic symptom is haematuria. Dysuria also can occur. Inflammatory reaction to eggs in the bladder wall and later fibrosis and calcification often leads to mucosal hyperplasia and papilloma formation In Egypt vesical schistosomiasis has been considered a common cause of malignancy of the bladder in male agricultural workers

Lab Diagnosis Microscopic identification of eggs in stool or urine is the most practical method for diagnosis Stool examination should be performed when infection with S. mansoni or S. japonicum is suspected, and urine examination should be performed if S. haematobium is suspected. Dark urine is a significant clinical sign of urinary schistosomiasis Tissue biopsy (rectal biopsy for all species and biopsy of the bladder for S. haematobium) may demonstrate eggs when stool or urine examinations are negative. The eggs of S. haematobium are ellipsoidal with a terminal spine, S. mansoni eggs are also ellipsoidal but with a lateral spine, S. japonicum eggs are spheroidal with a small knob.

Treatment Schistosomiasis is readily treated using a single oral dose of the drug Praziquantel

Prevention The main focus of prevention is eliminating the water-borne snails which are natural reservoirs for the disease. This is usually done by identifying bodies of water, such as lakes, ponds, etc., which are infested, forbidding or warning against swimming and adding niclosamide, acrolein, copper sulfate, etc., to the water in order to kill the snails. Individuals can guard against schistosomiasis infection by avoiding bodies of water known or likely to harbor the carrier snails

Liver Trematodes Clonorchis sinensis Dicrocoelium dendriticum
Opistorchis felineus Opistorchis viverini Fasciola hepatica

Clonorchis sinensis Epidemiologiy - China, Japan, Korea, Taiwan, Vietnam Habitat - Biliary tract, pancreatic tract Host - definitive : human, cat, dog - vector 1 : Water snail genus of Bulimus, Thiara, or species Melanoides tuberculatus

- Vector 2 : Fish family of Cyprinidae, Salmonidae, Gobiidae, Anabantidae Morphology - Elongated, flat, transparent, bulging on posterior - Oval egg, thickened on posterior, found within faeces

LIFE CYCLE Swallowed by vector1 (water snail) Sporocyst Redia
Eggs within faeces Mirasidium (cilliated larvae) Mating  Eggs Grow mature in biliary tract Cercaria Crossing fish (vector2) skin  forming metascercaria (cyst) in fish skin/muscle Swallowed by definitive host Metacercaria

Diagnosis Eggs within faeces Immunology diagnosis Prevention - Avoid eating raw fish  must be completely cooked

Dicrocoelium dendriticum
Epidemiology - Cosmopolite for lamb & other herbivores in Asia, Africa, Europe & America Morphology - Mature form: flat, slender - Eggs: dark brown, thick wall, contain completely-grown mirasidium Host Definitive: lamb Vector 1: snail genus of Abida, Zebrina Vector 2: ant, species Formica fusca Life Cycle : comparable to C. sinensis

Fasciola hepatica Epidemiology Is the first trematode found
Causes fasciolatic hepatic Is cosmopolite mainly in country with large farm (mostly sheep), infection in human often happens in Cuba, France, England, and Aljazair.

Habitat and host Habitat is mainly in billiary duct, may penetrate hepatic tissue causing abses. Definitive hosts are human, sheep and other cattle. Intermediate host I is family Lymnaeidae, especially genus Lymnaea. Intermediate host II is water plants especially Nasturtium officinale.

Morphology Big size, 30 x 13 mm Integuments is scaly
Posterior end without thorn Unique shape, like shoulder because it has kerucut kepala Batil isap kepala (1 mm) and stomach are almost same in size and adjacent

Caecum is hyper branching until posterior end
Hyper branching testis is lied between 2/4 – ¾ posterior body, one is behind the other Ovary branches, anterior to testis and smaller Uterus is short, curved, located between ootype and porus genital. Egg is x µ in size and has operculum. Immature eggs are lied in billiary duct and exit with feces.

