Kasr Alainy Students

Medical Parasitology in Tables

2nd Edition

Dr. Azza Al-Adawi (supervisor) Osama Esam Omar Aldurini Ibrahim Sehsah
This work is meant to help our friends in their medical course as undergraduates. We hope that this work will benefit all of them. So, please do not forget us in your do3aa. We depend on more than one source to get the information, but in the limits of our course as 3rd year medical students and the main source is the department book. There is no new information in this work but the arrangement of the information and some notes. We hope that it will help anyone who needs help as we did. Thanks to Dr. Azza for her time to review and put some comments on this work. Our best wishes for her are indescribable. Do not forget her in your do3aa too.

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Medical Parasitology in tables

Kasr Alainy Students

PLEASE NOTE (N.B.): a. This paper of work is not a 100% perfect information source, although we hope it is. b. Do not rely on this work (only) in study of medical Parasitology. This is just a bit of work to help you in your medical course. c. If you find any wrong information in here or you have an idea about it, please send any of us a message to the email or account or call us directly. d. This paper work is free to anyone. Please do not try to sell it anyway. e. The normal size of this paper is A3. f. Do not forget us in your do3aa. ---------------------------------------------------------------------------------------How to study medical Parasitology? 1. General characters & life cycle: read & understand. 2. General Distribution: Enough to know whether the parasite is present in Egypt or not (very important in cases). 3. Pathogenesis, Clinical picture and diagnosis: very important study them very well. 4. Treatment: enough to study the first drug written in your book (it is called the drug of choice) NO NEED to study any doses for drugs. ---------------------------------------------------------------------------------------Class: Trematoda
General characters: 1- Flattened dorso-ventrally, bilaterally symmetrical and unsegmented. 2- Provided with suckers: an anterior oral and ventral suckers, sometimes a third genital sucker. 3- Having a protective cuticle either smooth or provided with spines or tubercles. 4- Muscle fibers: longitudinal, circular and oblique help in the movement of the parasite. 5- Nervous and excretory systems are present but there is no respiratory or circulatory system. 6- The digestive system starts by mouth surrounded by oral sucker anteriorly. This leads to a short pharynx that bifurcates in front of the ventral sucker into two intestinal caeca that may be simple or branches and end blindly. 7- The genital system hermaphrodite (except Schistosoma) having both male and female reproductive organs in one worm. Usually there is crossfertilization between 2 separate adults but self-fertilization may occur. 8- General life cycle: adults eggs water miracidium snail Sporocyst redia cercaria infect man adults. Parasitic pharyngitis: In Lebanon & America, people have a habit of ingestion of fresh raw sheep & goat livers. If these livers are infected with Fasciola, living worms will attach to the pharyngeal mucosa causing: oedematous congestion of the pharynx, soft palate, larynx, nasal fossae and Eustachian tubes (suffocation known by the natives as Halzoun). Another cause for this condition is tongue worms (Linguatula serrata). Mode if infection: Infection occurs by ingestion of nymph stage in improperly cooked sheep viscera. Treatment: 1- Gargling with strong alcoholic drinks. 2- Administration of emetics. 3- Tracheostomy in laryngeal obstruction. Control: Proper cooking of animal tissues. General characters of schistosoma: 1- The adults have separate sexes. 2- The two sexes are dissimilar in appearance. 3- The adult worms parasitize blood vessels. 4- They lack a muscular pharynx and the two intestinal caeca reunite into a single caecum. 5- They produce non-operculared eggs. 6- The cercaria, with forked tail, invades the final host percutaneously. 7- No redia stage.

Classification of Helminthes
Fasciola hepatica/gigantica (Fascioliasis) Paragonimus westermani Lung fluke (Paragonimiasis) Flukes / Trematoda Intestinal fluke Heterophys (Heterophysiasis) (Disease) Schistosoma Haematobium, Mansoni & Blood fluke Japonicum (Schistosomiasis) (Swimmer's itch) Diphyllobothrium Latum (Diphyllobothriasis) Pseudophyllidea Diphyllobothrium Mansoni & Proliferum (Sparganosis) Taenia saginata (beef) (Taeniasis saginata) Taenia solium (pork) (Taeniasis Tapeworms solium/Cysticercosis) / Cestoda Echinococcus granulosus (Hydatid (Disease) Disease or Hydatidosis) Cyclophyllidea Echinococcus multilocularis (Alveolar Hydatid Disease) Multiceps multiceps (Coenurosis) Hymenolepis nana (Hymenolepiasis) Hymenolepis diminuta (Hymenolepiasis diminuta) Dipylidium caninum (Dipylidiasis) Ascaris lumbricoides (Ascariasis) Hookworms (Ancylostomiasis): o Ancylostoma duodenale o Necator americanus Strongyloides stercoralis In small intestine (Strongyloidiasis) Intestinal Trichostrongylus colubriformis nematoda (Trichostrongyliasis) Capillaria philippinensis (Intestinal Capillariasis) Trichinella spiralis (Trichinosis) Enterobius vermicularis (Enterobiasis) In large intestine Trichuris trichiura (Trichuriasis) Filaria (Filariasis): o Wuchereria bancrofti o Brugia malayi o Loa loa Adults o Onchocerca volvulus o Mansonella perstans o Mansonella ozzardi Dracunculus medinensis Tissue (Dracunculiasis, Dracontiasis) nematoda Trichinella spiralis (Trichinosis) Larva migrans o Cutaneous: Ancylostoma caninum Larvae Ancylostoma braziliense o Visceral: Toxocara canis Toxocara cati Liver fluke

-------------------------------------------------------------------------------------------------Cercarial dermatitis (Bathers itch or Swimmers itch): Schistosome of non-human species can penetrate the skin of man but cannot go beyond the germinal layer. Clinically: Dermatitis, irritation, itching, oedema and secondary infection. Diagnosis: History of contact with water followed by skin rash. Treatment: Anti-pruritics, local and general anti-histaminics, antibiotics for 2ry infections. Control: - Snail control - Avoiding dealing with polluted water. - Thorough drying of skin to prevent cercarial penetration.

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Nemathelminths (Round worms)

Platyhelminthes (Flat worms)

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Medical Parasitology in tables Name Parasite (Disease) Hepatic Flukes Fasciola (Fascioliasis) Fasciola hepatica: Common in sheep raising areas in Europe, Middle East (particularly Egypt), Central & South Africa. Fasciola gigantica: Common in cattle raising areas in South-East Asia & Africa including Egypt. Lung Flukes Paragonimus (Paragonimiasis)

Kasr Alainy Students Intestinal Flukes Heterophyes (Heterophysiasis)

Geographical Distribution

Asia (South-East), Africa (Nigeria & Cameron) and South America.

Middle and far east, south Europe and in Egypt in brackish water.

Definitive Host & Man in bile ducts of liver. Habitat Reservoir Host Herbivorous animals. Immature egg stage: Size: 140 70 um. Diagnostic Stage Color: yellowish brown. Shape: oval, operculated & thin shelled. Content: immature ovum. Intermediate Host Lymnaea cailliaudi (snail) in case of F.gigantica. Lymnaea truncatula (snail) in case of F.hepatica.

Man in lungs. Cats, dogs, pigs & monkeys. Immature egg stage: Size: 90 55 um. Color: brown. Shape: oval, operculated & thick shelled. Content: immature ovum. 1st I.H.: Semisulcospira snail. 2nd I.H.: Crabs, crayfish or shrimps. Encysted Metacercaria through eating insufficiently cooked crabs, crayfish or shrimps. Adult worms in lung Eggs coughed with sputum or swallowed & excreted in Faeces Fresh water Miracidium 1st I.H. Sporocyst Redia Cercariae (microcercous)Out to water 2nd I.H. Encysted metacercariae Ingestion small intestine Excysted metacercariae Migration through the intestinal wall Peritoneal cavity Penetrate the diaphragm & pleura Lungs.

Infective Stage & Encysted Metacercaria through eating contaminated Mode Of Infection vegetables or drinking contaminated water.

Man in between the villi of the small intestine. Fish eating animals. Mature egg stage: Size: 30 15 um. Color: yellowish brown. Shape: oval, operculated & thick shelled. Content: mature miracidium. 1st I.H.: Pirenella conica snail. 2nd I.H.: Tilapia Nilotica (Bolty) & Mugil Cephalus (Boury). Encysted Metacercaria through eating improperly cooked or freshly salted fish (less than 10 days, sweet Feseekh). Adult worms in intestineEggs Faeces Brackish water ingested by 1st I.H. Miracidium Sporocyst Redia Cercariae (lopho-cercous) Out to water 2nd I.H. Encysted metacercariae Ingestion Intestine Excysted metacercariae Become deeply embedded between the villi.

Life Cycle

Adult worms in bile ductsEggs FaecesFresh water Miracidium Snail host Sporocyst Redia Cercariae (lepto-cercous) Out to water Attach to aquatic vegetables Encysted metacercariae Ingestion Duodenum Excysted metacercariae Migration through the intestinal wall Peritoneal cavity Liver parenchyma Bile ducts. 1- If immature flukes migrate through the liver tissue destruction, necrosis & haemorrhage of the parenchyma. 2- Hyperplasia of biliary epithelium and fibrous thickening of the ducts as a result of mechanical obstruction, inflammatory responses & the activity of proline excreted by the flukes. 3- Periductal fibrosis causes pressure atrophy on adjacent liver tissue. 4- Minute abscesses can form around eggs trapped in the parenchyma. 5- Spontaneous healing appears to occur frequently and may result from inflammation and calcification. 6- Flukes that migrate out of the intestine may lose their way and form ectopic lesions. 1- Diarrhea & digestive disturbance. 2- Enlarged tender liver, pain in the right costal margin & substernal pain. 3- Cholangitis, cholecystitis and obstructive jaundice. 4- Fever, urticaria, anemia and marked peripheral eosinophilia up to 80%. 1- Clinical signs & symptoms (above) & diet history. 2- Detection of eggs in Faeces or duodenal aspirate is of limited use, because: a. It is only +ve 3 4 months after infection. b. Often eggs are undetectable in chronic phase. c. Spurious infection (False Facioliasis): eggs in stool duo to ingestion of liver of infected animals. The eggs disappear after 1 week of liver free diet. 3- Immunodiagnostic tests: by ELISA, Immuno-fluorescence & counter immunoelectrophoresis which can detect early & chronic infections & are highly sensitive. 4- Radiological imaging: ultrasonography, endoscopic retrograde & percutaneous cholangiography. 1- Triclabendazole. OR 2- Bithionol (Dichlorophenol). 1- Mass treatment of infected animal reservoir. 2- Pure water supply. 3- Snail control. 4- Human protection by proper washing or cooking of aquatic vegetations. It is advisable to soak vegetables in water containing vinegar for 5 minutes or to put them in water containing drops of potassium permanganate for 10-15 minutes to kill encysted metacercariae stuck to them.

Pathogenesis

Clinical Picture

1- Worms provoke granulomatous reactions 1- Light infection may pass unnoticed. In that lead to fibrotic encapsulation of the severe infections, irritation may worms. produce superficial necrosis, 2- Duo to aberrant migration, larvae may excessive mucous secretion & lodge in ectopic sites (brain, abdomen, skin hyperplasia of the mesenteric lymph or heart). nodes. 2- Patients may suffer from discomfort, colic pain, mucous diarrhea and eosinophilia. 3- Sometimes eggs may find their way to the circulation where they go as 1- Chronic productive cough with brownish emboli (ectopic lesions). purulent sputum containing streaks of blood and parasitic eggs. 2- Chest pain. 3- Eosinophilia (20-25 %). 4- Pleural effusion may occur. 1- Clinical signs (above) and diet history in endemic areas. 2- Detection of eggs in Faeces or sputum. 3- Adult worms may be expectorated after treatment. 4- Immunodiagnostic tests: complement fixation & ELISA detect early & chronic infections. 5- Plain x-ray of chest & tomography show nodular or ring shadows and cavities. 1212345Praziquantel. OR Bithionol (Dichlorophenol). Treatment of cases. Good cooking of crabs, crayfish & shrimps. Health education. Snail control. You should know that pigs & small animals are paratenic hosts that can transmit infection if eaten by man. Paratenic host is a host that harbours the parasite in an arrested state.

Diagnosis

1- Clinical signs (above) & diet history. 2- Finding the characteristic eggs in the stool.

Treatment

Praziquantel.

Prevention & Control

1- Proper cooking and salting of fish. 2- Periodic examination and treatment of fishermen. They should avoid defecating in water. 3- Snail control.

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Medical Parasitology in tables Name/Disease Classification Disease Geographical Distribution Definitive Host & Habitat Reservoir Host Schistosoma hematobium Urinary bilharziasis. Nile valley, Africa, Asia, Middle East, South Europe. Man in Vesical and pelvic venous plexuses. Blood flukes: Schistosoma / Schistosomiasis Schistosoma mansoni Intestinal bilharziasis. Nile delta, Africa, South America, Middle East.

Kasr Alainy Students Schistosoma japonicum Intestinal bilharziasis. Far East.

Man in inferior mesenteric venous plexus in the Man in superior and inferior mesenteric venous region of rectum and pelvic colon. plexuses. None. Monkeys and rodents. Domestic animals. Mature egg stage: Mature egg stage: Mature egg stage: Size: 14060 um. Color: Translucent. Size: 15060 um. Color: Translucent. Size: 8565 um. Color: Translucent. Diagnostic Stage Shape: oval with terminal spine. Shape: oval with lateral spine. Shape: oval with minute terminal curved spine. Content: miracidium. Content: miracidium. Content: miracidium. Intermediate Host Bulinus Trancatus snail in Egypt. Biomphalaria Alexandrina snail in Egypt. Onchomelania species snail. Furcocercous Cercariae through penetration of the skin of the D.H., aided by: Infective Stage & 1- The surface tension of the drying droplet of water. 2- Proteolytic enzymes secreted from penetration glands. Mode Of Infection 3- Strong lashing movements of the tail pressing the body into the skin. Male carries the female in its gynaecophoric canal towards the peripheral Shistosomula Venous circulation Migration to the lungs Heart capillaries Eggs pass to the lumen of intestine or urinary bladder Systemic circulation Intrahepatic branches of the portal vein Life Cycle Fresh water Miracidia Snail Sporocyst (no redia) Furcocercous Maturation Migration to the mesenteric veins or to the Vesical veins Cercariae Fresh water Penetrate the skin of D.H. Lose their tail Put their eggs. 1-Stage if invasion (1-4 days): Local dermatitis, irritation & rash duo to cercarial penetration. Acute toxemic schistosomiasis or Katayama 2-Stage of migration (3-4 weeks): syndrome: Lung: verminous pneumonitis, minute hemorrhages, cough & hemoptysis. - Occurs frequently with S. Japonicum & less Liver: enlarged and tender. commonly with S. Mansoni & very rare with S. Metabolic products: result in toxic and allergic manifestations as urticaria, eosinophilia, Hematobium. leukocytosis, fever, headache and muscle pain. - High antigenaemia duo to released soluble egg 3-Stage of egg deposition and extrusion (acute stage, 1-2 months): antigens may cross react with rapidly rising Eggs deposited in the venous plexus escape into the perivascular tissue and finally to the antibodies circulating immune complexes outside with urine or stool tissue damage & hemorrhage. With extrusion, there are: severe allergic reactions Katayama syndrome With schistosomiasis mansoni & japonicum: (acute fibril illness) with deposition of these o Dysentery with blood and mucus in stool. complexes in different sites. o Abdominal pain. - The patient suffers from fever (may last for o In S. Japonicum: there is bloody diarrhea and Katayama fever. several weeks), chills, diarrhea, generalized With schistosomiasis hematobium: lymphadenopathy and eosinophilia. Terminal haematuria. Frequent micturition. Burning pain. Embolic lesions: Pathogenesis & 4-Stage of tissue reaction (chronic stage, months-years): Liver: periportal fibrosis (common in S. mansoni Clinical Picture a. Tissue proliferation (delayed-type hypersensitivity): eggs trapped in the tissues stimulate & S. japonicum & may occur in S. hematobium). inflammatory reactions bilharzial granulomas reversible obstructive lesions. This lead to portal hypertension, hepatob.Tissue fibrosis (immune-suppression-fibroblast proliferation) irreversible obstructive splenomegaly, acitis and esophageal varices. lesions bilharzial nodules, papillomata and sandy patches egg output is reduced. Lung: granulomas in the perivascular tissue, In schistosomiasis mansoni and japonicum: pulmonary arteriolitis, obliterated blood flow, The intestinal wall becomes fibrosed, thickened and may be complicated with strictures, pulmonary hypertension and bilharzial sinuses, fistulae and prolapse. Eggs that fail to be fixed to the intestinal wall venules fall in corpulmonale (congestive right-sided heart the lumen and swept to the liver. This results in periportal fibrosis, portal hypertension, failure). This commonly occurs in S. mansoni & S. hepatosplenomegaly, acitis and esophageal varices. japonicum and less in S. hematobium. In schistosomiasis hematobium: Skin, CNS, pericardium and other organs: eggs Bladder: fibrosis, 2ry infection, stones and malignancy. embolize to ectopic sites via vascular by-pass. Ureter: stricture, hydro-ureter, hydro-nephrosis, 2ry infection and renal failure. Blood changes: Urethra: stricture and fistula. - Eosinophilia and leukocytosis. Genital organs: prostate, seminal vesicles, spermatic cord, vulva and vagina may be - Anemia: Iron deficiency: duo to haematuria. involved. Hemolytic: duo to hypersplenism. 1-History of infection and endemicity (living or coming from endemic area) and to assess efficacy of the drug. 2-Clinical picture according to the stage of infection. Rectal swab using a gloved finger lubricated with soap. The 3-Laboratory diagnosis: material obtained is put on a slide and examined. i. Direct parasitological methods: ii. Blood examination: anemia, leukocytosis and high eosinophilia. Detection of S. hematobium eggs in urine by sedimentation methods. iii. Indirect serological methods: resorted to in late or chronic cases Examination of the last drops of urine passed after 15 minutes of where massive fibrosis of the organs affected prevents the ova from physical exercise gives more positive results. excreta. The most common used tests are: - IHAT -ELISA -IFAT Diagnosis Eggs should be examined for viability: living eggs are translucent with iv. A recent direct technique is the detection of the adult Schistosome intact moving miracidium and hatch in fresh water. Dead eggs are circulating in serum or urine. They indicate active infection by enzyme opaque with dark granular contents and negative hatching test. immuno-assay & have high specificity & sensitivity. Detection of S. mansoni or S. japonicum eggs in stool by smear 4-Cystoscopy, colonoscopy and sigmoidoscopy: Done in chronic cases, technique or by concentration by sedimentation technique. when eggs are not obvious by routine way, to detect lesions and take Kato thick fecal smear is helpful for clinical & epidemiological studies. biopsies. It is a counting technique for detection of worm burden 5-Radiology. Treatment 1- Praziquantel (biltricide). 2- Oxamniquine (vansil). 3- Metriphonate. 1-Mass treatment and follow up of infected persons. - Lining banks of canals with concrete to prevent plant growth. 2-Protection: - Double canal system: one canal provides water for 6 months and the a. Health education, pure water supply, treatment of water canals to be other is allowed to dry alternatively. safe, proper sanitary measures as construction of latrines in houses, - Increasing the velocity of water by increasing the slopes of canals. schools and mosques. - Traps of palm leaves at canal inlets to prevent snails. b.Personal prophylaxis for exposed persons e.g. wearing boots & gloves. - Diverting the canal sources from passing through villages. Prevention & c. Quick drying of exposed skin on getting out of polluted water and Biological methods: Control application of alcoholic preparations reduce cercarial penetration. - Introduction of a natural enemy which predates on snails as ducks, d.Use of repellants as dimethyl or dibutyl phthalate or diethyl toluamid birds or snails (Marisa species). to prevent cercarial penetration. - Plantation of some plants toxic to snails as Balanites Aegyptiaca. 3-Snail control: Chemical methods (molluscicides): Physical methods: changing the environment to become unsuitable for - Copper sulphate 10 20 parts per million. snails to live. - Sodium pentachlorophenate (santobrite) 5 10 parts per million. - Clearing canals from weeds to deprive snails from food. - Bayluscide 2 parts per million. ~ IV ~ 2010/2011

Medical Parasitology in tables

Kasr Alainy Students

Class: Cestoidea Subclass: Cestoda

General characters: 1- Flat, ribbon shaped and segmented, hence called tape worms. 2- Covered by cuticle. 3- No body cavity, various systems are embedded in parenchymatous tissue. 4- No digestive system. They feed by diffusion through the cuticle. 5- Any cestode is formed of scolex (head), neck and strobila (chain of segments). 6- Excretory and nervous systems are present. 7- Genital system: hermaphrodite; each mature segment contains male and female genital systems. Common genital pores are either ventral or lateral. Adult intestinal cestodes are: D. latum, T. saginata, T. solium, H. nana, H. diminuta, D. caninum. Larval cestodes of man are: 1- Sparganum (plerocercoid) larva of D. mansoni and D. proliferum. 2- Cysticercus cellulosae of T. solium. 3- Hydatid cyst of E. Granulosus and E. multilocularis. 4- Coenurus cyst of M. multiceps. Man can act as definitive and intermediate host for the same cestode in: T. solium and H. nana.

