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Parasites by Mind Map: Parasites

1. TREMATODES

1.1. Blood

1.1.1. S. hematobium

1.1.1.1. Morphology

1.1.1.1.1. Egg

1.1.1.1.2. Adult male

1.1.1.1.3. Adult female

1.1.1.2. Transmission

1.1.1.2.1. Penetration of the skin

1.1.1.3. Habitat

1.1.1.3.1. Adult worm is found in vesical (bladder) venous plexus of Humans

1.1.1.4. Life cycle

1.1.1.4.1. Definitive host

1.1.1.4.2. Intermediate host

1.1.1.5. Clinical Features

1.1.1.5.1. dermatitis with papular, pruritic rash

1.1.1.5.2. Toxic metabolites from growing schistosomes can cause :

1.1.1.5.3. Eggs in bladder: can cause dysuria (difficulty in passing urine)

1.1.1.5.4. Genital disease is present in about 1/3rd of infected women vulvar and perineal disease, including ulcerative, fistulous, or wart-like lesions.

1.1.1.6. Lab diagnosis

1.1.1.6.1. Blood: Eosinophilia, anaemia, Hypoalbuminemia, high urea/ creatinin

1.1.1.6.2. Urine Examination: Centrifuged deposit shows eggs with terminal spine, RBCs.

1.1.1.6.3. Biopsy of Vesical mucosa: Granulomatous lesions around eggs.

1.1.1.6.4. X ray: to picture calcified eggs, strictures or dilatations of kidney, ureters & bladder

1.1.1.6.5. Immunological tests: ELISA, IHA -

1.1.1.7. TREATMENT

1.1.1.7.1. Praziquantel (Biltricide)

1.1.1.7.2. Oxamniquine (Vansil)

1.1.1.7.3. Metrofonate (Bilarcil)

1.1.2. S. mansoni

1.1.2.1. Morphology

1.1.2.1.1. EGG

1.1.2.1.2. ADULT

1.1.2.2. TRANSMISSION

1.1.2.2.1. penetration of the host skin.

1.1.2.3. HABITAT

1.1.2.3.1. smaller branches of the inferior mesenteric vein in the region of the lower colon.

1.1.2.4. Life cycle

1.1.2.4.1. Invective stage

1.1.2.4.2. Diagnostic stages

1.1.2.4.3. Intermediate hosts

1.1.2.5. Disease caused

1.1.2.5.1. Intestinal bilharziasis or Schistosomal dysentery or Snail fever

1.1.2.6. Commonest symptoms

1.1.2.6.1. Dysentery (diarrhoea and blood in stool)

1.1.2.6.2. Ectopic lesions in other parts of the body can be seen in

1.1.2.6.3. Clinical features

1.1.2.7. Lab diagnosis

1.1.2.7.1. Blood: Eosinophilia

1.1.2.7.2. Stool examination: for eggs of Schistosoma mansoni with a lateral spine

1.1.2.7.3. Biopsy: microscopic examination of the wall of the rectal tissue

1.1.2.7.4. Immunological test: antigen detection is better than antibody detection. ELISA (soluble egg antigen), Rapid Dip Stick tests, Immunoblots, IHA,

1.1.2.8. Treatment

1.1.2.8.1. Oxamniquine

1.1.2.8.2. Praziquantel

1.1.3. S. japonicum

1.2. Liver

1.2.1. F. hepatica & F. gigantica

1.2.1.1. Morphology

1.2.1.1.1. Egg

1.2.1.1.2. Adult

1.2.1.2. TRANSMISSION

1.2.1.2.1. eating plants containing an encysted metacercaria.