Life cycle Eggs are expelled within feces Metacercariae penetrate
Hepatic tissues are infiltrated with eggs, immature eggs are lied in billiary duct Eggs are expelled within feces Eggs mature in water and hatch after 9-15 days at optimum temperature C Penetrate Glisson’s capsule, hepatic tissue, then into billiary duct in 12 weeks in adult Miracidia enter intermediate host I and develop to become sporocysts, rediae I, rediae II in 3 weeks , and cercariae Penetrate intestinal wall, Enter peritoneal cavity Cercariae move toward Intermediate host II Metacercariae exit the cyst in duodenum At night, in 8 hours, become metacercariae Metacercariae penetrate definitive hosts

Clinical Symptom Until metacercaria penetrate Glisson’s capsule, these is no complain. But trauma and necrotic lesion rise during migration through hepatic tissues. In heavy infection, epithelia is scraped and young worm will return to hepatic parenchyma, form abscess pouch, and hepatic tissues are infiltrated with eggs. When larvae migrates to peritoneal cavity, focus ectopic may happen in blood vessel, lungs, subcutaneous tissue, brain ventricles, and eyes where abscess will be formed. Symptoms : colic, ikterus obstructiva, cough and vomiting, abdomen rigidity, acute epigastria pain, leukocytosist and eosinophily until above 60%

Diagnosis Eggs are found in feces, duodenal fluid, or bile. Patient, who will be examined, do not eat liver. Need early diagnosis to prevent fatal liver damage. Serodiagnostic test is very helpful, although it is not an routine diagnostic tool.

Prevention Treating patient and cattle that act as reservoir.
Incinerating water snails. Cooking vegetables that will be eaten.

Lung Trematode Paragonimus westermani Disease : Paragonimiasis ,
Pulmonary distomiasis

Paragonimus westermani
Epidemiology It is cosmopolite in human, mainly east in Japan, Philippine, Korea, China, Muangthai, Taiwan, Africa, etc. In Indonesia, it is autochthon infection in animal. In human, as import case.

Host Definitive hosts are human and mammalians such as dog and cat
Intermediate hosts I are Semisulcaspira libertina (Japan), Brotia asperata (Philipina), B. costula episcpalis (Malaysia), Syncera sp., and Melania. Intermediate hosts II are freshwater crabs genus Potamon, Eriocheir, Sesarma sp., and crayfish.

Life cycle Metacercariae penetrate definitive hosts
Sometimes, into ectopic place like mesentery, pleura or brain, and reach adulthood here From the pouch, eggs go out to bronchioles Then, they are coughed with sputum or swallowed and expelled with feces In 3-6 hours, enter abdominal cavity and penetrate abdominal wall, stay for several days before penetrating diaphragm, to pleural cavity and enter bronchioles Hatch in water after maturation (2-3 weeks) In intermediate hosts I, miracidia become Rediae I, Rediae II, and finally cercariae In duodenum, encystations happens, penetrate intestinal wall (in minutes) In intermediate hosts II, cercariae become metacercariae in 5 months Metacercariae penetrate definitive hosts

Clinical signs and pathology
Around parasite, leukocyte infiltration happens and is followed by forming fibrosis capsule and form cyst containing 2 worms, purulent blood, and eggs. Lungs : (1) nonsuppurative, (2) tubercle-like, (3) suppurative, (4) ulcerative. First fever, shaking chills, dry cough, then hemaptoe with sticky and rush-colored sputum mainly when wake up in the morning. Physical examination reveals a bronchopneumonia or bronchiectasi with pleural effusion.

Diagnosis Finding eggs in sputum, aspiration pleural fluid, and feces
Serology test with intradermal test, complement fixation test.