Class: Nemathelminths Subclass: Nematoda

General characters: 1- Elongated and cylindrical round in cross section. 2- Unsegmented with body cavity. 3- Separate sexes: posterior end is curved in most of males and straight in females. 4- Body wall consists of 3 layers: a. Outer laminated (cuticle). b. Sub-cuticle (hypodermis). c. Muscular. 5- Digestive system: simple tube extending from mouth to anus and formed of: mouth, esophagus and intestine. 6- Genital system: a. Male system: one genital set. b. Female system: two genital sets except in Trichuris and Trichinella. Female worm may either: - Give birth to larvae (larviparous). - Lay eggs (oviparous) either immature or mature. One cell e.g. Ascaris, Trichuris 4 cells e.g. Ancylostoma, Capillaria 16 32 cells e.g. Trichostrongylus e.g. Enterobius, Strongyloides

---------------------------------------------------------------------------------------Hydatid cyst of Echinococcus Granulosus: 1- Thy fully developed cyst is typically unilocular, spherical in shape and filled with fluid. 2- It reaches diameter if 10 cm or more (this takes many years). 3- In humans, 80 90 % of hydatid cysts are found in liver or lung, others are found in brain, bones and kidneys. 4- The cyst wall is formed of three layers from inside to outside: a. Cellular or germinal layer, capable of division. b. Elastic non cellular laminated layer. c. Host produced fibrous layer to prevent further growth of the cyst. 5- The cyst contains: a. Individual scolices (microscopic, 100 1000). b. Daughter cysts similar to the mother cyst. c. Brood capsules which are sacs enclosing a number of scolices. Scolices, daughter cysts and brood capsules may remain attached to the wall of the of the mother cyst or detach and fall into the cavity of the mother cyst (called hydatid sand). 6- Exogenous daughter cyst occurs as a result of herniation of germinal layer to the outside. 7- Sometimes, the germinal layer of the mother & daughter cysts and brood capsules fail to give scolices, thus we get sterile cyst. Eggs of nematoda Immature

Mature

---------------------------------------------------------------------------------------Tissue nematodes characters: 1- The adult worms live in the tissues of man (extraintestinal). 2- The oesophagus is filariform (cylindrical). 3- The female is larviparous (laying larvae). 4- An arthropod vector (Intermediate host) is required for transmission.

---------------------------------------------------------------------------------------Modes of infection of nematodes: 1- Ingestion either by: a. Ingestion of eggs: i. Eggs pass infective e.g. Enterobius. ii. Eggs become infective after a period of maturation outside e.g. Ascaris and Trichuris. b. Ingestion of larvae: i. In vegetables or water e.g. Trichostrongylus. ii. In pig muscle e.g. Trichinella. iii. In fish e.g. Capillaria. iv. In Cyclops e.g. Dracunculus. 2- Penetration of skin: a. Larvae penetrate the skin e.g. Ancylostoma, Strongyloides. b. Through bite of blood sucking insects e.g. Filaria.

---------------------------------------------------------------------------------------Parasite (Disease) Geographical Distribution Definitive Host & Habitat Diagnostic Stage Intermediate Host Infective Stage & Mode Of Infection Multiceps multiceps (Coenurosis) Cosmopolitan Small intestine of dogs and canines. See diagnosis. Sheep, goats and occasionally man. Ingestion of eggs with infected food, drink or hands. It develops the same way as hydatid cyst. The coenurus cyst develops chiefly in the brain and spinal cord. Symptoms of increased intra cranial tension. As a space-occupying lesion in the brain or spinal cord but confirmed as coenurus cyst after surgical removal. Surgical removal. As hydatid disease. Dipylidium Caninum (Dipylidiasis) Cosmopolitan S.I. of dogs, cats & man occasionally. Gravid segments or egg capsules. Flea larvae of dogs and cats. Ingestion of infected fleas. Adult worms on small intestine of D.H. eggs (oncospheres) faeces ingestion by I.H. cysticercoids ingestion of I.H. by D.H. small intestine Adults 1- Usually asymptomatic. 2- Abdominal pain and diarrhea may occur. By finding gravid segments or egg capsule in stool. As in taeniasis. ---------~V~

---------------------------------------------------------------------------------------Protective mechanisms of nematodes: 1- Intestinal nematodes resist the action of digestive juices by their cuticle and lytic enzymes secreted by the worm. 2- They maintain their position by: a. Oral attachment to the mucosa by teeth or plates (Hookworms). b. Partial penetration of the mucosa (Trichuris and Trichostrongylus). c. Complete penetration of the mucosa (Strongyloides, Trichinella and Capillaria). d. Retention of the folds of mucosa and pressure against it (Ascaris, Enterobius).

Life Cycle

Pathogenesis and Clinical Picture Diagnosis Treatment Prevention & control

2010/2011

Medical Parasitology in tables Parasite (Disease) Geographical Distribution Definitive Host & Habitat Reservoir Host Diphyllobothrium latum (Diphyllobothriasis) Lake regions, not in Egypt. Can be imported in fish. Small intestine of man. Diphyllobothrium mansoni & proliferum (Sparganosis) Far east, USA, East Africa. Taenia saginata (Taeniasis Saginata) Cosmopolitan especially in cattle raising countries. Small intestine of man only. Taenia solium (Taeniasis Solium)

Kasr Alainy Students Cysticercosis

Cosmopolitan especially in pork raising countries. Small intestine of man. Tissues of man. ----------

Small intestine of cats and dogs. Fish eating animals: dog & cat ---------Immature egg stage: Size: 70 50 um. Cannot be settled except Diagnostic Color: yellowish brown. after surgical removal and Stage Shape: oval, operculated & identification of plerocercoid thick shelled. larva in removed tissue. Content: immature ovum. 1st: Cyclops (water flea). 1st: Cyclops. Intermediate 2nd: fresh water fish: 2nd: frogs, snakes, mammals, Host Salmon. birds, or man (blind end). Plerocercoid larvae through: 1-Ingestion of undercooked flesh of 2nd I.H. Plerocercoid larvae through Infective Stage 2-Drinking water containing ingestion of undercooked or & Mode Of infected Cyclops. under salted contaminated Infection 3-Applying the flesh of 2nd (infected salmon) fish. I.H. as foment or poultice to inflamed tissue as skin or eye. Adult worms in small intestine Eggs Faeces Fresh water Coracidium 1st I.H. Procercoid larva 2nd I.H. eat 1st I.H. penetrate intestinal wall tissues & muscles plerocercoid larva or sparganum Ingestion by D.H. Small intestine Maturation (6 weeks) Eggs

------------------Immature egg stage: Size: 30-40 um in diameter. Color: yellowish brown. Shape: spherical with radially striated shell. Content: hexacanth oncosphere. Ziehl Nielsen stain: T. saginata stained well but T. solium not Cattle Pig

----------

---------Ingestion of eggs by: 1-Heteroinfection: through infected food or water. 2-External autoinfection: hand to mouth infection in infected patient. 3-Internal autoinfection: some detached segments of the worm ascend against peristaltic movement of intestine then descend again where they hatch and cause cysticercosis.

Cysticercus bovis through ingestion of undercooked infected beef.

Cysticercus cellulosae through ingestion of undercooked infected pork.

Life Cycle

Adult worms in small intestine gravid segment Adult worms in small detach singly out with intestine of dogs & cats faeces or by creeping 1st I.H. Procercoid larva perianal region Eggs 2nd I.H (occasionally man) grass ingestion by cattle plerocercoid larva or penetrate intestinal wall sparganum any tissue blood muscles (man is a blind end of the Cysticercus bovis cycle because he is not eaten Ingestion by D.H. Small by other animals) intestine Maturation ( 3 months) Eggs

Adult worms in small intestine gravid segment detach in chains through anus perianal region Eggs grass ingestion by pigs penetrate intestinal wall tissues & muscles Cysticercus cellulosae Ingestion by D.H. Small intestine Maturation Eggs

----------

1-May be asymptomatic. 2-Intestinal disturbance: colic, hunger pain, nausea, vomiting, diarrhea and loss of appetite. 3-Neurological manifestations: headache, Pathogenesis insomnia or convulsions and Clinical caused be absorbed toxins. Picture 4-Large no. may produce intestinal obstruction. 5-Pernicious anemia (macrocytic hyperchromic): a. Some toxins. b.Vit. B12 deficiency because the parasite competes for it.

1-Intestinal disturbance. 2-Neurological Depend on the tissue manifestations. 1-Intestinal disturbance, invaded: 3-Intestinal obstruction. Neurological manifestations, 1-Skin: inflammatory tender 4-Loss of weight & hunger Intestinal obstruction & loss swellings. pains as the parasite of weight. 2-Eye: painful edematous consumes much of 2-If man ingests the eggs, the conjunctivitis and ptosis. patients food. larval stage develops in 3-Degenerated larvae: cause 5-Appendicitis or cholangitis extra-intestinal tissues inflammation and necrosis caused by stray segments cysticercosis. This condition but no fibrosis. of the worm. occurs with T. solium only 4-Patient may suffer from: 6-Migrating segments which makes it more urticaria, edema, fever, creeping out of the anus dangerous. pain and eosinophilia. cause irritation, itching and worry of the patient.

1-Sites: brain, subcutaneous tissue, eye, heart or any other tissue. 2-Cysts produce inflammatory reactions which usually end by fibrosis and calcification. 3-Muscle pain, fever and eosinophilia. 4-Cysts in subcutaneous tissue are easily palpated (lipoma). In the eye may lead to visual disturbances. In neurocysticercosis leads to variable neurological disorders. 1-Intestinal infections. 2-Biopsy from a nodule in skin or muscles. 3-X-ray to visualize calcified lesions. 4-CT, MRI, ultrasonic or ophthalmoscopic examinations. 5-IHA, ELISA, eosinophilia & intra-dermal tests. 1-Surgical treatment. 2-Praziquantel. 3-Albendazole. 4-Simultaneous administration of steroids to relieve intense inflammatory reactions. 5-Vit D & calcium to help calcification. 1-Sanitary disposal of human excreta. 2-Pure water supply. 3-Proper washing of vegetables. 4-Treatment of infected patients. 5-Health education. 2010/2011

Diagnosis

1-Detection of eggs and segments in Faeces. 2-Blood picture shows anemia.

1-Detection of eggs or segments in Faeces. Cannot be settled except 2-Recovery of eggs from after surgical removal and perianal region by swab. identification of plerocercoid 3-Searching for gravid larva in removed tissue. segment in Faeces. If not found, give a saline purge.

1-Detection of eggs in Faeces & differentiation by Ziehl Nielsen stain. 2-Detection of gravid segments in Faeces.

Surgical removal (difficult in sparganum proliferum due to 1-Praziquantel. OR Treatment its proliferation and spread 2-Niclosamide. to other tissue). 1-Treatment of infected men. 2-Preventing contamination 1-Sanitary disposal of human of soil by human Faeces. excreta. 1-Water should be boiled or 3-Protection of I.H. by 2-Proper cooking of fish. filtered. preventing them from Prevention & 3-Treatment of infected 2-Thorough cooking of flesh grazing in infected areas. Control patients. of I.H. 4-Proper inspection of 4-Periodic de-worming of 3-Avoiding fomentation with slaughtered cattle. Infected reservoir hosts. the flesh of I.H. carcasses must be 5-Health education. condemned. 5-Proper cooking or deep freezing of meat.
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1-Praziquantel. OR 2-Niclosamide (Yomesan). 3-Supportive treatment: Vit. B12 given parenterally.

1-Praziquantel and Niclosamide. 2-A saline purge is given 1-2 hours later to wash the eggs to prevent cysticercosis. 3-Quinacrine hydrochloride (atebrine) for expulsion of the intact parasite.

Same as T. saginata but mainly directed towards pigs.

Medical Parasitology in tables Parasite Echinococcus granulosus (Disease) (Hydatidosis, Hydatid disease) Geographical Cosmopolitan, in sheep raising countries. Distribution Definitive Host Small intestine if dogs & canines but not man. & Habitat Diagnostic Stage Hydatid cyst Intermediate Host Echinococcus multilocularis In cold areas Small intestine of foxes, wolves and cats. The alveolar cyst Hymenolepis nana (Hymenolepiasis) Cosmopolitan, in warm areas, in Egypt too. Small intestine (S.I.) of man.

Kasr Alainy Students Hymenolepis diminuta (Hymenolepiasis diminuta) Cosmopolitan S.I. of rats, mice & occasionally man

Egg stage: Size: 30-50 um diameter Color: Translucent. Shape: spherical with two coverings. Content: mature hexacanth oncosphere. Flea larvae or grain beetles. Egg stage or cysticercoid larva, by: 1. Ingestion of contaminated food Ingestion of insect vector. and water. 2. Autoinfection (hand to mouth). Direct cycle: Adults in S.I. of D.H. eggs faeces ingestion by man penetrate S.I. mucosa cysticercoid larva after 1 weak return to the lumen adult stage. Indirect cycle: Adults in S.I. of D.H. eggs faeces eaten by I.H. cysticercoid larva ingestion of I.H. accidentally by man S.I. adult stage. (H. diminuta shows this cycle only).

Herbivorous animals.

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Infective Stage Egg stage through: & Mode Of - Hand to mouth from fur of infected animals. Infection - Food or drink infected by animal faeces. Adults in S.I. of D.H. eggs (oncospheres) faeces grass ingestion by I.H. penetrate S.I. pass to blood by lymphatics or venules various parts of body vesiculation grow slowly Hydatid cyst (take several years & may be single or multiple).

Life cycle

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Hepatic cyst (66%): Usually in the right lobe extending towards the abdominal cavity: 1-May cause no symptoms until it expands. 2-Obstructive jaundice. 3-Rupture of the cyst leads to: a. 2ry new cysts with hydatid sand or bits of germinal layer. b.Rupture into bile ducts leads to intermittent jaundice, fever and eosinophilia. c. Allergic manifestations up to anaphylactic shock in case of entrance of hydatid material to blood stream. Pulmonary cyst (22%): 1-Early symptoms include hemoptysis, transient thoracic pain and shortness of breath. Pathogenesis & 2-In majority of cases, the cyst transfer into chronic Clinical Picture abscess (if rupture is incomplete) and patient complains of sudden attack of cough with sputum contains frothy blood, mucous & hydatid material. Brain cysts (1%) Large cyst intracranial tension up to epilepsy Renal cysts (3%): Intermittent haematuria. Hydatid sand may be present in urine. Osseous cysts (2%): It has no fibrous nor laminated layers, but only germinal layer which develops in bone marrow cavity then extends to osseous tissue leading to: 1-Erosion of large area of bone. 2-Destruction of trabeculae. 3-Spontaneous fracture. Clinically by detection of slowly growing cystic tumor & history of contact with dogs. Ultrasonography & CT detect un-calcified cysts & of value in follow up of treated cases. X-ray imaging especially in pulmonary cysts and calcified cysts: 1-Round solitary or multiple sharply contoured cysts of 1 15 cm in diameter. Diagnosis 2-Internal daughters give a car wheel shape 3-Thin crescent or ring shape calcification. Serological tests: IHA, ELISA. Aspiration cytology: risky Molecular diagnosis: DNA analysis & PCR. Intradermal test of Casoni: was used but may give false results in 18% of cases. Now it is not preferred because it may give allergic reactions. 1-Surgical removal. Treatment 2-PAIR technique. 3-Medical ttt: i-Albendazole ii-Praziquantel 1-Proper disposal of infected viscera. 2-Elimination of dogs. Prevention & 3-Periodic examination of pet dogs and treatment of Control infected ones by Praziquantel. 4-Avoid dogs and prevent children from playing with them. 5-Protection of food and drink from infected dogs.

The alveolar cyst It is a porous spongy gelatinous mass formed of small irregular cavities that are lined by germinal layer with a very thin or no laminated layer with fibrous tissue strands in-between 1-Light infection: asymptomatic the cavities: 2-Heavy infection: It has irregular outline Abdominal pain which is not defined from Appetite loss the surrounding tissues. 1-Usually asymptomatic. Diarrhea or vomiting It behaves like a malignant 2-Mild GIT disturbances Nervous manifestations as tumor i.e. degeneration occasionally. dizziness, insomnia and and calcification in the convulsions due to absorption center and spreading at of toxic byproducts of the the periphery. It gives worm. metastasis through blood or lymph. Its commonest site is in the liver (90-100%). In human, the cyst is usually sterile (no scolices in the fluid medium of the cyst).

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Detection of eggs in faeces.

Surgical removal

1. Praziquantel 2. Treat all members of the family at the same time (mass ttt). 1-Personal hygiene. 2-Mass treatment. 3-Avoid infected food and drink. 4-Elimination of arthropods & rodent control. 5-Environmental sanitation.

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Rodent control.

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2010/2011

Medical Parasitology in tables

Parasite (Disease) Geographical Distribution Definitive Host & Habitat Ascaris Lumbricoides (Ascariasis) Trichuris Trichiura (Trichuriasis)

Kasr Alainy Students Enterobius vermicularis (Enterobiasis)

Cosmopolitan, common in temperate & cold climates. Man (only), in the caecum and adjacent parts of small & large intestine and appendix. Adult stage or egg stage, egg characters: Size: 50 25 um. Color: translucent. Shape: plano-convex, has 2 layers covered by outer sticky albuminous layer. Content: larvae (infective in few hours). Infective eggs containing larvae, through: Autoinfection (hand to mouth). Contaminated food or drink. Handling contaminated linen, clothing or articles. Air-born infection. Retro-infection. Adults female migrate towards the anal opening lay sticky eggs perianal area infection by any mode larvae hatch in S.I. moult twice adult

Cosmopolitan, common in warm areas with bad sanitation, in Egypt too (especially in children). Man, live free in the lumen of the small intestine. Man, in the caecum and adjacent parts.

Diagnostic Stage

Egg stage. Immature egg stage: Eggs are the most resistant. They can survive for months Size: 50 25 um. Color: brownish. and years in soil. Shape: barrel shaped, thick shelled with a mucoid plug at each pole. See the details in the next page. Content: immature ovum (1 cell stage). Rhabditiform larvae by ingestion of embryonated eggs through contaminated water, vegetable or hands.

Infective Stage & 2nd stage rhabditiform larvae through ingestion of Mode Of Infection embryonated eggs.