1.2.1.2.2. A pharyngeal form of the disease could be transmitted through eating raw liver infected with the adult worms.

1.2.1.3. Habitat

1.2.1.3.1. biliary passages of the liver of human

1.2.1.4. Life cycle

1.2.1.4.1. Life cycle of both F. hepatica and gigantica is similar however; the snail intermediate host is varied.

1.2.1.5. DISEASE

1.2.1.5.1. hepatobiliary disease with gastrointestinal disturbance

1.2.1.5.2. Massive infection with these worms could cause portal cirrhosis with all its manifestations

1.2.1.6. CLINICAL PICTURE

1.2.1.6.1. Fever, chills, right hypochondrial pain, tenderness, jaundice, and high esinophilia.

1.2.1.6.2. Chronic cholangitis with biliary obstruction could be suffered in long standing fascioliasis

1.2.1.6.3. Pharyngeal disease of fascioliasis could be seen when the patients eat raw infected liver. This is called Halzoun; young adult worms attach themselves to the pharyngeal mucosa causing pain, bleeding, edema and may be suffocation.

1.2.1.7. Diagnostic procedures

1.2.1.7.1. Laboratory

1.2.1.7.2. Immunological

1.2.1.7.3. Investigation

1.2.1.8. TREATMENT

1.2.1.8.1. Bithionol

1.2.1.8.2. Praziquantel

1.2.1.8.3. Triclabendazole

1.3. Intistine

1.3.1. Heterophyes h.

1.3.1.1. Morphology

1.3.1.1.1. Egg

1.3.1.1.2. Adult

1.3.1.2. Transmission

1.3.1.2.1. transmitted through eating undercooked or poorly salted fish infected with encysted metacercaria under the fish scales or in their flesh.

1.3.1.3. Habitat

1.3.1.3.1. small intestine

1.3.1.3.2. Sometimes it inhabits the biliary passages.

1.3.1.4. LIFE CYCLE

1.3.1.4.1. Infective stage: encysted metacercaria.

1.3.1.4.2. Diagnostic stage: eggs containing fully mature miracidium.

1.3.1.4.3. Intermediate host: the 1st is fresh water snail (Pirenella conica); the 2nd is fresh water fish.

1.3.1.4.4. Final host: fish eating animals and human.

1.3.1.4.5. Reservoir host: fish eating animals.

1.3.1.5. DISEASE

1.3.1.5.1. enteritis, indigestion and biliary problems.

1.3.1.6. CLINICAL PICTURE

1.3.1.6.1. Light infection usually passed unnoticed.

1.3.1.6.2. Heavy infection with Heterophyes is associated with:

1.3.1.7. DIAGNOSTIC PROCEDURES

1.3.1.7.1. detection of the characteristic eggs in the stool of the patients.

1.3.1.8. TREATMENT

1.3.1.8.1. Praziquantel (Biltricide)

1.3.1.8.2. Tetrachloroethylene

2. CESTODES

2.1. Intestinal

2.1.1. Taenia saginata & Taenia solium

2.1.1.1. Morphology

2.1.1.1.1. Egg

2.1.1.1.2. Adult

2.1.1.2. Transmission

2.1.1.2.1. Ingestion of infected meat carrying cysticerci

2.1.1.2.2. T. solium can also accidentally cause larval tissue infections in man. This is called as “Cysticercosis” Mode of infection: Ingestion of eggs

2.1.1.3. Habitat

2.1.1.3.1. Intestine

2.1.1.3.2. Tissue

2.1.1.4. Clinical Features:

2.1.1.4.1. INTESTINAL Infection (Taeniasis): (infection with adult tape worms) With few worms patient may be asymptomatic.If symptomatic common clinical features are: abdominal discomfort, hunger pain, loss of weight, chronic indigestion. Nausea, Vomiting, headache and diarrhea.Complications can be: Intestinal obstruction, appendicitis, cholangitis.