Treatment and Prevention
- Praziquantel PREVENTION Treating patients Cooking crab before being eaten

CESTODA

Scolex : organ of attachment,usually bearing suckers or hooks
Cestodes are members of phylum Platyhelminthes, also known as tapeworms. General morphology Scolex : organ of attachment,usually bearing suckers or hooks Neck : part which it grows Strobilla : the boby, consist of proglotids (segments)

Proglotids Immature :segment that is attached to the neck Mature : has a reproductive structure Gravid (pregnant): filled with eggs. Tegument: covers adult cestode, allows materials to enter and waste to be excreted from the body Hermaphrodite, each proglotid has a male and female reproductive structure. Mature embryo has six hooks and also known as onchosphere.

Diphyllobothrium latum

Morphology Is not yet found in Indonesia
Resides in ileum of human, dogs, and cats Morphology Adult worm 3 – 10m, can be as long as 60m, with proglotids. In the place of sucker or hooks, are two shallow sucking grooves called bothria. Operculated eggs

LIFE CYCLE Adult tapeworms resides in
ileum. Self fertilization will occur and eggs are produced Unembryonated eggs is release with feces. eggs will develop into onchosphere which contains a ciliated embryo. egg disintegrate releasing the ciliated embryo , coracidium, larva stage I. Coracidium is eaten by copepod, and inside it will develop to larva stage II called procercoid. If copepode is eaten by fish, procercoid will penetrate into fish’s muscle, and develop to larva stade III called plerocercoid/sparagnum. human will be infected by this larva. It will attach to mucous membrane of intestine and developes into adult tapeworms.

Pathogenesis Diagnosis Prevention Disease: diphyllobothriasis
Usually asymptomatic, can cause abdominal pain, weight loss, diarrhea, vomiting,deficiency of vit B12. Diagnosis Eggs or proglotids found in feces. Treatment Niclosamide, praziquantel, bithionol, atabrin Prevention Avoid ingestion of undercooked fish

Taenia Solium

Morphology Also called porkworm and resides in jejenum of human.
Larva is known as cycticercus celullosae 10 x 5 mm. usually inhabit the muscle. Morphology Adult worm is 2 – 4m Has a rostellum with two rows of hooks plus four suckers. Genital pores located lateral to proglotids. Eggs doesn’t have opperculum, but contains onchosphere.

L i f e cycle Eggs are digested out in the stomach of the pig.
Using its hook and lysis substrate, the oncosphere will then penetrate intestinal wall into blood stream and reside in muscle forming cysticercus celullose. Human will be infected by digestion of undercooked pork. The larva will attach inside the small intestine, and develop into adult tapeworms that can produce eggs. These eggs will then pass through feces

Diagnosis Treatment Pathogenesis Disease: cysticercosis
Most cases are asymptomatic. Diarrhea, abdominal pain may occur. If cysticercus migrate to brain, can cause neurocysticercosis. Headaches, seizures, even death can occur. Diagnosis Gravid proglotids or egg in feces, CT scan, MRI. Treatment Praziquantel and niclosamide, also surgical removal.

Taenia Saginata

Also known as beef worm. Larva is called cysticercus bovis, Morphology Adult beefworm is 5m,but can grow as far as 25m . Has four suckers, but no hooks.

Hymenolepsis diminuta

Habitat small intestine Definitive hosts rats, also common in humans Intermediate hosts grain beetle or flea Epidemiology cosmopolite, found in Indonesia

Morphology Adult worms mm long, 3-5 mm wide, have proglotids. Rounded scolex bears a small rostellum with four suckers, proglotid 0,8 mm long and 2,5 mm wide. Eggs without the polar filaments, sized 60-80μm.

Life cycle

Transmission Transmission or infection occurs by ingestion of infected beetles or other arthropods, usually in grains and cereals Pathogenesis Symptoms, if any, are mild, and usually include diarrhea, nausea, and slight abdominal pain Diagnosis Recovery of characteristic eggs in feces

Treatment Niclosamide, Praziquantel Prevention Limit exposure of grains and cereals to rats and insects.