Life Cycle

Pathogenesis

Clinical Picture

Adulteggsfaecessoil 1st rhabditiform larva 1st moult 2nd rhabditiform larva ingestion penetrate S.I. venous blood lung enter alveoli 2nd & 3rd moult ascend in the respiratory tracts swallowed S.I. 4th moult adult Tissue damage due to: 1- Large size of Ascaris (largest intestinal nematode). 2- Adults do not attach to intestinal wall, and may go ectopic places. 3- Toxic products stimulate immune response. 1- Usual infection (10-20) worms pass unnoticed. 2- During larval migration: a. Pneumonitis: fever, cough, dyspnea & eosinophilia. b. Allergic reactions asthmatic attacks & edema of lips c. Sputum examination reveals streaks of blood, eosinophils & may be larvae. d. Loefflers syndrome: x-ray shows scattered mottling. e. Ectopic lesions. 3- In the intestine: a. Abdominal pain, nausea, vomiting, colic, distention or dyspepsia due to production of anti-enzymes that interfere with digestion malnutrition. b. Changes in the bowel movements (diarrhea or constipation). 4- Complications: a. Traumatic effects due to irritation of the worms which may go to: Bile duct obstructive jaundice. Liver abscesses. Appendix appendicitis. Ampulla of Vater acute hemorrhagic pancreatitis Peritoneum Peritonitis. Stomach vomiting or escape through nares Trachea (rare) suffocation. b. Toxic effects by toxins that may produce oedema, asthma, insomnia, irritability & convulsions. c. Larvae in ectopic sites give the picture of visceral larva migrans.

Adults in caecum eggs soil shade & moisture Rhabditiform larvae ingestion lower part of S.I. caecum moult 4 times adult

The embedded anterior parts of the worms cause inflammation and irritation of the mucosa with hemorrhage. Secondary infection results in sub-mucosal abscesses & ulcers. Mild infection: Usually asymptomatic. Moderate infection: Frequent small blood-streaked stool 1- Pruritus ani: itching in the perianal area especially at (bloody diarrhea). night. Pain and tenderness in the lower 2- Nervous irritability, hyperactivity, insomnia and 2ry abdomen. enuresis. Nausea, vomiting & loss of weight. 3- Female migration to ectopic sites stimulate granuloma Heavy infection: formation, through migration to: Dysentery: the worms are distributed a. Vagina vulvo-vaginitis, they may migrate to throughout the colon & rectum leading uterus or fallopian tubes. to oedemtous hyperemic fragile b. Urinary tract infection & enuresis. mucosa. c. Appendix appendicitis. d. Intestine diarrhea & abdominal pain. Rectal prolapse: due to chronic straining e. Peritoneal cavity (through uterine tubes) pelvic due to dysentery leads to loss of anal peritonitis. tone & prolapse. Anemia: due to suction & bleeding causing microcytic hypochromic anemia. Toxic by-products may cause macrocytic hyperchromic anemia (Trichocephalic anemia). Rarely perforation: lead to peritonitis. May invade appendix: appendicitis. Eosinophilia: is persistent.

Diagnosis

Treatment

Prevention & Control

Clinically: Infection is suspected in children with pruritus at night. Laboratory: 1- Clinically: Adult worms may be seen in stool or anal area. Transient cough & dyspnea which disappear after 1-2 1- Finding eggs in stool. weeks followed by vague abdominal manifestations. 2- Rectal examination by proctoscopy: Eggs are rarely found in stool (about 5% only). 2- Laboratory investigations (findings): hyperemic edematous mucosa with Swabbing of anal or perianal area by: a. Eggs in faeces. hanging worms. o N.I.H. swab (National Institute of health): the peri-anal b. Adults in faeces, vomits, or intestinal obstruct. 3- Air-contrast barium enemas: linear area is swabbed in the morning before defecation or c. Larvae in sputum with blood & eosinophils. translucent adults in contrast to bariumbathing with a cellophane paper folded and tied to tip d. Eosinophilia: 20 % during migration then regresses coated bowel mucosa. of a glass rod and inserted in a test tube. The to 7 %. 4- Blood-test: cellophane is stretched in a slide and examined 3- Radiologically: - Eosinophilia (5 15 %). microscopically for eggs. a. Plain x-ray: adults appear as gas-filled loops. - Anemia. o Scotch adhesive tape swab: Scotch tape with sticky b. Barium meal: filling defects represent adults. side outwards is pressed against perianal area then spread on a slide with sticky side downwards and examined microscopically. 1- Albendazole OR Mebendazole. 1. Albendazole OR Mebendazole. 1. Albendazole OR Mebendazole: it should be repeated 2- In mixed infections, it is advisable to treat Ascaris 2. Repeated course may be necessary. We after 2 weeks. first (to avoid worm irritation ectopic lesions). have to give anti-diarrheal drug before 2. Local application of white oxide of mercury around the 3- Surgical treatment of complications. ttt. anus to relief the itching & kill the out coming worms. 1- Mass treatment. 1- Mass treatment. 2- Personal hygiene. 2- Washing hands before meals. 3- Toilet seats disinfected frequently. 3- Sanitary disposal of human faeces. 4- Food protection. 4- Proper washing of fruits and vegetables eaten raw. 5- Infected children should use tight trousers at night to 5- Night soil should not be used as fertilized unless treated by chemicals. prevent auto-infection.
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2010/2011

Medical Parasitology in tables Egg stage in Ascaris Lumbricoides Egg type Fertilized egg Unfertilized egg Decorticated egg Size 6045 um 9040 um ------------Oval, thick smooth Longer and narrow Fertilized egg but layer covered by Shape with ill-defined lacking the mamillated mamillations. mamillations. albuminous coat. Color Brownish content Immature(one cell stage) Life cycle of Strongyloides stercoralis: Direct cycle (similar to hookworm): Rhabditiform larvae soil moult infective filariform larvae penetrate the skin venous circulation lungs penetrate the alveoli migrate Hookworm - Ancylostoma duodenale (Ancylostomiasis) Mediterranean, North Africa, South America, India and China.

Kasr Alainy Students through the trachea swallowed small intestine 2 moults adults Indirect cycle (if the soil condition is optimal): Rhabditiform larvae soil four moults within 2 days adult (free-living) mature ova Rhabditiform larvae (free-living) as long as the conditions are suitable. If the condition becomes unfavorable, the rhabditiform larvae become infective filariform larvae. Autoinfection: When a person suffers from constipation, rhabditiform larvae have enough time to moult into infective filariform larvae. Then they penetrate the mucosa of large intestine then complete the cycle (internal autoinfection). Also, the infective filariform larvae can penetrate the perianal skin after coming out from the anus and then complete the cycle (external autoinfection).

Parasite (Disease)

Geographical Distribution Definitive Host & Small intestine S.I. (jejunum) of man only. Habitat Immature egg stage: Size: 40 60 um. Diagnostic Stage Color: Translucent. Shape: oval with rounded poles & thin shelled. Content: immature ovum with 4 cell stage. Infective Stage & Filariform larva through penetration of the skin Mode Of Infection results from handling soil without gloves or shoes Adults in S.I.eggs faecessoil 1st stage rahbditiform larva 1st moult 2nd stage rahbditiform larva 2nd moult infective Life Cycle filariform larva penetrate the skin venules or lymphatics lungs 3rd moult penetrate the alveoli migrate through the trachea swallowedsmall intestine4th moultadult Skin lesions: itching, erythema, vesiculation and pustulation at the site of penetration due to 2ry bacterial infection (ground itch or hookworm dermatitis). Pulmonary lesion: asthmatic bronchitis, minute hemorrhage, verminous pneumonitis, rise to: fever, cough, dyspnea, hemoptysis & eosinophilia (up to 70%) after 2-3 weeks (Loefflers syndrome) These 2 stages are seen in individuals who receive a primary infection. Intestinal lesion: - Hemorrhage (0.3 cc blood/day) results from attachment of the parasite to the mucosa by its cutting teeth. The worms leave the oozing site & attach to other site and so causing minute ulcers - Hypochromic microcytic anemia results from chronic blood loss & depletion of iron stores. It results in pallor, fatigue, dyspnea & tachycardia - Subcutaneous edema due to hypo-proteinaemia - GIT: nausea, vomiting & diarrhea due to mucosal ulcerations. Melaena & occult blood in stool may occur. - Pica i.e. habitual ingestion of non-food substances as soil. - Retardation of physical and mental development

Pathogenesis & Clinical Picture

Diagnosis

1-Clinical: above. 2-Laboratory: a. Stool examination for eggs. b. Determination of anemia. c. Testing for occult blood in stool.

Treatment

Prevention & Control

1-Albendazole OR Mebendazole (vermox). 2-Iron supplement and protein rich diet. 1-Sanitary disposal of human excreta. 2-Mass treatment. 1- Treatment of infected animals or patients. 3-Disinfection of human excreta used as fertilizers. 2- Proper washing of green raw vegetables and 4-Wearing shoes and gloves. pure water supply. 5-Killing the filariform larvae using soil larvicides. 6-Health education: avoid being barefooted and defecation on the ground and use of latrines (toilets)
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Strongyloides stercoralis Trichostrongylus colubriformis (Strongyloidiasis) (Trichostrongyliasis) Cosmopolitan, more in tropical and subtropical Cosmopolitan, especially in agricultural areas. countries. Man, in the duodenum and upper jejunum, but in Upper part of S.I. of herbivorous animals and heavy infection may involve the whole intestines occasionally man (may invade biliary passages). Immature egg stage: Size: 80 40 um. Color: Translucent. Filariform larvae. Shape: oval, thin shelled with one round pole & the other pointed. Content: immature (morula stage, 16-32 cells). Filariform larvae through penetration of skin or the Ensheathed filariform larvae through ingestion mucosa of the intestine. with green vegetables and water. Adults in S.I. eggs inside the mucosa of intestinal villi rhabditiform larvae lumen Adults in S.I. eggs faeces soil faeces has 3 types of life cycle: rhabditiform larvae moult 2 times within 4 5 1- Direct cycle (similar to hookworm). days ensheathed filariform larvae ingestion 2- Indirect cycle. S.I. another moult penetrate the villi 3- Autoinfection. remain for 4 days back to lumen Adults See the details above this table. Skin lesions: dermatitis & itching. Larvae may remain in the skin producing cutaneous larva migrans which usually seen in patients who develop external autoinfection. The lesion starts at the perianal region and extends as linear eruption across the buttocks, thigh & back at a fast rate (5 10 cm/hour) referred to as larva currens. Lung lesions: minute hemorrhage & pneumonitis as hookworms. Intestine lesions: Burning epigastric pain with tenderness (duodenitis). Infection is usually light producing no symptoms. Nausea and vomiting, diarrhea alternates with Heavy infections may cause anemia or signs constipation. of cholecystitis. Long-standing heavy infection results in weight loss, chronic dysentery, mal-absorption and steatorrhoea. Disseminated Strongyloidiasis: Occasionally some larvae pass through the pulmonary barrier to the left side of the heart to reach various organs of the body. In-patient with impaired immunity, the parasite produces massive number of larvae, which penetrate to extra intestinal organs and could be fatal. So it is considered as an opportunistic parasite. 1- Examination of faeces or duodenal contents for larvae either by: a. Direct or concentration methods which reveal the motile larvae in fresh specimen. 1- Finding eggs in stool or duodenal aspirate. b.Culture for 48 hours gives free living adult 2- Stool culture may give larvae. worms. 2- Examination of sputum for larvae. 3- Eosinophilia. 4- Serological test as ELISA. 1- Thiabendazole. OR Thiabendazole (Mintezol) 2- Ivermectin.

2010/2011

Medical Parasitology in tables Larva Migrans Name Parasite (Disease) Cutaneous larva migrans (CLM) Visceral larva migrans (VLM) Geographical ------------------------Distribution Not the man, so they cannot Definitive Host & Dogs & cats, not man so they invade man complete their cycle, instead Habitat viscera & cannot complete the cycle. they migrate under the skin. Diagnostic Stage ------------------------Infective Stage & Filariform larvae through Mode Of Infection penetration of skin. Infective egg through ingestion of contaminated food, drink or hands. Capillaria philippinensis (Intestinal Capillariasis) Philippines & Thailand, some cases detected in Egypt. Fish eating birds and occasionally man, embedded in the mucosa of jejunum & ileum. ------------Larval stage, through eating raw or poorly cooked fish and internal auto-infection. Adult female eggs fresh water embryonated eggs I.H. (fish) S.I. larvae ingestion of I.H. by D.H. S.I. of D.H. S.I. of D.H. hatch adult In autoinfection: Female eggs & larvaeinvade the mucosaadult

Kasr Alainy Students Trichinella spiralis (Trichinosis) Cosmopolitan, especially in porkeating countries. S.I. of man, pigs and rodents (rats). They act as intermediate hosts (I.H.) too. ------------Encysted larvae, through ingestion of improperly cooked infected pork. Larvae ingestion by pigs its muscles ingestion by man S.I. 3 moults adults female eggs in the mucosa larvae blood all tissues especially striated muscles coiled encyst encysted larvae

Life Cycle

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Pathogenesis & Clinical Picture

1.The lesion starts as a red itchy papule at the site of entry followed by a slightly elevated erythematous serpiginous tunnel 1-2 mm in diameter with itching and 2ry infection. 2.The lesion advances at a rate of 1-2 cm/day for several weeks or months till the larvae die. This commonly seen in the skin of hands, feet, back of buttocks.

Diagnosis

1. Clinically depends on the advancing serpiginous tunnels & history of contact of skin with soil. 2. Suspect migration of larvae in the tissues if there is high eosinophilia. The larva is always ahead of its track.

1. The rhabditiform larva hatch in the S.I. & penetrate the wall circulation viscera (liver mainly) wander for weeks or months or become dormant causing eosinophilic granulomatous lesion. 2. The characteristic granuloma consists of a gray elevated circumscribed area about 4 mm in diameter. It consists of eosinophils, lymphocytes & foreign body giant cells surrounding the larva. 3. Symptoms depend on location of larvae & the patients allergic response: - Asymptomatic with persistent eosinophilia. - The usual picture is: o Child 1- 4 years old. With history of contact with soil, dogs & cats. o Marked persistent eosinophilia (20 80 %). o Enlarged tender liver. o Pneumonitis & pulmonary infiltration may be seen in x-ray. o Visual or neurological disturbances. o Marked increased blood -globulins. 1. Clinically: a young child, with chronic eosinophilia, exposed to ascarid-infected pets, eating soil, hepatomegaly or chronic pulmonary disease is suggestive. 2. Laboratory diagnosis: - Laparoscopy & biopsy of liver nodules under vision is better than needle biopsy. - Hyper--globulins: IgG, IgM, IgE. - Eosinophilia (20 80 %). - Elevated anti-A & anti-B iso-haemoagglutinin titre due to cross reactivity with larval antigen. - Serological tests: IHA, IFA, ELISA.

1. Pathogenesis depends on the presence of parasitic stages in the mucosa chronic inflammation reactions atrophy mal-absorption of fats, sugars, proteins and electrolytes. 2. Abdominal pain, chronic diarrhea, vomiting, low-grade fever, dehydration, loss of weight & oedema of lower limbs (due to hypo-proteinaemia). 3. Death may occur due to severe electrolyte imbalance or due to superimposed bacterial infection.

Intestinal stage (1st week): Gastro-enteritis nausea, vomiting, abdominal cramps and diarrhea simulating ingestion of infected pork. Stage of larval migration (2nd week): Fever, oedema of eye lids, myositis & weakness of invaded muscles. There may be shallow rapid breaking eosinophilia 2050%. Stage of encapsulation (3rd week): Fever recovers slowly, muscle pain is persistent. Death may occur from myocarditis, pneumonia or encephalitis in case of severe infections.

Clinically: A history of eating pork with fever, 1. Clinical examination: above. eosinophilia, facial oedema & 2. Stool analysis: all stages of the myositis is suggestive. parasite are detected in watery Laboratory diagnosis: stool with a lot of Charcot 1- Muscle biopsy: examined for Leyden crystals. larvae. 3. Laboratory investigations: 2- Eosinophilia: 10-90% in the 3rd to - Low serum Na, K, Ca. 4th week. - Low serum proteins (especially 3- Intradermal test. albumin). 4- Serological tests: as IFAT & ELISA. 5- X-ray showing calcified cysts. 1. Specific: Mebendazole OR Albendazole. 2. Supportive ttt: fluids, electrolytes, high protein diet and vitamins. It impossible to control birds, but in human it is necessary to: 1- Detect & treat cases. 2- Prevent contamination of Lagoons by sanitary disposal of human excreta. 3- Warning people of the danger of eating raw fish. 1- Mebendazole (vermox) OR Thiabendazole. 2- Corticosteroids. 3- Symptomatic treatment: for fever, headache & muscle pain. 1. Destruction of rats & proper breeding of pigs. 2. Heat ttt of garbage fed to swine. 3. Avoidance of eating pork. 4. Meat inspection of slaughter houses (Trichinoscope). 5. Destruction of larvae by proper cooking & freezing (at -15 for 20 days or quick at -37). 6. Pork roasts cooked in microwave ovens does not kill larvae.

Treatment

1.Albendazole. 2.Thiabendazole ointment. OR 1. Thiabendazole (Mintezol). 3.Thiabendazole (Mintezol). 2. Corticosteroids in severe cases. 4.Antibiotics for 2ry infection. 5.Anti-histaminics.

Prevention & Control

1. Avoid skin contact with soil 1-Dogs & puppies should be kept away from polluted with dog or cat children. faeces. 2-Pets should be de-wormed regularly & 2. Regular examination & elimination of stray ones. treatment of pet animals and 3-Avoid contamination of food, drink & elimination of stray dogs & hands by excreta of dogs & cats and soil. cats.

Other causes of cutaneous larva migrans: 1-Human and non-human strains of Strongyloides (larva currens; fast moving). 2-Cutaneous myiasis caused by larvae of flies as Gastrophilus and Hypoderma. N.B. In case of heavy infection by VLC, some larvae of Ascaris, Ancylostoma & Strongyloides, during their cycle, pass from the lungs to the left side of the heart to the systemic circulation and settle in different organs producing visceral larva migrans.

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2010/2011

Medical Parasitology in tables Name Parasite (Disease) Geographical Distribution Definitive Host & Habitat Reservoir host Diagnostic Stage Intermediate host Infective Stage & Mode Of Infection

Kasr Alainy Students

Dracunculus medinensis Wuchereria bancrofti (Dracunculiasis, Dracontiasis) (Bancroftian filariasis, Elephantiasis) In areas where people depend on wells for water In tropical and subtropical areas in Africa, Asia & South America. It is found in Egypt in Kalyobia, supply. Most cases are in Africa (Sudan, Mali & Ghana) Dakahlia, Sharkia, Cairo, Giza and Assiut. Man, in tissues (extra-intestinal). Dog, horse, cattle Larval stage: Size: 60020 um Shape: comma shaped with rounded anterior end, long tapering tail and a rhabditiform esophagus. Cyclops Infective larvae, through drinking water containing the infected cyclop. Adults copulation male die female migrate to subcutaneous tissue especially that become contacted with water during contact with water uterus prolapses discharges larvae until they finished ingestion by cyclops body cavity moult twice infective larvae ingestion of cyclop by D.H. or R.H. larvae migrate through the wall of S.I. retro-peritoneal tissues maturation Man only, in lymph vessels and glands. ---------------Mainly microfilariae (but adults may be seen too): Sheath: loose Size: 250 8 um Curves: smooth Tail nuclei: free Periodicity: nocturnal in blood Mosquito (Culex, Aedes, Anopheles). Infective filiform larvae, when mosquito bites the man.