2.1.1.4.2. CYSTICERCOSIS: (infection with larvae/cysticerci) Incubation Period: 15 days to years after infection.

2.1.1.4.3. Neurocysticercosis

2.1.1.4.4. Larval cystic lesions

2.1.1.5. Lab diagnosis

2.1.1.5.1. TAENIASIS

2.1.1.5.2. CYSTICERCOSIS

2.1.1.6. TREATMENT

2.1.1.6.1. TAENIASIS: anthelmintic therapy usually suffices.

2.1.1.6.2. CYSTICERCOSIS: anthelmintic therapy is chosen, albendazole, praziquante, glucocorticosteroids and surgery.

2.1.2. Hymenolepis nana

2.1.2.1. Morphology

2.1.2.1.1. Egg

2.1.2.1.2. Adult

2.1.2.2. TRANSMISSION

2.1.2.2.1. Ingestion of the eggs

2.1.2.2.2. Ingestion of the infected arthropods.

2.1.2.2.3. Internal autoinfection.

2.1.2.3. HABITAT

2.1.2.3.1. small intestine

2.1.2.4. LIFE CYCLE

2.1.2.4.1. Infective stage: eggs.

2.1.2.4.2. Diagnostic stage: eggs

2.1.2.4.3. Intermediate host: no intermediate host (accidentally beetles and fleas may act as intermediate hosts)

2.1.2.4.4. Final host: man.

2.1.2.5. DISEASE

2.1.2.5.1. dwarf tapeworm infection.

2.1.2.6. CLINICAL PICTURE

2.1.2.6.1. H. nana adult worm infection is asymptomatic especially in light infection. Heavy infection is associated with abdominal pain, diarrhea, headache and anorexia.

2.1.2.6.2. IMMUNE RESPONSE: 1. Experimental evidence on mice suggests a certain degree of immunity to reinfection with H. nana in the same host. 2. In immunocompromized host the process of internal autoinfection with heavy infection is demonstrated.

2.1.2.7. DIAGNOSTIC PROCEDURES

2.1.2.7.1. Diagnosis of H. nana is done by detection of the characteristic eggs in the stool of the infected patient. The presence of the polar filaments is diagnostic.

2.1.2.8. TREATMENT

2.1.2.8.1. Niclosamide (Niclocide)

2.1.2.8.2. Praziquantel

2.2. Tissue

2.2.1. Echinococcus granulosus.

2.2.1.1. Morphological forms

2.2.1.1.1. Adult stage (sexual stage):

2.2.1.1.2. Egg:

2.2.1.1.3. Hydatid cyst (Larval stage or asexual stage):

2.2.1.2. Mode of Transmission

2.2.1.2.1. Definitive host: Dog (and other canines) are infected after eating infected meat of sheep and other herbivores carrying hydatid cyst (Larval stage)

2.2.1.2.2. Intermediate host: Herbivores such as sheep are infected by accidentally ingesting eggs of E. granulosus along with grass. Man is also infected by ingesting food or water contaminated with parasite eggs.

2.2.1.3. Habitat

2.2.1.3.1. Adult worm inhabits the small intestine of canine animals e.g. dogs, foxes, wolves, jackals

2.2.1.3.2. Hydatid cyst (larval stage) in humans and in herbivores (sheep, goat, pig, cattle, camel and deer) localizes mainly in liver, lungs, spleen and CNS. Sometimes in bones.

2.2.1.4. Clinical Features

2.2.1.4.1. E. granulosus causes unilocular hydatid cyst Patients are usually asymptomatic mostly. Silent or latent cysts.

2.2.1.4.2. Symptoms depend on site of cyst Commonly Lungs, liver, spleen

2.2.1.5. Diagnostic procedures

2.2.1.5.1. Casoni’s test: hypersensitivity test: (Intradermal injection of 0.2ml hydatid fluid on left forearm): Wheal formation occurs in positive cases in few hours: >5 cm diameter reaction is considered positive.