Dyphilidium caninum

Dyphilidium caninum Synonym Double-pore dog tapeworm Definitive hosts
Cats and dogs,,, also found in humans’ small intestine. Intermediate hosts Dog/cat flea; Ctenocephalides canis and C.felis.

Dyphilidium caninum Morphology
Adult tapeworm is 10 to 50 cm in length. Several rows of tiny hooklike spines are present on the cone-shaped rostellum. The uterus in the gravid proglottid contains numerous packets of eggs, each packet containing 5 to 20 eggs. Colorless eggs ~ 30-60μm in diameter, with a six hooked oncosphere present in each egg. The eggs are enclosed in membrane-bound packets.

Dyphilidium caninum Transmission
Infection after ingestion of cysticeroid larvae. Pathogenesis Most of infected individuals are asymptomatic, although some with a heavy worm burden may experience mild gastrointestinal symptoms, such as nausea, diarrhea, indigestion, and slight abdominal pain.

Human host Life cycle

Dyphilidium caninum Diagnosis
Recovery of characteristic gravid proglottids and egg packets (following rupture of proglottids) in human feces. Treatment Niclosamide, Praziquantel. Prevention Good veterinary care of cats and dogs, keeping animal freely from parasites. Good personal hygiene.

Hymenolopsis nana

Hymenolopsis nana Morphology:
smallest tapeworm, 25-40mm, found in mice and other rodents, doesn’t need intermediate host the scolex bears a short rostellum with one row of hooks, along with four suckers proglottids 2 mm wide and 1mm long Sac-like gravid uterus is usually full of eggs Egg: round to oval thin-shelled, micrometer, contains an inner envelope with two polar thickenings, each having four to eight filaments, which extend into the space within the shell

Hymenolopsis nana Transmission: Infection is usually transmitted by ingestion of infective eggs. Although most cases are asymptomatic, mild gastrointestinal symptoms, such as diarrhea, abdominal pain, and weight may occur

Hymenolopsis nana Laboratory Diagnosis: recovery of characteristic eggs in human feces. Adult worms and proglottids are rarely seen in the stool

Hymenolopsis nana Treatment and Prevention: Praziquantel is the treatment of choice for infection with H. nana. Niclosamide is also effective. Good sanitary practices are essential in the prevention of infection

Echinococcus granulosus

Morphology: hydatid tapeworm, 4 mm in length, scolex bearing four suckers, numerous hooks, and three proglottids Eggs: although not found, but it is identical to those of Taenia species

Transmission and Pathogenesis Ingestion of eggs, usually by hand-to-mouth contact with infected dog feces. Symptoms vary, depending on the location of the cyst in tissue. Although cysts may form in many areas of the body, the lung and the liver are most commonly affected. Pulmonary symptoms, such as cough and chest pain, may develop with lung infection. One serious complication of hydatid cyst disease is the risk of anaphylactic shock, following rupture of the cyst.

Laboratory Diagnosis: The eggs are not found in human feces. The diagnosis of hydatid cyst disease may be made by radiographic and serologic studies. A combination of assays, including enzyme immunoassay and immunoblot techniques, has been suggested ti diagnose hydatid cyst disease. The demonstration of hydatid sand is also diagnostic.

Treatment and prevention Although surgical removal of hydatid cyst has long been considered the treatment of choice, several antihelminthic agents are now available. These include praziquantel and mebendazole. Infection is also prevented by good personal hygiene to prevent hand-to-mouth transmission of eggs from dogs to humans, avoidance of ingestion of sheep viscera by dogs, and antihelminthic treatment of dogs, as necessary

Thank You

MEDICAL HELMINTHOLOGY

Similar presentations

Presentation on theme: "MEDICAL HELMINTHOLOGY"— Presentation transcript:

Similar presentations

About project

Feedback

Log in

Auth with social network:

MEDICAL HELMINTHOLOGY

Similar presentations

Presentation on theme: "MEDICAL HELMINTHOLOGY"— Presentation transcript:

Similar presentations

About project

Feedback