Life Cycle

Adults in lymph vessels & glands of man (D.H.) microfilariae blood appear in peripheral blood by night (nocturnal periodicity) mosquito during biting and sucking (I.H.) cyclodevelopmental transmission (just developing) infective filiform larvae go to man again during biting it can enter by penetration or through bite wound or any abrasion pass to lymph nodes and vessels maturation adults
1- Many infections are a symptomatic, & occur only in blood examination. 2- Main pathological features caused mainly by adult worms. 3- The disease pass in 2 phases: a. Acute inflammatory phase: due to immunological reaction to toxic products of worms. 2ry infection by streptococci may be added. o Symptoms appear about one year after the infective bite. o Recurrent attacks of lymphangitis: affected vessels appear as raised, red hot, swollen & tender. Commonly in limbs especially in legs & genitalia (epididymo-orchitis & funiculitis). o Attacks of lymphadenitis: enlarged & tender regional lymph nodes. 2ry infectionabscess o Filarial or elephantoid fever: sudden onset with rigors & sweating lasts for few hours to several days & often recurs. o Bacterial & fungal super-infection. b. Chronic phase: o Hydrocele (most common): results from accumulation of straw colored fluid in sacs around testicles. o Obstruction of lymphatics: occurs slowly & usually follows years of repeated attacks of lymphangitis & fibrosis of lymph nodes & vessels by coiled worms inside lymphatics. o Distension & varicosities of lymphatics distal to obstruction o Persistent lymphatic edema. o Rupture of distended lymphatics: in pleural sac (chylo-thorax), peritoneal cavity (chylous ascitis), tunica vaginalis of testis (chylo-cele), intestine (chylous diarrhea) or in urinary tract (chyluria) with passage of microfilaria in urine. o Elephantiasis: permeability of the walls of obstructed lymphatics leakage of lymph with high concentration of protein under the skin proliferation of connective tissue & deposition of fibrous tissue. The skin & underlying tissues becomes hard, dense & non-pitting (hard edema). The skin appears thickened, rough & fissured susceptible to 2ry infection. There may be huge enlargement of the affected parts usually dependent one e.g. legs, scrotum, vulva, breast, & arms. Elephantiasis occurs after persistent high infection for 5 10 years. 1- Clinical signs and symptoms: above. 2- Laboratory investigations: a. Recovery of microfilariae in blood at night. They are highest in capillary blood (ear lobe & fingers) o Examination of a drop of fresh blood shows movement of microfilariae. o Di-ethyl-carbamazine (DEC) provocative test: giving 100 ml & taking blood 45 minutes later. Thus, microfilariae can be demonstrated at any time of the day. o Concentration of microfilariae if they are scanty by Knotts technique: the sediment is examined for microfilariae. b. Detection of microfilariae in chylous urine from hydrocele: ether dissolves chyle. c. Detection of adults in lymph node biopsy. d. Immuno-diagnosis (serology): o Detection of circulating antigen: is of great value. o Detection of antibodies is of lower value because of cross reactivity (+ve in endemic areas). e. Molecular techniques: PCR f. High eosinophilia. 3- Imaging techniques: a. Ultrasonography to visualize adults in lymphatics. Viable adults may be seen moving actively. b. Lymphoscintography will reveal lymphatic abnormalities especially dilatation of vessels.

1.Migration of female under the skin causes allergic reaction due to release of metabolic products urticarial rash, nausea, vomiting, diarrhea or asthmatic attack. 2.The skin opposite the anterior end shows red papule then blister which ulcerates. The worm lies in a Pathogenesis & subcutaneous tunnel & its course may be marked Clinical Picture with induration and oedema. 3.2ry infection of the ulcer leads to abscess, cellulitis and even septicemia. 4.Severe allergic reactions occur if the worm is broken during forced extraction & the larvae escape into the subcutaneous tissue.

Diagnosis

Clinically: The outline of the worm under the skin may be seen. Skin lesions: papule, blister & ulcer. Laboratory: Larvae are obtained by placing the affected part in cold water for few minutes. X-ray shows calcified females. Intradermal test & C.F.T. (Complement Fixation Test). Eosinophilia.

Treatment

Prevention & Control

1.Removal of the worm: o The ancient method: rolling the worm on a stick & pulling gradually each day until resistance is felt to avoid rupture of the worm. o Surgical removal. 2.Drugs: anti-inflammatory drugs that help in expelling worms spontaneously or manually. o Thiabendazole (Mintezol) OR o Diethylcarbamazine (DEC, Hetrazan) OR o Metronidazole (Flagyl). 3.Symptomatic treatment: antiseptic dressing, antibiotics, antihistaminics and corticosteroids. 1.Eradication of cyclops in wells by regular steaming or by chemicals as chlorine, copper sulphate & calcium oxide or breeding of fish that feed on them. 2.Boiling or filtering of wells water 3.Use of pumps.

1- Di-ethyl-carbamazine (DEC): the drug of choice. It kills adults and modifies microfilariae in a way that they are effectively removed by the host. The dose is given orally and repeated once every 6 months as long as the person remains microfilaraemic or has symptoms. It does not reverse the pathology already established but limits its progression. Antihistaminics & corticosteroids are given to alleviate allergic reactions induced by the rapid destruction of the parasite 2- Ivermectin: effectively removes microfilariae from the blood, but does not affect adults. Thus, microfilariae reappear in the circulation. Treatment should be repeated half yearly or yearly. 3- Combine of DEC & Ivermectin: gives better results. 4- Symptomatic treatment: foot care, antibiotic and antifungal therapy to prevent and cure adenolymphangitis. Physiotherapy and banding to reduce and alleviate lymphoedema. 5- Surgical management: chronic hydrocele and elephantoid skin may be corrected surgically and should be preceded by a course of DEC. 1- Control of mosquito vector. 2- Mass treatment of patients to destroy microfilariae.
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N.B. See occult filariasis in page 13

2010/2011

Medical Parasitology in tables Name Brugia malayi Parasite (Disease) (Malayan filariasis) Geographical Far east. Distribution Definitive Host & Lymph nodes & vessels of Habitat man. Monkeys and cats (for certain Reservoir host strains) Sheath Loose Size 250 8 um Curves Kinky Tail nuclei 2 nuclei Periodicity Nocturnal in blood Mosquito (Mansonia mainly, Vector (I.H.) Aedes & Anopheles) Infective Stage & Infective filiform larvae, when Mode Of Infection infected mosquito bites man. Microfilaria Loa loa : Eye African worm (Loaiasis or Loiasis) West and central part of tropical Africa. Subcutaneous tissue of man. ----------Tight 250 8 um Kinky Full Diurnal in blood Chrysops fly. Microfilariae when the fly bites the man. Adults subcutaneous tissue of man microfilariae appear in blood in day time (diurnal periodicity) chrysops fly during biting cyclodevelopmental transmission man through biting again subcutaneous tissue mature Onchocerca volvulus (Onchocercosis or Onchocerciasis) Central Africa, Central & South America, Yemen & Saudi Arabia. Subcutaneous tissue on bony parts (in the form of nodules) of man. ----------Unsheathed 300 10 um Smooth Free Non-periodic in skin & subcutaneous tissue Simulium (also called black or buffalo fly). It is a daytime biting fly. Microfilariae stage, when the man is bitten by the Simulium. Adults subcutaneous nodules microfilariae shedding Simulium fly during biting cyclodevelopmental transmission man through biting again subcutaneous tissue maturation Adult

Kasr Alainy Students Mansonella Mansonella perstans ozzardi Central Africa, South South America. America. Serous cavities & retroperitoneal tissue. ---------------------

Unsheathed Unsheathed 100 5 um 200 5 um Smooth Smooth Full Free Non-periodic in blood Cullicoides ---------------------

Life Cycle

As Bancroftian filariasis

-----------

-----------

Pathogenesis & Clinical Picture

Diagnosis

Treatment

Prevention & Control

1- Onchocerca nodule: usually found over bony prominence as scalp, elbow, knee, ribs, iliac crests & scapula. They are firm, painless, rounded or oval, movable & vary in size from few mm in diameter to several cm. They do not cause medical problems unless they 1- Calabar swelling: most commonly press on a vital organ. observed on hands, wrists and 2- Eye lesions (River or Sudan Blindness): forearms, but may appear o Cause: due to toxic or allergic reactions to anywhere in the body. They are living & dead microfilariae migrating from painless and non-pitting. They last 1- Milder disease than nodules especially in the scalp. from few hours to several days and Bancroftian filariasis. o Manifestations: keratitis, iridocyclitis, may recur for years. They are due 2- Elephantiasis affects legs retinitis & optic neuritis. Subsequent fibrosis to hosts immune response to the below knees and arms leads to complete blindness. parasitic antigens. below elbows. o Early symptoms: photophobia, lacrimation, Usually non-pathogenic 2- Generalized pruritus, fatigue and 3- Genital involvement is rare. blepharospasm & foreign body sensation. arthralgia are common. 4- Chyluria is rare. 3- Skin lesions: 3- Adult worms may be seen under 5- Allergic manifestations are o Severe dermatitis & edema at first then the conjunctiva or skin & disappear common. granuloma & fibrosis with severe itching. in about 15 minutes leaving no o Later on, loss of elasticity, atrophy & trace. wrinkling of skin giving premature senility 4- Serious complications: occur when appearance. microfilariae invade CNS, kidneys, o In the groin it leads to hernia and hanging heart. groin, which is composed of pendulous folds of skin that may contain enlarged lymph nodes. o De-pigmentation producing leopard skin or hyper-pigmentation (in Yemen; Sowda) with popular itchy eruptions Clinical manifestations: above. Laboratory investigations: Clinical: Demonstration of microfilariae in aspirate or Worms seen under conjunctiva & bloodless skin snips. history of Calabar swellings. Biopsy of nodules reveals adults. Laboratory: Serological tests: to detect antibodies. Blood film at any time for As Bancroftian filariasis o Detection of microfilariae in blood Molecular techniques: PCR. microfilariae. in day time (10 am 2 pm). Mazzotti test: oral dose of DEC provokes o Serology. intense pruritis within few hours due to death o PCR. of microfilariae. Local application of it on skin o Eosinophilia. is safer (called patch teat). Corticosteroids are given in severe reactions. 1- Chemotherapy as in Bancroftian 1- Surgical removal of the nodules. Unnecessary in asymptomatic filariasis. As Bancroftian filariasis 2- Ivermectin (mectizan). cases. 2- Surgical removal of adult if seen 3- DEC (Hetrazan). Ivermectin. under the conjunctiva. 1- Treatment of patients. 1- Treatment of patients. 2- Control of chrysops is difficult As Bancroftian filariasis 2- Control of Simulium fly is difficult, larvae & --------------------because it breeds in swampy areas pupae attach to submerging rocks in rivers. of forests.

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2010/2011

Medical Parasitology in tables Occult filariasis; Tropical Pulmonary Eosinophilia (TPE) It is a filarial infection where the microfilariae are not found in blood but found with adult forms in tissues. Cause Immunologic hyper-responsiveness to microfilariae in the lung. In the circulation: 1. Absence of microfilariae from the circulation. 2. High eosinophilia (> 3000/ul). 3. Elevated titre of anti-filarial antibodies and IgE level. In the tissue: Characters 1. Presence of microfilariae surrounded by aggregates of eosinophils in the lungs. In X-ray there is diffuse miliary lesions in the lungs. 2. Extrapulmonary lesions may occur as splenomegaly, lymphadenopathy and hepatomegaly. Presence of microfilariae surrounded by aggregates of eosinophils are seen too. Paroxysmal cough, breathlessness & wheezing that is worse at Clinical night. There is impairment of lung function that may become Picture irreversible in the chronic stage. DEC: leads to rapid suppression of the symptoms and reduction of Treatment number of eosinophils. Definition Classification of Protozoa This classification is for reading only. Phylum Subphylum Class

Kasr Alainy Students

Members

Sarcodina

Lobosea (Amoeba)

Sacro-mastigophora

Mastigophora

Zoomastigophora (Flagellates)

Entamoeba histolytica Commensal amoebae Potentially pathogenic amoebae Neglaria fowleri Acanthamoeba: o Granulomatous Amoebic Encephalitis o Acanthamoeba keratitis Giardia lamblia Trichomonas vaginalis Leishmania o Cutaneous o Visceral Trypanosoma: o African o American

Ciliophora

---------

Kinetofragmino Balantidium coli phora (Ciliates) Cryptosporidium parvum Cyclospora cayetanensis Isospora belli Plasmodium Babesia Toxoplasma Microsporae

-----------------------------------------------------------------------------------------------Class: Protozoa
General characters: 1- The protozoon: consists of: a. Protoplasm: consists of Outer ectoplasm &Inner endoplasm: b. Nucleus 2- Nutrition: through the ectoplasm by: a. Pseudopodia (amoebae). b. Cilia and flagella (Ciliates & Flagellates; Mastigotes). 3- Locomotion: by pseudopodia (amoebae), cilia (Ciliates) and flagella (Flagellates). 4- Excretion: by diffusion through body surface or by contractile vacuoles. 5- Secretions: include digestive enzymes, toxins, antigenic substances & cyst walls to resist unfavorable conditions. 6- Reproduction: a. Sexual: by i. Syngamy: Union of male & female gametes to form the zygote. ii. Conjugation: Exchange of nuclear materials between 2 organisms. b. Asexual: by i. Binay fission: nuclear division followed by cytoplasmic division (mostly all protozoa). ii. Endodyogeny: 2 daughter cells enclose in the cell membrane of the mother cell. iii. Schizogony:the nucleus divides into several nuclei followed by division of cytoplasm forming several segments (daughter cells) and give rise to a schizont. iv. Budding: the parent cell does not divide, but puts out a small budlike process (daughter cell) with its proportionate amount of chromatin; the daughter cell then separates to begin independent existence. Apicomplexa --------Sporozoa

Microspore

---------

Microspore

Classification of Protozoa According to Habitat This classification is for understanding & studying. Giardia lamblia Cryptosporidium Small Isospora intestine Cyclospora Intestinal Luminal Microsporidia (affecting small intestine) Large Entamoeba histolytica intestine Balantidium coli Urogenital Trichomonus vaginalis Visceral Leishmania (L. donovani complex) African trypanosomes: o T. gambiense Haemo-flagellates o T. rhodeseinse American trypanosomes: o T. cruzi Blood protozoa Plasmodium: o P. vivax Intra-erythrocytic o P. ovale sporozoa o P. malariae o P. falciparum Babesia Cutaneous leishmania o Old world (OWCL): L. tropica L. major L. aethiopica o New world (NWCL): L. peruviana L. braziliensis L. Mexicana L. pifanoi Toxoplasma gondii Free living amoeba (FLA): o Naegleria fowleri o Acanthamoeba species: Granulomatous Amoebic Encephalitis (GAE) Acanthamoeba keratitis Microsporidia

Tissue protozoa

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2010/2011

Medical Parasitology in tables Parasite (Disease) Entamoeba histolytica (Amoebiasis) Geographical Cosmopolitan (more in areas of overcrowding and bad sanitations) Distribution Definitive Host & Man in the wall and lumen of colon especially caecum and sigmoido-rectal region Habitat Reservoir Host -----------------------Diagnostic Stage Cyst or Trophozoite stage Quadrinucleate (mature) cyst, through: Auto-infection Hetero-infection: Infective Stage & o Eating raw vegetables fertilized with human faeces. Mode Of Infection o Open source of water contaminated with human excreta. o Flies & cockroaches carrying cysts to food or drink. o Food handlers, especially chronic asymptomatic cyst carriers. Quadrinucleate cyst ingestion pass stomach acidity small intestine lower ileum excystation 8 small amoebae multiply by binary fission EITHER: remain in the lumen feed on starch & mucus OR invade the wall by their lytic enzymes flask-shaped ulcers. (In chronic cases, they produce cysts and pass with faeces). There are 2 forms of E. histolytica. They are similar in morphology & can inter-change in certain condition.: 1-Pathogenic or tissue form. 2-Non-pathogenic or lumen form. The pathogenic activity of E. histolytica depends on: 1-Virulence of organisms. 2-Resistance of the host. 3-Condition of the intestinal tract. The amoebae secretes histolytic enzymes produce necrosis of the intestinal mucosa with rapid lateral & downward extension of ulceration flask-shaped ulcer (wide base & narrow opening). This is followed by: 1. Proliferation of connective tissue, which lead to fibrous thickening of intestinal wall 2. Intensive ulceration may accompanied by 2ry bacterial infection. 3. Extra-intestinal invasion: mainly to liver. Asymptomatic Infections: Extra-intestinal Amoebiasis: The most common type. The parasite is Hepatic Amoebiasis: found in the lumen with no invasion of Amoebic hepatitis: enlarged tender liver with pain mucosa and pass with stool (cyst passer). in the right hypochondrium. Symptomatic Infections: amoebic liver abscess: enlarged tender liver and Intestinal Amoebiasis: leukocytosis. Taping of abscess reveals thick, Acute stage: anchovy-sauce or chocolate-colored pus The onset is gradual with dysentery, containing trophozoites. abdominal pain & tenderness. Pulmonary Amoebiasis: Tenesmus, painful spasms of anal sphincter Fever, leukocytosis & evidence of consolidation. is a sign of ulcerations. Trophozoites may appear in the sputum in case of Stool contains blood, mucus, shreds of bronchial erosion. necrotic tissue & trophozoites. Complications: Chronic stage: 1. Amoeboma: granuloma around the ulcer. It may Recurrent attacks of dysentery with be confused with malignant tumors. intervening GIT disturbances & 2. Haemorrhage: due to erosion of a blood vessel in constipation. the intestinal wall. Localized tenderness. 3. Perforation of an amoebic ulcer peritoneal In long standing infections, there is loss of infection (peritonitis). weight & cachexia. 4. Stricture: due to healing by fibrosis. 5. Appendicitis. Intestinal Amoebiasis: Sigmoidoscopy (invasive): Clinical:See above (N.B. it should be To visualize lesions or take a biopsy. differentiated from bacillary dysentery). Indirect diagnosis: Laboratory: Radiological (barium enema). Direct stool examination: Serological. Bulky, offensive, acidic, scanty exudate: Detection of copro-antigen in stool. reveals blood, epithelial cells, Charcot Leyden Molecular techniques. crystals & amoebae are present. Extra-intestinal Amoebiasis: Examination for the trophozoites: Clinical: - Wet preparation using saline, reveals According to the organ affected. highly refractile shining bodies with Laboratory: progressive directional crawl and ingested Aspirate examination from lung or liver abscess red blood cells. for trophozoites if accessible. - Stained smears will reveal the morphology Liver scanning. - Permanent preparation using iron Radiology for diaphragm level and pulmonary heamatoxylin or trichrome stain. lesions. Examination for the cysts: Serology. - Smear stained with iodine or trichrome. Leukocytosis can be found due to 2ry bacterial - Concentration techniques. infection. Intestinal Amoebiasis: Extraintestinal Amoebiasis: Metronidazole (Flagyl) followed by Metronidazole OR Tinidazole followed by Diloxanide fluroate for 10 days each. OR Diloxanide fluroate. Tinidazole (Fasigyn) for 2 3 days followed Aspiration of abscesses or open surgical drainage by Diloxanide fluroate for 10 days. may be needed. 1- Treatment of patients. 2- Food handlers should be examined and treated. 3- Environmental sanitation. 4-Human faeces should not be used as fertilizers. 5-Personal prophylaxis.
~ XIV ~

Kasr Alainy Students Balantidium coli (Balantidiasis) Cosmopolitan, widely distributed In pig raising areas. Lumen, mucosa and sub-mucosa of large intestine of man, especially the caecum. Pigs Cyst or Trophozoite stage Cyst stage, through: Auto-infection. Ingestion of cysts with food or water contaminated by pigs or human excreta. Cyst ingestion small intestine excystation single parasite multiplication EITHER remain in the lumen with no symptoms OR invade the intestinal wall produce flask-shaped ulcers after period encystment cysts in stool.

Life Cycle

Pathogenesis

Clinical Picture

1-Invasion of the mucosa is affected by: a. Cytolytic enzyme hyaluronidase. b. Boring action of cilia. 2-Secondary bacterial infection may follow the invasion. This leads to formation of flask-shaped ulcers as in acute amoebic infection with signs and symptoms of dysentery. 3-Extra-intestinal spread is rare. 4-Complications: a. Hemorrhage. b. Perforation. c. Peritonitis. d. Appendicitis.