2.2.1.5.2. Demonstration of the hydatid cysts: on USG, X ray (in bones), CT scan, MRI

2.2.1.5.3. Serological Assays: ELISA, CF, IFA, IHA (Cross reactions have been noted between cysticercosis and hydatid disease)

2.2.1.5.4. a combination of assays including immunoblot and ELISA has been suggested Aspiration of the hydatid fluid and detection of the hydatid sand is also diagnostic (although it is not recommended because of anaphylactic risk)

2.2.1.6. Prevention & Control

2.2.1.6.1. Good sanitary practices are essential in prevention

2.2.1.6.2. Anti-helminthic treatment of dogs

2.2.1.6.3. Avoidance of ingestion of sheep viscera by dogs

3. NEMATODES

3.1. SMALL INTESTINAL

3.1.1. Ascaris lumbricoides

3.1.1.1. Morphology

3.1.1.1.1. Unfertilized Egg

3.1.1.1.2. Fertilized Egg

3.1.1.1.3. Adult Male

3.1.1.1.4. Adult Female

3.1.1.2. Transmission

3.1.1.2.1. Ingestion of fertilized embryonated eggs with uncooked vegetables (especially from gardens or farms where human stool is used as fertilizer) or contaminated drinking water. Flies and paper money may rarely disseminate embryonated eggs.

3.1.1.3. Habitat

3.1.1.3.1. Adult worms inhabit the small intestine (jejunum & ileum)

3.1.1.4. disease

3.1.1.4.1. Ascariasis

3.1.1.5. Clinical features

3.1.1.5.1. Symptoms are related to the worm burden

3.1.1.6. Diagnosis

3.1.1.6.1. Blood picture: Eosinophilia especially during the migratory phase

3.1.1.6.2. Stool Examination: Characteristic Eggs/worms can be observed

3.1.1.6.3. Radiological: USG can show the adult worm sin intestine

3.1.1.6.4. Immunological tests: ELISA, CFT

3.1.1.6.5. Endoscopy: adult worms can be seen in the small intestine

3.1.1.7. Treatment

3.1.1.7.1. Mebendazole

3.1.1.7.2. Albendazole

3.1.1.7.3. Surgical treatment: may be required in hyper-infected cases for removal of blockage produced from worms

3.1.2. Ankylostoma duodenale

3.1.2.1. Morphology

3.1.2.1.1. Eggs

3.1.2.1.2. Adult Male

3.1.2.1.3. Adult Female

3.1.2.1.4. Rhabditiform larvae

3.1.2.1.5. Filariform larvae

3.1.2.2. Transmission

3.1.2.2.1. Penetration of the human skin, usually that of the foot.

3.1.2.3. Habitat

3.1.2.3.1. Adult worms live in the small intestine of Man (Jejunum mainly)

3.1.2.4. Life Cycle

3.1.2.4.1. Definitive host: Man (only 1 host is required)

3.1.2.4.2. diagnostic stage : Eggs in stool

3.1.2.5. Clinical features

3.1.2.5.1. Ground itch: develops at the site of entry of filariform larvae. Disappears in 1-2 weeks

3.1.2.5.2. Creeping eruption: cutaneous larva migrans: Marking on the skin due to the migration of filariform larvae through the skin at rate of 1-2cms/day

3.1.2.5.3. Bronchitis / bronchopneumonia: due to moulting and migration of larvae through the lungs

3.1.2.5.4. Chronic blood loss (0.03-0.2 ml/day/worm)

3.1.2.5.5. Anemia (Hypochromic-microcytic): Hb less than 10mg% Nutritional defects: Iron, vitamin B12, Folic acid

3.1.2.5.6. Gastric acidity/ dyspepsia In heavy infestations (which may involve more than 500 larvae

3.1.2.5.7. general symptoms include pallor of the skin and mucous membranes, fluid retention in the face and extremities, constipation alternating with diarrhea, abdominal tenderness, increased appetite for strange substances (e.g., clay), delayed puberty and stunted growth in young, fatigue, dullness, and apathy.

3.1.2.6. Diagnostic procedures

3.1.2.6.1. Blood picture: Anaemia

3.1.2.6.2. Stool examination: characteristic eggs. and live worms at times.

3.1.2.6.3. Endoscopy: duodenum

3.1.2.6.4. Immunology: ELISA, CFT

3.1.2.7. Treatment

3.1.2.7.1. Mebendazole

3.1.2.7.2. Albendazole

3.2. LARGE INTESTINAL

3.2.1. Enterobius vermicularis

3.2.1.1. Morphology

3.2.1.1.1. Egg

3.2.1.1.2. Adult Male

3.2.1.1.3. Adult Female

3.2.1.2. TRANSMISSION

3.2.1.2.1. Oxyuriasis is transmitted through oral route ( hand to mouth), insect ( house fly), contaminated food and beverages, and through autoinfection. Familial spread is very common.

3.2.1.3. HABITAT

3.2.1.3.1. Caecum and the adjacent portions of the large intestine

3.2.1.4. LIFE CYCLE

3.2.1.4.1. Infection with E. vermicularis takes place by three ways

3.2.1.4.2. Infective stage: fully embyronated egg

3.2.1.4.3. Diagnostic stage: eggs or sometimes the adult worms in the stool

3.2.1.5. DISEASE

3.2.1.5.1. Oxyuriasis (enterobiasis)

3.2.1.6. CLINICAL PICTURE

3.2.1.6.1. Generally, oxyuriasis is a symptomatic infection however, the following symptoms are diagnostic:

3.2.1.7. DIAGNOSTIC PROCEDURES

3.2.1.7.1. Laboratory

3.2.1.8. TREATMENT

3.2.1.8.1. Pyrantel pamoate

3.2.1.8.2. Mebendazole (Vermox)

3.2.2. Trichuris trichiura

3.2.2.1. Morphology

3.2.2.1.1. Egg

3.2.2.1.2. Adult Male

3.2.2.1.3. Adult Female

3.2.2.2. TRANSMISSION

3.2.2.2.1. Feco-oral transmission

3.2.2.3. HABITAT

3.2.2.3.1. Large intestine

3.2.2.4. LIFE CYCLE

3.2.2.4.1. Infective stage: fully embyronated eggs

3.2.2.4.2. Diagnostic stage: characteristic barrel shaped eggs

3.2.2.5. DISEASE

3.2.2.5.1. Trichuriasis

3.2.2.6. CLINICAL PICTURE

3.2.2.6.1. Light T. trichiura infection usually is asymptomatic

3.2.2.6.2. Heavy T. trichiura infection is characterized by:

3.2.2.6.3. IMMUNE RESPONSE

3.2.2.7. DIAGNOSTIC PROCEDURES

3.2.2.7.1. Laboratory

3.2.2.8. TREATMENT

3.2.2.8.1. Mebendazole (Vermox)

3.2.2.8.2. Loperamide (Imodium)

3.3. TISSUES

3.3.1. Wuchereria bancrofti

3.3.1.1. Morphology

3.3.1.1.1. Larvae (microfilaria):

3.3.1.1.2. Adult Male

3.3.1.1.3. Adult Female

3.3.1.2. TRANSMISSION

3.3.1.2.1. infected female mosquito carrying a stage 3 (L3) larvae bites a human

3.3.1.3. Habitat

3.3.1.3.1. Adult worms live in the lymphatics and lymph nodes of human body. Microfilaria can be found in blood after they move out of the lymphatics.

3.3.1.4. Life cycle

3.3.1.4.1. infective stage : L3 stage larvae

3.3.1.4.2. intermediate host : Mosquito

3.3.1.4.3. definitive host : human

3.3.1.5. Disease caused

3.3.1.5.1. Filaria

3.3.1.6. Clinical features

3.3.1.6.1. Inflammatory phase:

3.3.1.6.2. Obstructive Phase:

3.3.1.7. Diagnosis

3.3.1.7.1. Collection of blood at night as the microfilariae are periodic and appear in blood during night time (between 10pm and 4am) or 1 hour after giving DEC drug: if we wish to collect the blood in the day time. (DEC challenge test) .