Diagnosis

Clinically: Clinical manifestations of dysentery. Laboratory: Finding trophozoites in diarrhoeic stool and cysts in formed stool. Stool should be examined several times since discharge of the parasite is intermittent.

Treatment

Metronidazole (Flagyl) OR Oxytetracycline The same as in amoebic infections, plus: Care of pigs excreta is of great importance where they are raised. 2010/2011

Prevention & Control

Medical Parasitology in tables Parasite (Disease) Geographical Distribution Giardia lamblia (Giardiasis) Cryptosporidium parvum (Cryptosporidiasis) Worldwide Small intestine of man, intracellular within the brush border Oocyst stage Cyclospora cayetanensis (Cyclosporiasis) Worldwide Isospora belli (Isosporiasis) Worldwide

Kasr Alainy Students Trichomonas vaginalis (Trichomoniasis) Cosmopolitan

Cosmopolitan, more in warm climates The duodenal mucosa, upper part Definitive Host of small intestine, bile duct & gall & Habitat bladder of man, especially children Diagnostic Stage Cyst or Trophozoite stage

Enterocyte (intracellular) of upper part of small intestine of man Unsporulated oocyst stage Mature sporulated oocyst, Cyst stage, through: Sporulated oocyst, through: through ingestion of: Auto-infection Auto-infection: Infective Stage Contaminated vegetables & o Thin-walled endogenous Hetero-infection: & Mode Of fruit. Contaminated food (vegetables) o Thick-walled exogenous Infection Contaminated chlorinated by Musca fly or food handlers. Ingestion of contaminated food & filtered water arising Contaminated water. or drink from water-storage tanks. Merogony: asexual reproduction Not completely known meronts (contains merozoites) Asexual & sexual cycles are initiate new cycles adjacent cells believed to occur Cyst duodenal lumen Gametogony: sexual reproduction Unsporulated, immature, excystation multiply by gamonts contains micro non-infective oocysts are Life Cycle longitudinal binary fission attach &macrogametes fertilization shed in patients faeces. to the mucosa some encyst & zygotes thin- & thick Sporulation occurs outside pass in stool walledoocysts infection (thin the host (5 days) mature, walled can cause endogenous sporulated & infective infection) oocyst (No autoinfection).

Intracellular of Man (vagina , urethra , epithelial cells of small prostate) intestine of man Oocyst stage Trophozoite only Sporulated oocyst, through: Auto-infection. Ingestion of contaminated food or drink. Oocyst small intestine sporozoites penetrate epithelial cells immature sporulated oocyst sporulation (may occur in the lumen or outside the host) 1. Inflammatory changes: villous atrophy and crypt hyperplasia of affected area. 2. In immunocompetent subject: Often asymptomatic. Self-limited diarrhea may develop Chronic diarrhea with abdominal cramps are seen in some cases 3. In immunocompromised subject (opportunistic infection): Severe diarrhea with malabsorption and dehydration can develop and be life threatening.

Trophozoite stage, through sexual intercourse, directly from an infected partner.

------------------

Pathogenesis and Clinical Picture

1- Inflammatory changes: villous 1-Asymptomatic if the parasite just atrophy and crypt hyperplasia. feed on mucus. 2- In immuno-competent subject: 2-Symptomatic cases: Hyperaemia Mild self-limited diarrhea & duodenatis, manifested by lasting for 2 weeks. Epigastric pain In some cases, especially in Disturbances of digestion children, the condition is Diarrhea & flatulence accompanied by abdominal 3-Severe symptoms: as: discomfort, anorexia, fever, Persistent diarrhea, steatorrhea, nausea & loss of weight. hypoproteinaemia & fat-soluble 3- In immuno-compromised vitamin deficiencies. subject: Mal-absorption due to villus The disease is severe, especially atrophy. in AIDS patients & could be life Cholangitis & cholecystitis may threatening (opportunistic lead to jaundice & colic pain infection). Occur in patients with impaired Severe diarrhea, malabsorption immunity such as: dehydration. Hypo--globulinaemia Dissemination of the parasite to Diminished secretory IgA in SI other organs can develop, as Dimished gastric acidity or esophagus, gall bladder, urinary achlorohydria bladder, & respiratory tract.

1- Inflammatory changes: villous atrophy and crypt hyperplasia of affected area. 2- In immuno-competent subject: Watery-diarrhea that tends to occur in a relapsing or cyclical pattern. Accompanied by nausea, vomiting, flatulence & abdominal cramps. May cause anorexia, loss of weight, fatigue & lowgrade fever. 3- In immuno-compromised subject: In AIDS patients, the illness is severe, prolonged & tend to recur. Biliary affection may develop.

Diagnosis

Treatment

Prevention & Control

Clinically: suggestively Laboratory: Direct stool analysis: reveals Trophozoite in diarrheic stool Clinically: as above. Laboratory: Cyst &trophozoite in formed Stool analysis: Clinically: as above. stool. Simple smear & concentration Laboratory: Concentration technique gives methods (Sheathters sugar Stool analysis: the specimen higher positivity. floatation) are used. Oocyst can can be examined fresh If the result is ve the test be detected by: unstained or stained with should be repeated again after Staining by acid-fast stain (MZN acid-fast stain (MZN stain). some days because the stain). Jejunal biopsy: to detect excretion of the parasite is Immunofluorescence assay. asexual stages. irregular. Intestinal biopsy: String test (Enterotest) To detect meronts and gamonts. Indirect through: Serological tests (of little value) Detection of copro-antigen. In immuno-competent patients: Metronidazole (Flagyl) OR self-limited Tinidazole (Fasigyn) Trimethoprim combined In immuno-compromised patient: with Sulphamethoxazole Albendazole, recently Nitazoxanide Nitazoxanide Fluid & electrolyte replacement 1. Measures against faeco-oral transmission Infection can be prevented 2. Proper filtration of drinking by proper washing of As Amoebiasis water vegetables and fruits and 3. Boiling of drinking water to boiling of water. immuno-compromised patients.
~ XV ~

In women: Trophozoites found in vagina & urethra feed on the mucosal surface sloughing of sq. epith. cells 50% are asymptomatic. The rest suffer from profuse odorous discharge associated with burning, itching, dyspareunia, frequency of urination & dysuria On examination: diffuse vulval erythema , excessive discharge & vaginal wall inflammation In Men: Frequently asymptomatic When infection involves prostate or higher urogenital tract, symptoms may appear as: thin discharge, dysuria & nocturia enlarged prostate & epididymitis. 1. Microscopic examination of wet films prepared from discharge or urine. 2. Culture of discharge on suitable media (as Clinically: as above. Modified Diamond's Laboratory: medium) when Stool analysis: microscopy fails. The oocyst can be seen 3. Detection of antigens by in fresh unstained or immunological tests as: stained with acid-fast Enzyme immunoassay stain (MZN stain). Direct fluorescent antibody test using labeled monoclonal antibodies 4. Molecular techniques as DNA probe. Trimethoprim combined with Metronidazole (Flagyl Sulphamethoxazole Treatment of the sexual Fluid & electrolyte partner replacement 1. Treatment of patients & their partners. Measures against 2. Diagnose &ttt of faeco-oral asymptomatic carriers. transmission 3. Use of condoms is very effective. 2010/2011

Medical Parasitology in tables

Visceral Leishmania (Kala-azar, Dum-dum fever, black fever) Parasite (Disease) Old world Leishmaniasis: L. donovani & L. infantum New world Leishmaniasis: L. chagasi & L. amazonensis African (Sleeping Sickness) T. brucei gambiense West Africa & western part of tropical Africa T. brucei rhodesiense Trypanosoma

Kasr Alainy Students

American (Chagas disease) T. cruzi

Geographical Distribution DH & Habitat Reservoir Host Diagnostic Stage

Man, less in blood abundant in blood Goats, cattle & pigs Wild game animals Multi form trypanosomes Jungle Tsetse fly as: Tsetse fly: Glossina palpalis Vector Sand fly: Phlebotomus Sand fly: Lutzomyia Glossina morsitans Infective Stage & Promastigote stage, through bite of sand fly & inoculation of Short stumpy metacyclic trypanosomes, through bite of Mode Of Infection promastigotes. tsetse fly Development Multi form trypanosomes taken by tsetse fly by bite Amastigote taken by female sand fly by bite change into inside Vector change into amastigote midgut longitudinal binary promastigote multiply by longitudinal binary fission (Mechanism of fission migrate back to the salivary gland multiply migrate back to the buccal cavity infect another host Disease epimastigote short stumpy metacyclic trypanosome during biting (Biological transmission) Transmission) infect another host during biting (Biological transmission) Chronic course ( 3 years) with these stages: 1. Incubation period ( 14 days). 2. Trypanosomal chancer: local 1. Promastigotes that engulfed by skin macrophage inflammatory nodule at the site transforms to amastigotes and start multiplication. of bite (lasts 1-2 weeks). 2. A local papule (leishmanioma) are rarely seen but 3. Parasitaemia: trypanosomes described in children. pass to the blood & multiply 3. The parasites are present in few numbers in blood & are irregular fever, headache, joint taken by reticulo-endothelial system cells & other organs & muscle pain and rash. that show hyperplasia. 4. Invasion of lymph nodes: 4. The onset is usually gradual with initial fever (intermittent especially posterior cervical with double daily rise). region (Winterbottom's sign) 5. Diarrhea & dysentery are common. generalized weakness, 6. Splenomegaly, hepatomegaly & lymphadenopathy are hepatomegaly, splenomegaly, seen. irregular erythematous rash & 7. Invasion of bone marrow results in aplastic anemia, anaemia. The trypanosomes are Pathogenesis and leukopenia & thrombocytopenia. There is reversal of Clinical Picture present in lymph nodes, blood & albumin/globulin ratio due to elevation of gammabone marrow. globulins. 5. Invasion of the CNS: gradually 8. Skin changes may occur in the form of: dark pigmented with perivascular cellular erythematous areas or depigmented macules distributed infiltration ischemic softening over the body. A butterfly distribution over the nose is of tissues & petechial common. haemorrhages diffuse 9. Post-kala-azar dermal leishmaniod in the form of meningioencephalitis & depigmented skin nodules may develop due to meningiomyelitis. There is spontaneous arrest of the disease or incomplete treatment mental apathy & retardation, with antimony compounds. slow speech, tremors, 10. Weight loss and emaciation (abnormally thin & weak), involuntary movements & which render the patient to secondary infections. This convulsion. Lastly, the sleeping may lead to death. stage develops & the patient falls into coma. Death occurs either from the disease or from inter-current infection.

L. donovani: Southeast Asia & central Africa. Central & south America. L. infantum: Mediterranean area, Europe & Africa. Man in Reticulo-Endothelial System -------------------Amastigote in biopsy and promastigote in culture.

East & central part of Central and south America tropical Africa Man, domestic & wild animals ----------C-shaped trypanosomes Winged bug: Triatoma & Rhodnius As African but through contamination of the site of bite or mucous membranes with faeces As African but: Pass to the hindgut. Dont go to the salivary gland Infective stage pass with faeces

The acute form: 1. Organisms proliferate at the site of infection and produce erythematous indurated area called Chagoma, which occur frequently in the face. 2. Organisms spread rapidly to the regional lymph nodes blood organs and More rapid & fatal tissues. They usually appear in phagocytes course even before of liver (Kuppfer cells), spleen & cardiac the appearance of muscle. neurological 3. Sudden unilateral edema of the eye lids manifestations. without conjunctivitis (Romanas sign). The incubation 4. Signs and symptoms of generalized period is short. infection: high fever, muscle pain & Bouts of fever & exhaustion. Epistaxis is more common in rigors are more young children. frequent & severe. 5. Generalized glandular edema, It appears in blood hepatosplenomegaly and rarely skin rash. early in infection & 6. In severe infections, there are signs of in abundant meningioencephalitis & cardiac involvement numbers. and heart failure. Myocarditis & 7. Complications include: death, chronicity or emaciation are recovery. prominent. The chronic form: CNS is involved More common in adults & manifestations early. depend on the site invaded. Untreated patient 1. In the heart: ECG changes with signs & die within one year symptoms of heart failure. after infection. 2. Dilatation of parts of the GIT: as megaoesophagus & mega-colon manifested by dysphagia & constipation. 3. Invasion of CNS or thyroid gland is commonly less. 4. Immunosuppression results in exacerbation of the infection. 1. Demonstration of the parasite in the blood by: a. Direct thick smear b. Special concentration techniques. c. Culture on suitable medium. d. Xenodiagnosis: feeding laboratory-bred winged bug on the patients blood then examining the gut of the bug for trypanosomes. 2. Serodiagnosis 3. Biopsy of enlarged lymph nodes may reveal amastigotes. 4. Cruzin test: intradermal test, gives delayed reaction +ve cases. 5. Molecular techniques as PCR 1.Nifurtimox: it inhibits intra-cellular growth 2.Primaquine: destroy trypanosomes in blood

Diagnosis

Treatment

Prevention & Control

Clinically: as above. 1. Clinically: as above especially fever with double daily rise, Demonstration of trypanosomes leukopenia & splenomegaly. in aspirate from chancre, lymph 2. Detection of the parasite in the blood or material from nodes, blood, CSF by : As T.brucei the spleen, liver, bone marrow or lymph nodes: o Microscopic examination of gambiense but: specimens are examined by 3 methods: fresh unstained or stained films More frequently a. Microscopy: blood examined by thick drop preparation o Culture on suitable medium. appear in blood. or by buffy coat method. Smears are stained with o Animal inoculation fails unless More readily Giemsa stain. the animal is irradiated to demonstrated with b. Culture of specimens on suitable medium. decrease its immunity. animal inoculation c. Intra-peritoneal inoculation of material in hamsters. with appearance of Detecting an increase in total 3. Immunodiagnosis: serum IgM level: always elevated posterior nuclear a. Montenegro (leishmanin) test: gives delayed reaction (after shift. due to antigenic variation of the 3 days). Usually negative in active infection & becomes surface coat of the organisms. positive after successful treatment. Serological tests: not available b. Serological tests. commercially. 1. Antimony sodium gluconate (Pentostam) 1. In the early stages: Pentamidine Suramin 2. Pentamidine 2. In the late stages: Trypasamide 3. Allopurinol (for AIDS patients) 3. For both stages: Eflornithine (Ornidyl) 1. Treatment of the patients. 1. Treatment of patients. 2. Control of vector. 2. Control of vectors. 3. Protection by using wire screens, mosquito or repellents. 3. Chemoprophylaxis: one dose of Pntamidine every 5 6 4. Vaccination in endemic areas using suspension of living months. promastigotes resulting in lasting immunity.

1. Detection and treatment of cases. 2. Control of vector.

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2010/2011

Medical Parasitology in tables Plasmodium (Malaria) Parasite (Disease) Geographical Distribution Diagnostic Stage Vector Infective Stage & Mode Of Infection P. vivax (Vivax or Benign tertian malaria) World-wide P. ovale (Ovale or Oval tertian malaria) Tropical area P. malariae (Malariae or Quartan malaria)

Kasr Alainy Students P. falciparum (Falciparum, Babesia Species (Babesiosis) Subtertian or Malignant malaria) Europe, North & South America Merozoites Hard ticks Sporozoites, through bite of hard tick inoculating them Sexual multiplication in hard tick sporozoites salivary glands bite RBCs (directly) asexual multiplication by budding merozoites release other cells

Subtropics & temperate Tropical area zones Ring, trophozoite, schizont, gametocyte stages in infected RBCs, but with P. falciparum ring & gametocyte stages only. Female Anopheles Mosquito Sporozoite stage, through bite of female Anopheles mosquito & inoculation of sporozoites. Merozoite stage, through blood transfusion. In man: N.B. Some P. ovale & vivax enter asexual multiplication exo-erythrocytic. Infected Mosquito Sporozoites 40 minutes in blood Hepatocyte Hypnozoites (resting stage) Trophozoites Schizonts rupture Liver Merozoites Blood RBCs Ring stage Ring stage Tropozoites Schizonts (reythrocytic) rupture 6 36 Blood Merozoites Some Merozoites form Gametocytes Mosquito during biting Life Cycle (man become infective to mosquito) In Mosquito Vector: Gametocytes (exflagellation microgamete & macrogamate fusion (sexual)) Zygote Ookinete Oocyst Sporocyst Salivary glands Sporozoites man during biting (mosquito become infective to man) 1. Infection starts with incubation period (liver phase) Complications: followed by prodromal symptoms which are influenza like. 1. P. vivax, ovale & malariae malaria are relatively benign. 2. Then malarial paroxysms, which coincides with: 2. Chronic P. malariae infection results in immunoa. Rupture of RBCs (due to osmotic fragility). complex deposition on the glomerular walls nephrotic b. Liberation of metabolites of the parasites. syndrome. c. Immunologic response to the parasitic antigens. 3. P. falciparum is usually severe & fatal (thus called 3. Malarial paroxysms (clinical attacks), include 3 stages: Pernicious): a. Cold stage: the patient complains of sudden chill, extreme a. In this infection, the parasitized RBCs develop knobs cold & his temperature is elevated (lasts 10 15 on their surface. So they adhere together & to specific minutes). receptors on the endothelial cells of the capillaries of b. Hot stage: headache, high fever & hot dry flushed skin internal organs partial occlusion anoxia & (lasts 2 6 hours). necrosis which may be fatal. The clinical picture differs c. Sweating stage: profuse sweating, temperature falls & the according to the site of occlusion: patient is weak & exhausted (may last for several hours). Cerebral malaria: severe headache, drowsiness, 4. Malarial paroxysms is repeated as follows: confusion & coma a. Every 48 h in P. vivax & P. ovale tertian malaria. Dysenteric malaria: abdominal pain, vomiting & b. Every 72 h in P. malariae quartan malaria. bleeding Pathogenesis and c. Every 36-48 h or irregular in P. falciparum subtertian Pulmonary edema Clinical Picture malaria. Algid malaria: Because of pulmonary edema, GIT It is repeated for 2 weeks with intensity thin stop bleeding or gram ve septicemia. Hypotension rapidly Its termination may mean elimination of infection but develops impaired capillary perfusion, vascular relapse or recrudescence may presented : collapse & shock. Relapse: recurrence of attacks due to reactivation of Hypoglycemia: may result from impaired hepatic hypnozoites in liver (occurs with P. ovale & vivax) gluconeogenesis. Recrudescence: recurrence of attacks in patients having Renal failure: Renal anoxia acute renal failure. low-grade parasitaemia when they become debilitated b. Hyperactive malarial splenomegaly: characterized by (occurs with P. malariae & falciparum). chronic splenomegaly with marked elevation of IgM. No relapse with blood transfusion. This may be due to reduction of suppressor T-cells that 5. Anemia: due to destruction of RBCs. Merozoites of P. vivax control B-cell activation in P. falciparum infection. & P. ovale invade reticulocytes only. Merozoites of P. c. Black water fever: may be the result of repeated malariae invade old RBCs. This restricts the infection. attacks of P. falciparum infection & incomplete However, those of P. falciparum invade RBCs of any age quinine therapy. Massive intravascular haemolysis causing severe hemolytic anemia. occurs with anemia, jaundice & hemoglobinuria (dark 6. Hepatosplenomegaly: because of enhanced phagocytosis red or black urine). The cause may be autoimmune of RBCs remnants & other debris. with development of antibodies to the infected RBCs.

1.Invasion of RBCs their rupture. 2.Infection is asymptomatic or mild and self-limited in most cases. 3.It is characterized by fever (not periodic), chills, headache, myalgia & backache. 4.Mild to moderate haemolytic anaemia jaundice. 5.More severe forms with rapidly progressive illness characterized by fever, anaemia, jaundice & renal failure may develop. 6.In splenectomized patient, the infection is fulminating & may be fatal.

Diagnosis

Treatment

Prevention & Control

1.Blood film examination: reveals multiple small rings 1. Examination of thin and thick blood smears from the patient during the febrile conditions. This shows ring, trophozoite, in RBCs that can be schizont and gametocyte stages of the parasite. In P. falciparum, only rings & gametocytes are seen. RBCs harbouring differentiated from P. trophozoites & schizonts of P. falciparum are trapped in blood capillaries of the internal organs (due to the surface falciparum by absence of knobs they developed). malaria pigment. 2. Detection of the circulating parasite antigens using monoclonal antibodies. 2.Serology: is useful 3. Use of DNA and RNA probes. especially in presence of low parasitaemia. 3.PCR Classification of drugs that treat human malaria: The recommended regimens for malaria treatment: 1. Drugs that destroy parasite stages in the liver (tissue 1. Treatment of clinical attacks: Chloroquine. schizonticides): Primaquine (kills hypnozoites too). 2. Radical treatment: Primaquine is given after treatment of 2. Drugs that destroy parasite stages in the blood (blood clinical attack to kill hypnozoites of P. vivax & P. ovale. schizonticides): Quinine, Chloroquine & recently 3. Anti-malarial chemoprophylaxis: for healthy persons 1.Combination of Artimesinin (plant extract). entering a malaria endemic area: Clindamycin & Quinin. 3. Drugs that destroy gametocytes in the blood (blood a. Causal prophylaxis as Primaquine. 2.Blood transfusion in severe gametocyticides): b. Suppressive prophylaxis as Chloroquine during stay in cases. a. Chloroquine kills gametocytes of P. vivax, P. ovale & P. malaria endemic area. malariae. 4. Drug resistant malaria: is overcome by drug combination b. Primaquine kills all gametocytes of all four species. Thus as Coartem (artemether and lumifantrine) is recently they render the patient non-infectious to the mosquito. developed. 1. Early detection and treatment of human cases. In Egypt, malaria is under control. However 2. Control of mosquito vector it is threatened by falciparum malaria from Tick control measures 3. Chemoprophylaxis of healthy human entering a malaria endemic area. neighboring countries especially Sudan prevent infection. 4. Vaccination against malaria. A vaccine is already tested in South America where falciparum malaria is endemic. and some parts of Africa with promising results.
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Medical Parasitology in tables

Kasr Alainy Students

Cutaneous Leishmania (Cutaneous Leishmaniasis; CL) A-Old World Cutaneous Leishmaniasis (OWCL) B-New World Cutaneous Leishmaniasis (NWCL) Parasite L. maxicana (Disease) L. major (Wet or L. brazilinesis L. tropica (Dry or Urban CL) L. aethopica L. peruviana (Uta) (Chiclero ulcer, Bay L. pifanoi Rural CL) (Espundia) sore) Geographical Middle East, Asia & Africa in Middle East, Asia & Ethiopia & Kenya Central & south America. Distribution people living in big cities. Africa in rural areas. Vector Snad fly (Phlebotomus fly species) Snad fly (Lutzomyia fly species) Diagnostic Amastigote in the early lesion biopsy. Stage Promastigote in culture. Infective Stage & Mode Of Promastigote form, through bite of(Phlebotomaus , lutzomyia) fly. Infection Development Amastigote taken by female sand fly by bite change into Promastigote multiply by longitudinal binary fission migrate back to the buccal cavity Inside the infect another host during biting (Biological transmission). Vector 1. The lesion develops in exposed parts of the body, usually face. It may 1. It produces an It produce Produce Chiclero acute infection Also, produce skin be single or multiple. diffuse CL . ulcer or Bay sore. ulcers. 2. At the site of bite, there is with duration of 3 The parasite Usually single & 6 months. a localized nodule due to Lymphatic spread proliferate affects the ear 2. The lesions occur multiplication of the result in wide indefinitely causing 1ry on the lower organisms in the skin spread ulcerations forming many destruction of limbs. macrophages and & involvement of lesions. Disease known cartilage. The initial lesion granulomatous reactions 3. The lesions are mucous is single then This probably the locally as Uta. Occurs in the moist with serous around them. membranes & can Pathogenesis spreads slowly result of not only May one or small forest workers exudate and tend 3. The lesion is dry and cause erosion of and Clinical like lepromatous deficient cellnumber of skin who collect the to ulcerate very ulcerated only after the nasal septum, Picture leprosy. mediated lesions that are chicle gum. early. several months giving an palate or larynx immunity but self-healing similar Does not Rarely cause ulcer with cut edges, with oedema, also of some to L. tropica. ulcerate or heal. diffuse cutaneous raised indurated margin Resistance to retissue destruction characteristics of lesions with and scanty exudate. It is infection with the & 2ry bacterial the parasite nasopharyngeal known as Oriental sore. same species (L. infection. itself. mucosal 4. 2ry bacterial infection is tropica or major) This result in great Lesions resemble involvement & common, the ulcer heals following a 1ry deformity that is lepromatous regional spontaneously if infection is strong called Espundia. leprosy. lymhadenopathy. untreated after about and long lasting. one year leaving a disfiguring scar. a. Clinically. b. Detection of the parasite : Examination of material aspirated or scraped from the edge of lesion. A biopsy could be taken & submitted for histologic examination. Amastigotes can be seen & are numerous in the early than in late lesions . Diagnosis Culture on suitable medium may demonstrate promastigote forms. c. Montenergo test: is an intradermal test using antigen from cultured promastigotes. It is +ve in more than 95% of infections. It gives a delayed reaction that appears as an indurated area after 3 days. d. Serological tests. Systemic treatment: Local treatment: Pentavalent antimony as antimony sodium gluconate or pentostam. Physical methods as surgical excision, curettage, heat and freezing therapy. Pentamidine is given in diffuse cutaneous leishmaniasis caused by L. Chemical methods using topical preparations as 2% chlorpromazine and Treatment aethiopica. clotrimazole 1%. Allopurinol, Ketoconazole and Dapsone are proved useful. Intradermal injection of interferon gamma around the lesion promotes healing of ulcers. 1- Treatment of patients. Prevention & 2- Control of vector. Control 3- Protection by using wire screens, mosquito nets or repellents. 4- Vaccination in endemic areas using suspension of living promastigote resulting in lasting immunity.

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Medical Parasitology in tables Parasite (Disease) Geographical Distribution DH & Habitat I.M. host Diagnostic Stage Toxoplasma gondii (Toxoploasmosis) Worldwide distribution

Kasr Alainy Students

Cat Wide range of avian and mammalian intermediate hosts including man and cats (Obligate Intracellular) Toxoplasma trophozoites Tachyzoite (trophozoite), bradyzoite, tissue cyst, pseudocyst and sporulated oocyst except for Unsporulated oocyst. Infection can occur through: Oral route: most common route of infection , includes: Ingestion of sporulated oocyst in contaminating food, drinks, objects, hands, etc Ingestion of cysts present in undercooked meat of intermediate hosts. Infective Stages & Parenteral route: Mode Of Trans-placental transmission: pregnant woman with parasitaemia. This can occur during: Infection o Acute primary infection of pregnant woman during or shortly after pregnancy. o Old latent infection when the woman is immunosuppressed. Blood and leukocyte transfusions if the donor has parasitaemia. Organ transplantation, particularly heart transplants. Contamination of mucous membranes and skin abrasions. Asexual cycle (in the intermediate hosts; man, cattle, goats, poultry & cats). Life Cycle Sexual cycle (in the definitive host; cats only). 1. Congenital infection: At first, there is generalized infection of the fetus then the parasite localizes in the CNS. Ocular lesions start by proliferation of the parasite in the retina and cause inflammation of the choroid (Retinochoroiditits). 2. Acquired infection: Pathogenesis In acute stage: focal areas of inflammation and necrosis in various tissues. In chronic or latent stage: subsidence of inflammation and formation of inactive cysts (with development of immunity in immuno-competent hosts). 3. Recrudescence: during immunosuppression, cysts reactivated resulting in flaring up and possibility for disseminated infection. Toxoplasmosis is asymptomatic in the great majority of cases, the sequelae of infection depend on: Infected persons immunity and age. Virulence of the infecting strain of the parasite (possibly). I. Congenital toxoplasmosis: The effect depends on age of the fetus at the time of infection and the protective immunity of the mother. Higher severity of infection occurs with early pregnancy infection. 1. Loss of fetus due to abortion or still birth. 2. Early neonatal manifestations in the form of: CNS affection: microcephaly, hydrocephalus, spasticity, palsy and convulsions. Cerebral calcifications could be seen on X-ray examination. Eye affection: retinochoroiditis (the most common sequelae of toxoplasmosis). Systemic manifestations: as fever, pneumonitis, hepatomegaly, jaundice and lymphadenitis. Clinical Picture 3. Late manifestations: infected baby appears healthy, manifestations appears late in life. - CNS involvement including mental retardation. - Eye affection. II. Acquired toxoplasmosis : Lymphadenitis is the most clinical form of infection. It may be associated with fever, headache, myalgia and sometimes splenomegaly and skin rash. Retinochoroiditis: it may be due to congenital infection that did not detected early. It can result in blindness. III. Toxoplasmosis in immuno-compromised patients (Opportunistic infection) : Encephalitis: it is the most important manifestation in immuno-compromised patient and a major cause of death in AIDS patients. It is usually due to reactivation of latent cerebral cysts. Organ transplant patients can develop acute disseminated toxoplasmosis. Clinical: suggestive as above Imaging: X-ray reveals cerebral lesions. Ultrasound, fetal examination can detect lesions as enlargement of cerebral ventricles. Laboratory diagnosis: Serology: Diagnosis mostly relies on serology. Detection of IgM is important as it indicates: Active infection Congenital infection as the maternal IgM does not cross the placental barrier. Diagnosis Detection of IgG indicates: Acute infection (rising titre): appears later than IgM and usually persists for a year. Chronic latent infection: stable or declining titre. Techniques: various as ELISA, IFT, etc Sabin Feldman dye test: serum of patient is added to Toxoplasma organisms and methylene blue. If antibodies are present, the organism will not take the dye positive reaction. Frenkle test (Toxoplasmin intradermal test): positive in active and chronic infections and has limited clinical applications. Molecular techniques: PCR is especially important in immuno-compromised patients in whom immuno-diagnosis is not reliable. Also, it can be used on amniotic fluid samples and infant urine for diagnosis of congenital infection. Combination of Pyrimethamine and Trisulphapyrimidines. Treatment Spiramycin can be given for infected pregnant women. 1. Proper washing of hands, vegetables and fruits, clean water supply and safe disposal of cats litter boxes. Prevention & 2. Washing of hands and utensils after handling raw meat & proper freezing and cooking of meat. Control 3. Health education of pregnant women and routine antenatal serological screening to detect maternal infection.

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Medical Parasitology in tables Potentially pathogenic free-living amoeba Acanthamoeba species Naegleria fowleri (Primary Amoebic Granulomatous Amoebic Acanthamoeba Keratitis Meningioencephalitis; PAM) Encephalitis (GAE) Reported in some parts of the Sporadically reported worlds Water (fresh, brackish & salt), moist soil, decaying vegetation. Amoeboid trophozoite form trophozoite form Trophozoites & cysts Amoeba, through: Amoeboid trophozoite, through Corneal trauma. Trophozoite, through: nasal route during swimming in contaminated water & air: Exposure to or sniffing of contaminated 1ry infection nasal route contaminated water. water & inhalation of 2ry infection blood spread Wearing contaminated contaminated air. contact lenses. Flagellate form Amoeboid form cyst stage 1. Amoeboid trophozoite invades the nasal mucosa and cribriform plate and reaches the brain along the olfactory nerves. 2. Flagellate & cyst give rise to Amoebae prior of invasion, which is the only form detectable in brain tissue. 3. Naeglaria produces diffuse meningio-encephalitis with hemorrhagic inflammation and necrosis of brain tissue. Pam is an acute fulminant rapidly fatal disease that affects mostly children and young adults 1. There is fever, headache, nausea & vomiting, stiffness of neck and convulsions. 2. Disturbance in the sense of smell or taste can occur. 3. The patient enters in coma and death occurs early. 4. The entire course usually takes 3 6 days. Trophozoite (active) Cyst (resting) 1. 1ry infection occurs in the lower respiratory tract and ulcerated skin & mucosa. 2. Invasion of CNS (2ry infection) by blood spread causes single or multiple 1. Acanthamoeba cause focal granulomatous chronic progressive lesions in the brain & other ulcerative keratitis. affected organs. Corneal ulceration may 3. In AIDS patients progress to perforation. disseminated infection can 2. In AIDS patients, developed. infection may cause endophthalmitis. Takes subacute or chronic 3. The infection is course (days to years) characterized by sever Manifested by nausea & ocular pain and vomiting, altered mental affection of vision. state, headache, convulsions and stiffness of the neck. In AIDS patients, the disease may be fulminating resembling Naeglaria infection.

Kasr Alainy Students

Parasite (Disease) Geographical Distribution Habitat in Nature Diagnostic Stage

Microsporidia

Reported from various parts of the world. ----------------Spore stage The spores, through uncertain methods but the infection is most likely acquired by ingestion. Others include inhalation, ocular exposure & sexual intercourse. Spores Ejects the tubular polar filaments Sporoplasm Cytoplasm of the host cell Cycles of Merogony followed by Sporogony Spores

Infective Stage & Mode Of Infection

Life Cycle

Pathogenesis

Clinical Picture

It depends on the type of the microsporidia: Intestinal microsporodiosis: The most clinical form & is usually seen in AIDS patients. It produces prolonged diarrhea, malabsorption, wasting and dehydration. Cholangitis and rhinosinusitis can develop due to spread to other epithelial cells. Systemic disease can also develop due to spread to multiple organs. Ocular microsporidiasis: Ocular lesions affect both healthy and HIV infected subjects. Infection can lead to conjunctivitis, keratitis and corneal ulcers. Microsporidial myositis: The patient suffers from generalized muscle weakness, myalgia, fever and weight loss. Systemic infection: Infection can involve several systems in both immunocompetent and immunocompromized patients. There may be intestinal, biliary, ocular, hepatic, renal and respiratory affections.

Diagnosis

1. History of swimming mainly. 2. CSF examination: Microscopic examination reveals amoeba forms. CSF examinationreveals the Suspension in fresh water parasite. incites transformation into flagellate forms that confirm the diagnosis. Culture on suitable medium 1. At present, there is no complete treatment. 2. Amphotericin B can be given IV or intrathecally. 1. Avoidance of swimming in contaminated water. 2. Proper chlorination of public water supplies & pools. There is no complete satisfactory treatment. However, there are some reported successful regimens: Excision of focal lesion & treatment with Ketoconazole. Penicillin & Chloramphenicol

Identification of trophozoites & cysts in corneal scraping directly and after culture.

Direct methods: Biopsy: identification of organisms in stained biopsy material. Examination of excreta and body fluids: identification of stained spores in faeces, urine, bile and duodenal, bronchial or nasal fluisds. Electron microscopy: to identify the ultra-structure of the parasite. Molecular techniques: Assays are being developed.

Treatment

Prevention & Control

Oral Itraconazole Albendazole: for intestinal and disseminated infections. combined with topical Nitazoxanide: is effective in intestinal microsporidiosis. Miconazole. Topical fumagillin: in ocular lesions. Corneal transplant. 1. Proper care of contact lenses. 2. Avoidance of exposure ----------------of the eye to contaminated water.

Commensal amoebae They are characterized by: Etnamoeba coli: 1- All move by pseudopodia, giving rise to a sluggish hesitant motility. It lives in the large intestine in 10 30 % of people. It resembles E. histolytica but 2- Endoplasm is not clearly differentiated from the ectoplasm with food vacuole differs in: containing bacteria and tissue debris showing a dirty endoplasm (contrary to 1- Average size of trophozoite is larger being 30 um. E. histolytica) 2- More granular endoplasm containing ingested bacteria but no red cells. Etnamoeba dispar: 3- Narrower and less differentiated ectoplasm. It is morphologically similar to E. histolytica but differs in being non-invasive living 4- Broader and blunter pseudopodia. in lumen of large intestine. 5- Sluggish movement. Etnamoeba hartmanni: 6- Peripheral chromatin granules of the nucleus are more coarse irregular. It is morphologically similar to E. histolytica and only differs in size: 7- Karyosome is large and eccentric. 1- Trophozoite: range from 4 12 um in diameter and ingest bacteria only. 8- Cysts are larger (average size is 25 um) with slender aplinter-chromotoid 2- Cysts: range from 3 10 um in diameter. bodies, glycogen vacuole and 8 nuclei similar to those of the trophozoite 3- It is non-pathogenic (not tissue invader). stage.

N.B. Enough to study the names of commensal amoebae & know that E. coli is bigger, E. hartmanni is smaller & E. dispar is morphologically identical to E. histolytica
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Medical Parasitology in tables

Kasr Alainy Students Immunodiagnosis of Parasitic Infections Situations where immunodiagnosis is important: 1. When we cannot precisely locate the parasite e.g. visceral larva migrans. 2. When parasitic stages may not appear in patients excreta e.g. early and chronic phases of infection. 3. To differentiate true from spurious (false) infections e.g. Fascioliasis. 4. When large numbers of specimens are simultaneously tested e.g. epidemiological studies. 5. When sampling may be dangerous to the patient e.g. hydatidosis, cerebral toxoplasmosis, trichinosis. 6. Follow up after treatment. Serology is better than skin testing. Detection of antigen is superior to detection of antibody. Progress in Molecular Parasitology Molecular techniques are now being progressively applied in parasitology especially in these fields: Molecular classification of parasites: 1. Morphologically similar parasites can be classified into species, subspecies, etc according to DNA & RNA sequences. 2. Molecular analysis can identify evolutionary relationship between parasites. The more similar the sequences in two organisms, the more likely they are related. Study of parasite biology: Such as metabolism, host invasiveness, virulence factors, etc Development of new drugs: 1. Identification of vital targets in the parasite that are lacking in the host allows the development of more effective and less toxic drugs. 2. Detection of the drug resistance genes and understanding their mechanism of action permits the development of drugs that overcome this resistance. Diagnostics: 1. Molecular diagnosis as PCR and DNA hybridization techniques. 2. Molecular methods can be used to prepare sensitive and specific reagents to be used in immunodiagnosis. Vaccine development. Epidemiology and control measures: Determination of geographical distribution of various strains of the parasite allows the implementations of control measures most suitable for local strains. ------------------------------------------------------------------------------------

Immunology of Parasitic Infections

Vaccination No efficient vaccine preparations have yet been approved for human use against parasites. The causes include: 1. Difficulty of identification and isolation of protective antigens to be used as vaccine. 2. Possibility of induction of immunopathological lesions in response to the vaccine. 3. Parasites may evade the immunity produced by the vaccine. 4. The complexity of the life cycles of the parasites makes the choice of the stage to be targeted difficult. 5. Vaccine preparations may not be equally effective in different countries. This is due to the existence of various strains for the same parasite in different geographical regions. Immunopathology of parasitic infections 1. Allergic reactions (Type 1 hypersensitivity): IgE mediated allergy commonly occur with helminthic infections. They include: Systemic reactions (anaphylaxis): life-threatening condition, e.g. after leakage of hydatid cyst fluid. Bronchial asthma: e.g. Fascioliasis and Larva migrans. Allergic dermatitis: e.g. early stages of Schistosomiasis, Fascioliasis and Ascariasis. 2. Eosinophilic pneumonia: results from helminthic larvae, e.g. Ascaris & Hookworms. 3. Autoimmune reactions: They are due to cross-reaction with the host antigens. They can lead to hemolytic anemia as in falciparum malaria and produce damage to the heart and neuronal tissue in Chagas disease. 4. Deposition of immune complexes (Type 3 hypersensitivity): may deposited systemically or on basement membranes. e.g. Plasmodium malariae Nephrotic syndrome Schistosomiasis Katayama fever (serum sickness-like disease). 5. Granuloma formation (Delayed type hypersensitivity): e.g. in Schistosomiasis, granuloma formation around the eggs. 6. Immunosuppression: Variable degrees of immunosuppression is observed in parasitic infections. e.g. infants infected with visceral Leishmaniasis may suffer severe immunosuppression. Death of these patients often results from secondary infections (e.g. pneumonia). Parasite Immune Evasion 1. Sequestration of the parasite: It means the hiding of the parasite. It can be achieved through: Intracellular habitat; e.g. Plasmodium & Toxoplasma. Presence of surrounding cyst wall; e.g. Trichinella. 2. Luminal habitat: e.g. Ascaris and Enterobius. 3. Parasite movement: .e.g. Ancylostoma, Larva migrans. 4. Antigen modification: through: Antigen variation: e.g. African trypanosomes, malaria. Antigen disguise: Parasites cover themselves with various host proteins; e.g. Schistosomiasis. Antigen mimicry: Presence of similarity between host and parasite; e.g. Schistosomiasis. Antigen shedding: Parasites shed their surface antigens to neutralize the antibodies at a distance from the parasite; e.g. S. mansoni & P. falciparum. 5. Production of blocking antibodies: These are antibodies of little protective effect. They combine with helminth antigens making them unavailable for antibodies of high protective effect, e.g. Schistosomiasis. 6. Inhibition of immune factors: Cleavage of antibodies: by protease enzyme, e.g. Trypanosoma cruzi Inactivation of complement: o Protease activity: e.g. Schistosoma larva o Acceleration of decay of complement: e.g. Trypanosoma cruzi o Ejection of membrane attack complexes from their surface: e.g. Leishmania Inhibition of macrophages: e.g. Leishmania, Toxoplasma & Trypanosoma cruzi 7. Immunosuppression e.g. visceral Leishmaniasis.

Medical Entomology
Medical importance of arthropods: I. Arthropods as agents of diseases and discomfort: a. Inoculation of poisons: e.g. ticks, spiders & scorpions. b. Invasion of tissues: e.g. scabies & myiasis. c. Dermatitis and allergic skin lesions: e.g. fleas, mosquitos, bugs & lice. II. Arthropods as transmitters of diseases: a. Mechanical transmission: i. Indirect: They act as passive carriers of organisms on their hairs, mouthparts or legs. e.g. Musca domestica. ii. Direct: They pick the organisms from a diseased person and inoculate them to healthy one. e.g. stomoxys. b. Biological transmission: i. Propagative: multiplication of the organisms without developmental changes. e.g. yellow fever virus (Aedes aegypti) & plague organisms (fleas). ii. Cyclopropagative: multiplication and developmental changes of the organisms. e.g. malaria (Anopheles) & Leishmania (Sand fly). iii. Cyclodevelopmental: developmental changes without multiplication. e.g. filaria (mosquitos). iv. Transovarian: organisms transmitted from the infected mother to offspring through the ova. e.g. organisms transmitted by hard & soft ticks. v. Trans-stadial (stage to stage): e.g. organisms of scrub typhus which pass from larvae (as ectoparasite of man) to nymph to adults to next larvae.

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Medical Parasitology in tables Arthropod Geographical Distribution Medical Importance Mechanism of Transmission

Kasr Alainy Students Control (Read only) i. Aquatic stages (larvae & pupae): a. Mechanical (physical) control: Removal of plants where larvae breed in shaded areas and development of shade when they need sunshine. Filling or drainage of breeding places. Production of turbidity in clear water. Changing the current and the level of water to prevent permanent growth. b. Biological control: Natural enemies such as frogs, ducks and fish. c. Chemical control: Malariol (larvae & pupae): cheap non-volatile oil, which cause suffocation of aquatic stages. Paris green (larvae, not pupae): a spray for the surface of water. It acts as stomach poison to larvae. It does not affect pupa as it does not feed. Insecticides (DDT): produce poisoning whether ingested or contact the cuticle. ii. Adult stages: Wire screening. Mosquito repellents. Spraying with insecticides. Animal barriers. Sterilization of males by irradiation produces infertile eggs. Using of natural enemies.

Culex

Transmission of: Wuchereria bancrofti (chief transmitter). Viral encephalitis. Rift valley fever (viral disease)

Aedes

Cosmopolitan but more prevalent in tropical and temperate countries.

Transmission of: Yellow fever virus. Dengue fever virus. Wuchereria bancrofti. Rift valley fever.

Transmission is only by females, which bites man sucking his blood.

Anopheles

Transmission of: Human malaria. Wuchereria bancrofti & B. malayi. Viral encephalitis (occasionally).

Prevalent in 1. Transmission of diseases: Mediterranean a. Protozoal (Leishmaniasis) coasts, Middle east, b.Bacterial (Oroya fever = Carrions disease = Phlebotomus Africa, India China Bartonellosis) (Sand Fly) and America. c. Viral (Sand fly fever = Papatasii fever = 3 day N.B. Phlebotoms fever): similar to influenza. papatasii is present 2. Harrara: allergic reaction to the bite of sand fly. in Egypt It is considered as efficient disease agent transmitter: Musca 1. Indirect mechanical transmission of domestica Cosmoplitan microorganisms (Typhoid, Poliomye-litis and (House Fly) bacillary dysentery), cysts of protozoa and eggs of helminthes. 2. Accidental myiasis. 1. Direct mechanical transmission of blood Stomoxyscalparasites as trypanosomes. citrans Cosmoplitan 2. Accidental myiasis. (Stalble fly) 3. Painful bites. 4. Skin allergy. G. palpalis: West Glossina (Tse- Africa Tse fly) G. morsitans: East Africa Calliphorinae (Calliphora, Lucilia) Cosmopolitan Sarcophaginae (Sarcophaga, Wohlfahrtia) Cosmopolitan, the Cimicidae commonest one in (Bed Bugs) man is Cimex lectularius Reduviidae North & South (Winged Bug) America

1. Filling the cracks in walls and ground to deprive the fly from its breeding places. Transmission is only by female 2. Screening of windows and doors by nets with bite, feed by night and hide by narrow meshes. day time. 3. Insecticides against larvae and adults. 4. Repellents to the skin.

The tiny hairs covering the body, the mouth-parts and the legs have sticky pads, all help to collect organisms and transmitting them.

1. Elimination of breeding places. 2. Spraying with insecticides (DTT). 3. Wire screening of inlets and outlets of the house. 4. Basic sanitation and health education (Musca develops resistance to ordinary insecticides).

Direct mechanical transmission of blood and painful bites.

As musca but mainly to animal stables.

1. Transmission of trypanosoma that cause sleeping sickness in man. 2. Transmission of Nagana to animals.

By biting of tsetse fly

1. Changing the nature of breeding places to become unsuitable for the fly and periodic cleaning of riverine vegetation (deforestation). 2. Collection of larvae and pupae. 3. Application of insecticides. 4. Treatment of patients. 5. Campaign against wild animals.

They cause semi-specific myiasis

By sucking mouth

As Musca

1. Their persistent biting by night causes insomnia and nervous irritability. 2. They may act as mechanical carriers but they are not biological vectors of human diseases. 3. Recently, there is evidence to indicate that they may transmit hepatitis B virus. Also called: winged bug, cone-nosed, kissing, Assassin & Barbers bug. They are the vectors for T. cruzi that causes Chagas disease and T. rangeli which is non-pathogenic to man. Act as Intermediate host for: D. latum, D. mansoni & D. medinensis.

1. Application of insecticides to hiding places. 2. Fumigation with sulfur. 3. Collection and destruction of bugs. As bed bugs. Regular steaming or addition of calcium oxide, chlorine or copper sulphate. Fish (Barbus): can feed on Cyclops. Wells water should be boiled, filtered, covered and provided with pumps.

Cyclops

Live in fresh water.

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2010/2011

Medical Parasitology in tables Arthropod Geographical Distribution Medical Importance Mechanism of Transmission Control

Kasr Alainy Students

Siphonaptera Cosmopolitan (Fleas)

Anoplura (Lice)

Worldwide, wherever there is low hygiene

Acarina (Ticks)

As vector of diseases: 1. Plague: (causative organism is Yersinia bacilli) Ingestion of infected blood fleas stomach multiplication & block of the stomach next ingestion of blood blood cannot pass the obstruction regurgetation with bacilli (Anterior station transmission) 2. Endemic or murine typhus: (causative organism is Rickettsia mooseri; R. typhi): Rickettsia epithelial lining of mid-gut multiplication faeces (Posterior station transmission) Man is infected trough: a. Contamination of skin by flea faeces or by scratching. b.Inhalation of dried flea faeces (bacilli still alive for 40 days). c. Crushing the fleas. As intermediate host of parasitic diseases: 1. Rat fleas act as IH for H. nana & H. diminuta. 2. Dog and cat fleas act as IH for D. caninum. Fleas attacking their host: Tunga penetrans causing Chiggers or Jiggers disease. It is found in tropical & subtropical regions. The fertilized female burrow into the skin of the sole of foot or between the toes to take its blood meal. As eggs develop they project to live in the soil. Clinical picture: painful nodular swelling which may ulcerate. Treatment: surgical removal of flea with antiseptic dressing & antibiotics. Prevented by wearing shoes. Lice as vectors of diseases (Body lice): 1. Epidemic typhus: causative organism is Rickettsia prowazekii. Mechanism of transmission: Rickettsia lice gut cells multiplication rupture of cells lumen pass with faeces Infection occurs by: Contamination of bite wound with lice faeces (posterior station) Inhalation of dust containing the dried infected faeces of lice. Crushing the lice against skin abrasions. The source of the epidemic infection is either: A case of typhus from neighboring area. A case of Brill-Zinsser disease: it is a mild form of typhus. It is a late recrudescence of long dormant infection (may be 30 years of 1st infection). 2. Trench fever (5-day fever): causative organism is Rickettsia Quintana. Mechanism of transmission: Contamination of skin wound with lice faeces (posterior station). Crushing the lice against skin abrasions. 3. Epidemic relapsing fever: causative organism is Borrelia recurrentis. Mechanism of transmission: Only by crushing the lice against the skin. Lice as a cause of Pediculosis (Vagabonds disease): It occurs in persons who have lice for long periods. The skin becomes thickened and shows spots of hyperpigmentation. Pubic louse (Phthirus pubis): 1. It is not known to transmit any disease. 2. It causes irritation of the skin which shows bluish patches. 3. If present in the eyelashes, it causes inflammation of lid margin (blepharitis). Diseases caused by ticks: 1. Dermatosis: during biting, they produce trauma to the skin Occurs in hard by the mouth-part. This provokes inflammatory reaction. ticks either by: Forcible removal of the tick may be complicated by 2ry Saliva in the infection and ulceration. bite wound 2. Paralysis: a rapid ascending flaccid paralysis with difficulty in Contamination swallowing and respiration that may lead to death especially of skin in children & aged adults. It caused by toxins in their saliva. abrasions by Most of the patients recover after removal of the tick. faeces. Diseases transmitted by hard ticks: Trans-ovarian Rickettsial diseases:as Q-fever by Coxiella burneti. transmission. Bacterial & spirochaetal diseases: as Lyme disease by Borrelia Occurs in soft burgdorferi. It is a systemic illness with skin lesions, fever, ticks either by: arthritis, carditis or meningitis. Saliva Viral disease: as viral encephalitis & Haemorrhagic fever. Coxal fluid Protozoal diseases: Babesiosis by Babesia divergens. Trans-ovarian Diseases transmitted by soft ticks: transmission Endemic relapsing fever by Borrelia duttoni. Q-fever by Coxiella burnetti .

Human fleas: 1. Application of insecticides under the carpets. 2. Use of vacuum cleaners Dog and cat fleas: Dusting animals and their homes with insecticides. Rat fleas: 1. Dusting rat holes with insecticides. 2. Using of rodenticides (warfarin). 3. Strict quarantine measures against ships coming from foreign parts by fumigation to kill rats.

Body lice (Pidiculus humanus corporis): Frequent bathing and boiling of clothes. Head lice (Pidiculus humanus capitis): The current drugs of choice are: Synthetic pyrethrin as a spray. Anticholine esterase inhibitors. Pubic lice: Boil the underwear. Shave the pubic and axillary hairs. Removal of the lice from eyelashes with forceps and application of yellow oxide of mercury ointment .

1. Careful search for ticks in persons exposed to infected areas and early removal of ticks by gentle extraction after applying chloroform, ether, kerosene or a glowing match or cigarette to the tick avoiding breaking down the capitulum. 2. Soft ticks are killed by spraying their hiding places with insecticides. 3. Hard ticks being permanent ecto-parasites, insecticides should be applied directly by spray or dipping the domestic animals in basins containing 5% gammaxane. 4. Using repellents, wearing high boots and clothes treated with diethyltoluamid. 5. Rodent proofing buildings. 6. Anti-tick vaccine is proved to effective in veterinary practice.

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Medical Parasitology in tables Arthropod Geographical Pathogenesis (Medical Importance) & Clinical Distribution Picture Diagnosis Treatment

Kasr Alainy Students Control

Sarcoptes scabiei & Scabies (Itch mite)

Demodex folliculorum (Follicle mite)

Trombiculid mites

House dust mites

Storage (Forage) mites

Domestic mites

Scorpion

1. Clinical picture: Common sites: previously. Inter-digital spaces, flexor aspects of wrist and 2. Examining the skin 1. The patient must take hot forearm, elbow, axillae, back, inguinal region surface with a hand lens soapy bath using a rough and genitalia. to find the burrows & brush (to open the tunnels). The lesions: opening one of them by a 2. Many acaricides are used, the 1. Elevated reddish tracks in the skin with needle to see the mites. most effective are: Worldwide, minute vesicles. 3. Scraping the infected area a. Pyrethrin as 5% cream. especially 2. The patient suffers from intense itching, with a scalpel and b. Crotamiton (Eurax) 10% is among poor which is aggravated by warmth and material obtained is preferred in infants, children classes or sweating causing scratching. examined microscopically, and pregnant women. when there is 3. This spreads the lesions and induces 2ry immediately after adding c. Lindane 1% cream. over crowding bacterial infection. 10% KOH to avoid d. Benzyl benzoate 20%. or lack lf 4. This results in multiple popular vesicular & dissolving of the mites. hygiene. pustular lesions with widespread eruptions. 4. A better method is by The drug must be applied to Crusted or Norwegian scabies: applying mineral oil to the the whole body for 8 12 1. This is a generalized dermatitis with skin before scraping. This hours then washed off. extensive scaling and crusting. enables organisms to 3. Antihistaminics for itching and 2. It may occur in immuno-deficient or very adhere better to the antibodies for 2ry infections. debilitated patients with hundreds of mites blade and the slide and in the lesion. will not dissolve the mites. 1. They rarely cause any harm but the may be associated with acne and comedones (black heads). Pressing the lesion and 1. Washing the face with soap 2. They may cause dry erythema with scaling examining the extruded and water. Cosmopolitan and blepharitis. material microscopically for 2. Lindane 0.5% in vanishing 3. Infestations are usually higher in aged parasitic stages. cream combat them. persons and in women using cleansing creams instead of soap and water. They are called Chiggers mites, Harvest mites or Red bugs. Vectors of scrub typhus: by trans-ovarian & ----------------------------------------------------trans-stadial transmission. Chiggers mites causing dermatitis: by larvae in North America & Europe. 1. Bronchial asthma: especially in children. 1. History taking. 2. Perinnial rhinitis: sneezing, nasal 2. Clinical examination. congestion, watery discharge and 3. Determine sensitization --------------------------------conjunctival itching. by skin tests and serum 3. Dermatitis: erythematous scaling & assays of specific IgE and lichenified areas. IgG4 antibodies. Pests of stored food products e.g. flour, cereals, cheese and macaroni. They affect workers handling these products (exposed to crushed mite products and their excreta) e.g. bakers itch or grocers itch. A lotion of worm water and 1. Dermatosis: by contact or bite of mites.it vinegar or sat. solution of picric produces itching, urticarial and papular acid in 90% alcohol. ------------eruptions of exposed parts of the body. -------------------- Saline purge in GIT troubles. 2. Digestive troubles: if swallowed, they cause Arsenicals for respiratory irritation of intestinal crypts with colic & symptoms. they are recovered in faeces (intestinal acariasis). 3. Respiratory symptoms: if inhaled, they are recovered in sputum (respiratory acariasis). 4. Allergic conjunctivitis. These are blood-sucking mites that cause dermatitis in man. ------------- Rat mites are found in ware houses. Bird ----------------------------------------mite are found in air-conditioning ducts or eaves of houses. 1. Application of tourniquet just above the site of bite to decrease the absorption of the toxin. 2. Suction of the venom or Scorpion sting is very painful. incision at the site of the Its toxin causes twitching, muscle spasms, --------------------------------wound. convulsions, shock & may cause heart failure, 3. Doctors should be ready with especially children & elders. anti-scorpion serum. 4. Treatment of shock if present. 5. Analgesics like aspirin, spraying anesthetics or corticosteroids in severe cases.

1. Frequent bathing and boiling of bed linen. 2. Avoid contact with patients and infected animals. 3. Treatment of patients and domestic animals.

Personal protection by impregnation of socks and trousers with a repellent (pyrethrin or diethyl-tolumid). This will prevent attack of mites. 1. Exclusion of dust from beds and bedrooms of patients. 2. Indoor humidity control. 3. Vacuum cleaning. 4. Dallergen (acaricidal and allergen reducing agent).

---------------------

---------------------

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2010/2011

Medical Parasitology in tables Myiasis Definition: It is the invasion of tissue of animals or humans by the larval stages of dipterous flies. Classification: I. According to habitat (type of tissue invaded): a. External myiasis: i. Cutaneous myiasis: Invasion of intact skin: by larvae: a. Creeping eruption: form tunnel under the skin e.g. Gastrophilus & hypoderma. b.Nodular swelling: invade the intact skin & produce nodular swellings e.g. Cordylobia & Dermatobia. Traumatic (wound) myiasis: invade wounds or ulcers e.g. Calliphora, Lucilia, Chrysomyia & Cochlyomyia. ii. Nasal myiasis: e.g. Chrysomyia, Sarcophaga & Wohlfahrtia. Eggs nasal cavity hatch larvae burrow into tissue bone brain meningitis & death. Clinical picture: nasal obstruction, sneezing & epistaxis. iii. Ocular myiasis: External ophthalmomyiasis (Oestrus): Adult Oestrus eye eggs hatch larvae which possess hooks conjunctival irritation & severe pain. Internal ophthalmomyiasis (Oestrus, Gastrophilus, Hypoderma): It involves the orbit and eye. It is very destructive & leads to loss of eye. iv. Aural myiasis: Severe pain accompanied by deafness & tinnitus and the drum can be perforated e.g. Chrysomyia, Sarcophaga & Wohlfahrtia. b.Internal myiasis: i. Intestinal myiasis: Through ingestion of eggs or larvae in contaminated food, e.g. Musca, Calliphora & Sarcophaga. Larvae deposited around the anus then reach the intestine, e.g. Fannia. Clinical picture: abdominal discomfort, vomiting & diarrhea. Larvae may appear in the vomit or stool leading to patients anxiety. ii. Gastric myiasis: e.g. Eristalis, Clinical picture: vomiting. iii. Urogenital myiasis: e.g. Fannia, Clinical picture: inflammation of urinary tract, pain during urination. II. According to the habit of the fly: a. Specific: the larvae of this group are obligatory tissue parasites and can only develop on or in living tissue. i. Dermatobia: e.g. Dermatobia lays its eggs on mosquito when mosquito stands on human skin, eggs hatch.. The hatched larvae penetrate the skin and forms a nodule. ii. Cordylobia: e.g. Cordylobia. Larvae are acquired from lying on the ground or from the clothes as the eggs are laid on contact to human skin, larvae come out of eggs & attack the skin. iii. Oestrus, Gastrophilus and Hypoderma. b.Semi-specific: The larvae of this group usually grow on dead tissue of man and animals but they may invade neglected wounds. e.g. Calliphora, Lucilia, Sarcophaga & Wohlfahrtia. c. Accidental: Larvae may accidently get in the tissue when the eggs are ingested accidently with food. e.g. Musca & Piophila. Diagnosis: Only by finding the larvae in the lesion & demonstrating its characteristic posterior spiracles. Treatment: 1. Removal of the larvae: a. Manually if larvae are in skin, eye, nose and ear. b.By saline purge if larvae are in stomach or intestine. c. By douches if larvae are in vagina or bladder. d.Through a cystoscope in urinary myiasis. 2. Treatment of secondary infection (Antiseptics & Antibiotics). Prevention and Control: 1. Control of adult flies with insecticides and by the use of nets. 2. Preventions of intestinal myiasis by protection of food from flies. 3. Preventions of wound myiasis by cleaning and covering the wounds by gauze.

Kasr Alainy Students Serological tests are not necessary for the diagnosis of: Trematoda: Heterophyes Cestoda: Multiceps multiceps Dipylidium Caninum Diphyllobothrium latum Diphyllobothrium mansoni & proliferum Hymenolepis nana Hymenolepis diminuta Nematoda: Enterobius vermicularis Trichostrongylus colubriformis Cutaneous larva migrans Protozoa, As regards the following Protozoa IT IS RECOMMENDED TO DO SEROLOGICAL TESTS IN THE FORM OF COPRO-ANTIGEN DETECTION using ELISA for example: Balantidium coli Cryptosporidium parvum Cyclospora cayetanensis Isospora belli Artropods: Skin tests: Cestodes: All arthropods

Protozoa:

Arthropods:

Cysticercosis; Taenia solium (Taeniasis Solium) Echinococcus granulosus (Hydatidosis, Hydatid disease) Trichinella spiralis (Trichinosis) Dracunculus medinensis (Dracunculiasis, Dracontiasis) Leishmania (Montenegro (leishmanin) test) T. cruzi (Cruzin test) Toxoplasma gondii (Frenkle (Toxoplasmin intradermal) test)) House dust mites

Special tests: 1. Blood flukes (Schistosomiasis): Hatching test 2. Enterobius vermicularis (Enterobiasis): a. N.I.H. swab (National Institute of health) b. Scotch adhesive tape swab 3. Wuchereria bancrofti (Bancroftian filariasis, Elephantiasis): Di-ethylcarbamazine (DEC) provocative test 4. Onchocerca volvulus (Onchocercosis or Onchocerciasis): Mazzotti test 5. Giardia lamblia (Giardiasis): String test (Enterotest) 6. Toxoplasma gondii (Toxoploasmosis): Sabin Feldman dye test Surgical treatment: Cestodes:

Nematodes:

Protozoa:

Diphyllobothrium mansoni & proliferum (Sparganosis) Taenia solium (Cysticercosis) Echinococcus granulosus (Hydatidosis, Hydatid disease) Echinococcus multilocularis Multiceps multiceps (Coenurosis) Wuchereria bancrofti (Bancroftian filariasis, Elephantiasis) Loa loa: Eye African worm (Loaiasis or Loiasis) Onchocerca volvulus (Onchocercosis or Onchocerciasis) Entamoeba histolytica (Amoebiasis; Cysts in tissues) Cutaneous Leishmania (Cutaneous Leishmaniasis)

Biopsy (not absolute): Cestodes: Cysticercosis Nematodes: Visceral larva migrans (VLM) Trichinella spiralis Wuchereria bancrofti Onchocerca volvulus Protozoa: Entamoeba histolytica Cryptosporidium parvum Cyclospora cayetanensis Trypanosoma Leishmania (Visceral & Cutaneous) Microsporidia Animal inoculation: Trypanosoma

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2010/2011

Medical Parasitology in tables

Kasr Alainy Students

Life cycles of some Helminthes

Trematoda
Adults Intrahepatic branches of portal veins Systemic Circulation Heart Lungs Fasciola: leptocercous Skin penetration 2nd I.H.: Crabs, crayfish or shrimps 2nd I.H.: Tilapia Nilotica (Bolty) & Mugil Cephalus (Boury). Paragonimus: microcercous Cercaria Hterophyes: lophocercous Schistosoma: furcocercous Snail (1st I.H.) Ingestion Eggs

2010 / 2011

(operculated except Schistosoma which have a spine)

Mature Heterophyes Schistosoma

Immature Fasciola Paragonimus

Water Encysted metacercaria

(miracidium hatch from the egg except in Heterophyes which is eaten by 1st I.H.)

Cestoda
(1, 2)

Adults in S.I.
All in man except: 2,5 Occasionally in man: 6, 9

(All)

Eggs
(4, 7)

(3, 4, 5) (7, 8)

Grass

Water

Man

Autoinfection
(4, 7)

Trash & bad sanitation

(7, 8)

(5, 6, 9) (3, 4)

Coracidium 1st I.H. 2nd I.H.

I.H.

Ingestion
1: D. latum 6: M. Multiceps 2: D. mansoni & proliferum 3: T. saginata 7: H. nana 8: H. diminuta 4: T. solium 9: D. caninum

5: E. granulosus

Intestinal Nematodes
Lungs
(1, 4, 5)

Intestine
(2, 3, 6, 7, 8)

Adult

(1, 2, 4, 5, 6, 7, 8)

Immature egg

(3)

(1)

Ingestion Larva
(6)

(1, 2, 3)

Mature egg
(7) (4, 5, 6) (8)

Skin penetration

Encysted larva
(4, 5, 6)

(4, 5)

Filariform larva

Rhabditiform larva
4: Ancylostoma duodenale 8: Trichinella spiralis
2010/2011

1: Ascaris lumbricoides 2: Trichuris trichiura 5: Strongyloides stercoralis 6: Trichostrongylus colubriformis

~ XXVI ~

3: Enterobius vermicularis 7: Capillaria philippinensis

Medical Parasitology in tables

Kasr Alainy Students

Infective and diagnostic stages of Protozoa

Protozoon Entamoeba histolytica Balantidium coli Giardia lamblia Cryptosporidium parvum Cyclospora cayetanensis Isospora belli Trichomonas vaginalis Diagnostic stage Cyst or Trophozoite stage Cyst or Trophozoite stage Cyst or Trophozoite stage Oocyst stage Infective stage Quadrinucleate (mature) cyst Cyst stage Cyst stage Both thin & thick-walled Sporulated oocyst Oocyst Diagnostic stages C. parvum Cyclospora Isospora belli T. vaginalis Plasmodium Trophozoite T. gondii Acanthamoeba E. histolytica B. coli Cyst or Trophozoite Giardia lamblia Acanthamoeba Keratitis Ring, trophozoite, schizont & Plasmodium except P. falciparum gametocyte stages Ring & gametocyte P. falciparum stages only Infective stages Entamoeba histolytica (Quadrinucleate (mature)) Cyst Balantidium coli Giardia lamblia Cryptosporidium parvum Cyclospora cayetanensis (Mature) sporulated oocyst Isospora belli Toxoplasma gondii Promastigote Visceral & Cutaneous Leishmania Trichomonas vaginalis Toxoplasma gondii Trophozoite Naegleria fowleri (Amoeboid) Acanthamoeba; (GAE) Short stumpy metacyclic Trypanosoma trypanosomes Plasmodium Sporozoite Babesia Amoeba Acanthamoeba Keratitis

Unsporulated oocyst stage Mature sporulated oocyst Oocyst stage Trophozoite only Sporulated oocyst Trophozoite stage

Amastigote in blood or Visceral Leishmania biopsy and promastigote in culture. African Multi form trypanosomes Trypanosoma American C-shaped trypanosomes Trypanosoma Ring, trophozoite, schizont, gametocyte Plasmodium stages in infected RBCs, but with P. falciparum ring & gametocyte stages only. Babesia Merozoites Cutaneous Amastigote in biopsy and Leishmania Promastigote in culture.

Promastigote stage

Short stumpy metacyclic trypanosomes

Sporozoite stage

Sporozoites Promastigote form Tachyzoite (trophozoite), bradyzoite, tissue cyst, pseudocyst and sporulated oocyst except for Unsporulated oocyst. Amoeboid trophozoite

Toxoplasma gondii Toxoplasma trophozoites

Naegleria fowleri Acanthamoeba; Granulomatous Amoebic Encephalitis (GAE) Acanthamoeba Keratitis Microsporidia

Amoeboid trophozoite

trophozoite form

Trophozoite

Trophozoites & cysts Spore stage

Amoeba The spores

Diagnostic and Infective Stages of Helminthes

Diagnostic Eggs Immature Fasciola Paragonimus D. latum Ascaris lumbricoides Trichuris trichiura Trichostrongylus colubriformis Hookworms Capillaria philippinensis Mature Cestoda Larvae Nematoda Cestoda Eggs Nematoda Infective Larvae Encysted metacercaria: Fasciola, Paragonimus, Heterophyes. Cercaria: Schistosoma. Plerocercoid: D. latum, Spargana. Procercoid: Spargana. Cysticercus: Taenia. Cysticercoid: H. nana, H. diminuta, D. caninum. Filariform larva: Hookworms, Cutaneous larva migrans, Strongyloides, Trichostrongylus. Filiform larva: Wuchereria bancrofti, Brugia malayi. Infective larvae: Loa loa, Onchocerca. Encysted larva: Trichinella. Infective larva: Capillaria, Dracunculus Nematoda Osis (larva, tissues) Man act as I.H. Larviparous (Requires I.H. or vector) I.H. Vector

Heterophyes Schistosoma Taenia Hymenolepis Dipylidium caninum Enterobius vermicularis

Ascaris Capillaria Visceral larva D. mansoni Taenia migrans Echinococcus Strongyloides M. multiceps Trichinella Dracunculus Filariae

Embryonated Ascaris Taenia lumbricoides Echinococcus Embryonated M. multiceps Trichuris H. nana trichiura Enterobius vermicularis

Cestoda Asis (adult, S.I.) Man act as D.H.

Oviparous (Does not require I.H.) Intestinal Extra-intestinal Ascaris D. latum Diphyllobothriasis D. mansoni & proliferum Sparganosis Trichuris Taenia Taeniasis Larva migrans Taenia solium Cysticercosis Enterobius H. nana Hymenolepiasis nana (visceral & Echinococcus granulosus Hydatidosis Trichostrongylus H. diminuta Hymenolepiasis diminuta cutaneous) M. multiceps Coenurosis Hookworms D. caninum Dipylidiasis Strongyloides

Capillaria Trichinella

Dracunculus Filariae

~ XXVII ~

2010/2011

Medical Parasitology in tables

Kasr Alainy Students

Parasites affecting different organs

Organ Trematoda Cestoda D. latum Taenia H. nana H. diminuta D. caninum Nematoda Ascaris Ancylostoma duodenale Trichostrongylus Strongyloides Trichinella Capillaria Enterobius Trichuris Protozoa Arthropods Giardia lamblia Cryptosporidium Isospora Cyclospora Intestinal myiasis Microsporidia Leishmania (in macrophage) Plasmodiunm (in blood vessels) Al amoebae except E. gingivalis Balantidium coli Intestinal myiasis Leishmania P. falciparum Entamoeba histolytica Giardia lamblia Visceral Leishmania ---------- T. cruzi Plasmodium toxoplasma

Small intestine H. heterophyes

Large intestine Schistosoma mansoni

-----------

Liver

Fasciola Schistosoma

Echinococcus granulosus Cysticercus cellulosae

Ascaris Visceral larva migrans

Lungs

Schistosoma Paragonimus

Echinococcus granulosus

Ascaris (larva) Ancylostoma (larva) Strongyloides (larva) Visceral larva migrans M. perstans (pleura) M. ozzardi (pleura) W.bancrofti( tropical pulmonary eosinophilia)

Entamoeba histolytica

-----------

Brain

Eggs act as emboli: Paragonimus Schistosoma

Echinococcus granulosus Cysticercus cellulosae Coenurus cyst

Eye

-----------

Sparganum Cysticercus cellulosae Cysticercus cellulosae Echinococcus granulosus -----------

Heart

Heterophyes: eggs act as emboli -----------

Lymph nodes

Entamoeba histolytica Neglaria Visceral larva migrans Acanthamoeba Strongyloides (disseminated Trypanosoma larva) P. falciparum Toxoplasma gondii Visceral larva migrans Acanthamoeba (Keratitis) Trichinella (larva) T. cruzi (Romanas sign) Loa loa Toxoplasma gondii Onchocerca (retinochoroiditis) Visceral larva migrans T. cruzi amastigotes Trichinella (larva) M. perstans Toxoplasma gondii M. ozzardi Wuchereria bancrofti Trypanosoma Brugia malayi Leishmania O. volvulus Toxoplasma gondii Cutaneous larva migrans Dracunculus Loa loa Onchocerca Trichinella Leishmania African Trypanosome (chancre) T. cruzi (Chagoma) T. cruzi Toxoplasma gondii Trypanosome Leishmania Plasmodium Babesia Trichomonas vaginalis E. histolytica trophozoite (from amoebic lung abscess eroding a bronchus) E. gingivalis trophozoite

-----------

Ocular myiasis Phthirus pubis

-----------

----------Cutaneous myiasis Sarcoptes scabiei Tunga penetrans Demodex folliculorum House dust mites Storage mites -----------

Skin & Subcutaneous tissue Muscles

-----------

Sparganum Cysticercus cellulosae Sparganum Cysticercus cellulosae

-----------

Blood

-----------

Urine

Schistosoma haematobium egg Eggs of: Paragonimus S. haematobium

Wuchereria bancrofti Brugia malayi ----------Loa loa (microfilaria) M. perstans M. ozzardi Enterobius (in females) Hydatid sand from ruptured Urogenital myiasis kidney cyst Wuchereria bancrofti (microfilaria) Ascaris (larva) Hydatid sand from ruptured Ancylostoma (larva) lung cyst Strongyloides (larva)

-----------

Urogenital myiasis

Sputum

-----------

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Medical Parasitology in tables

Kasr Alainy Students

Modes of transmission of parasites

Mode Trematoda Cestoda Taenia solium egg H. nana Echinococcus M. multiceps Sparganum Taenia solium H. nana Echinococcus M. multiceps Nematoda Ascaris Enterobius Trichuris Toxocara (VLM) Trichostrongylus Ascaris Enterobius Trichuris Toxocara (VLM) Trichostrongylus D. medinensis Capillaria Protozoa Amoebae Giardia lamblia B. coli Toxoplasma gondii Cryptosporidium Isospora Cyclospora Potentially pathogenic free-living amoebae arthropods Eggs of flies as Musca causing gastric or intestinal myiasis.

Vegetables

Fasciola

Water

Fasciola Schistosoma

-----------

Undercooked fish Heterophyes Paragonimus Undercooked Fasciola viscera/ muscles Linguatula nymphs

D. latum Sparganum Taenia H. nana Taenia solium

-----------

-----------

Trichinella spiralis Enterobius Strongyloides Capillaria Enterobius -----------

Toxoplasma gondii Entamoeba histolytica Balantidium coli Giardia lamblia Cryptosporidium Isospora Potentially pathogenic free-living amoebae Toxoplasma gondii Plasmodium T. cruzi Leishmania Trypanosome Plasmodium Babesia Cysts

-----------

Auto-infection

-----------

-----------

Inhalation Congenital

---------------------

--------------------D. latum Sparganum H. nana H. diminuta D. caninum -----------

---------------------

Through arthropods

Biological

-----------

D. medinensis All filaria -----------

-----------

Mechanical

Eggs

Blood parasites

Geographical Distribution (in Egypt or not?) All Trematodes are present in Egypt except: Paragonimus westermani, Schistosoma japonicum. All Cestodes are present in Egypt except: D. Latum and D. mansoni. All intestinal Nematodes are present in Egypt except: N. americanus. The only tissue Nematode present in Egypt is Wuchereria bancrofti. All protozoa are present in Egypt except: L.donovani, L. chagasi, L. amazonensis, T. cruzi, P. ovale, P. malariae, P. falciparum, Babesia, L. aethopica & New World Cutaneous Leishmaniasis (NWCL). All arthropods are present in Egypt except: Glossina palpalis & Glossina morsitans & Reduviidae (Winged Bug), Trombiculid mite. Man as definitive host In all Trematodes. In all Cestodes except: E. granulosus, E. multilocularis, M. multiceps and D. mansoni. In all intestinal nematodes except A. caninum, A. braziliense, T. canis, T. cati. In all tissue nematodes. Intermediate host All Trematodes have one I.H. except: Heterophyes, Paragonimus have two I.H. All intestinal Cestodes have one I.H. except D. latum (two I.H.) Nematodes: o Intestinal nematodes: all have NO I.H. except: T. spiralis, C. philippinensis. o Tissue nematodes: all have I.H. Special notes on Trematoda and Cestoda: 1- All are flat worms (Trematoda & Cestoda). 2- All are intestinal except Fasciola & schistosoma which are extra intestinal cestodes. 3- No gravid segment in Pseudophyllidea (D. latum & D. mansoni) because their uterus spell out eggs by its pores. 4- Any worm in small intestine nausea, diarrhea, vomiting & colic. 5- 4 worms have 2nd I.H.: Paragonimus (Crabs, crayfish or shrimps), Heterophys (Tilapia Nilotica (Bolty) & Mugil Cephalus (Boury)), Diphyllobothrium Latum (Salmon) and Diphyllobothrium Mansoni & Proliferum (frogs, snakes, mammals, birds, or man). 6- Intestinal obstruction constipation surgical treatment. 7- All eggs are yellowish brown except: Schistosoma, H. nana, Enterobius, Ancylostoma, Trichostrongylus (translucent).

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2010/2011

Medical Parasitology in tables

Kasr Alainy Students

Clinical presentations caused by helminthes (VERY IMPORTANT TABLE)

Disease Trematoda Cestoda Nematoda Hook worms Ascaris Strongyloides Trichinella Capillaria Protozoa Giardia lamblia Cryptosporium Cyclospora Isospora Intestinal microsporidia Visceral Leishmania Malignant malaria (P. falciparum) Entamoeba histolytica Balantidium coli P. falciparum Visceral Leishmania Amoebae Potentially pathogenic amoeba Trypanosome Visceral Leishmania Plasmodium Babesia Toxoplasma --------------------Plasmodium Babesia Leishmania Trypanosome Amoebae Plasmodium Toxoplasma Amoebae Visceral Leishmania Trypanosome Plasmodium Toxoplasma Visceral Leishmania Trypanosome Plasmodium ----------Arthropods

Diarrhea

Heterophyes

All adult Cestoda

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Dysentery

Schistosoma mansoni

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Trichuris

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Fever

Fasciola Schistosoma

VLM Echinococcus granulosus (if Trichinella ruptured into the blood) Filaria (bancrofti & malayi)

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Anemia

Microcytic Schistosoma hypochromic Macrocytic ----------hyperchromic Normocytic Hypoplastic Jaundice Schistosoma ----------Fasciola Schistosoma

----------D. latum (vit. B12 deficiency) --------------------Echinococcus granulosus

Trichuris Hookworms Trichuris (due to toxic products) --------------------Ascaris Visceral larva migrans (VLM)

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Hepatomegaly

Fasciola Schistosoma

Echinococcus granulosus

VLM

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Splenomegaly

Schistosoma

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----------Hook worms CLM Onchocerca Loa loa Enterobius ----------Trichuris Ascaris Trichuris Trichuris Ancylostoma D. medinensis

----------Sarcoptes scabiei Insect bites House dust mites ----------------------------------------Siphonaptera (Fleas) Acarina (Ticks) Myiasis

Itching

Cercarial dermatitis

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Pruritis ani Haematuria Rectal prolapse Appendicitis

----------Schistosoma haematobium -----------

Taenia saginata --------------------T. saginata E. vermicularis

----------Plasmodium E. histolytica B. coli E. histolytica B. coli Cutaneous Leishmania Acanthamoeba Microsporidia

Ulcer

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Best wishes: Your friends & Drs.

~ XXX ~

2010/2011