3.3.1.8. Treatment

3.3.1.8.1. DEC: Diethylcarbamazine

3.3.1.8.2. Ivermectin

3.3.1.8.3. Surgical treatment has to be undertaken in cases with huge deformities

3.3.2. Dracunculus medinensis

3.3.2.1. Morphology

3.3.2.1.1. Adult Female

3.3.2.1.2. Rhabditiform larva

3.3.2.1.3. Adult Male

3.3.2.2. TRANSMISSION

3.3.2.2.1. drinking water contaminated with infected copepods (Cyclops).

3.3.2.3. HABITAT

3.3.2.3.1. Adult female D. medinensis inhabits the subcutaneous tissues particularly that of the lower limb, while its rhabditiform larva infest Cyclops.

3.3.2.4. LIFE CYCLE

3.3.2.4.1. Infective stage: rhabditiform larvae after 21 days in the Cyclops.

3.3.2.4.2. Diagnostic stage: rhabditiform larvae or the worm in its position.

3.3.2.4.3. Intermediate host(s): Cyclops.

3.3.2.4.4. Final host: man.

3.3.2.4.5. Reservoir host: infected host.

3.3.2.5. CLINICAL PICTURE

3.3.2.5.1. Onset of fever, urticaria, itching, allergic manifestations e.g. asthma or periorbital edema in the allergic patients. There is a relief of symptoms after the blister is ruptured. Worms is detected under the skin with serpentine pattern

3.3.2.6. IMMUNE RESPONSE

3.3.2.6.1. The main immune reaction against medina worm infection is a Localized cellular immune reaction to limit the infection, together with increased IgE level in the serum.

3.3.2.7. DIAGNOSTIC PROCEDURES

3.3.2.7.1. Diagnosis is typically based on clinical manifestations. In endemic areas the characteristic worm’ containing lesion is easily recognizable

3.3.2.7.2. The worm can be stimulated to discharge larvae by submerging the ulcer with water.

3.3.2.7.3. Plain x-ray may demonstrate the calcified dead worms in the subcutaneous tissues.

3.3.2.8. TREATMENT

3.3.2.8.1. Niridazole (Amblihar)

3.3.2.8.2. Metronidazole

3.3.2.8.3. Thiabendazole

3.3.3. Onchocerca volvulus

3.3.3.1. Microfilaria

3.3.3.1.1. 280-330 x 6-9 µm unsheathed body head is characteristically expanded cuticle is striated head and tail are free of nuclei cephalic space (1.5-2:1) they have no periodicity

3.3.3.2. Adult Male

3.3.3.2.1. 20-40 x 0.15-0.2 mm variable number of anal papillae and 2 spicules threadlike filarial worm both ends of the body are tapered the anterior end has 2 circles of 4 papillae and 1 large lateral pair cuticle has characteristic annular thickening (rugae)

3.3.3.3. Adult Female

3.3.3.3.1. 300-500 x 0.25-0.4 mm vulval opening at .85 mm from the anterior end threadlike filarial worm both ends of the body are tapered the anterior end has 2 circles of 4 papillae and 1 large lateral pair cuticle has characteristic annular thickening (rugae)

3.3.3.4. TRANSMISSION

3.3.3.4.1. O.volvulus is spread through the bite of the blackfly (buffalo giant) which breeds in fast-flowing rivers, streams and the lands along the river bank.

3.3.3.5. HABITAT

3.3.3.5.1. Adults: Inhabit the subcutaneous tissue (nodule) especially at the junction of the bones, scalp, pelvis, chest and spine. Microfilariae: : Inhabit the skin/ eye

3.3.3.6. LIFE CYCLE

3.3.3.6.1. Infective stage: infective microfilariae inside the vector

3.3.3.6.2. Diagnostic stage: microfilarae in skin snip

3.3.3.6.3. Intermediate host(s): Simulium spp.,

3.3.3.6.4. Reservoir host: infected persons

3.3.3.7. DISEASE

3.3.3.7.1. Onchocerciasis includes two diseases:

3.3.3.8. CLINICAL PICTURE

3.3.3.8.1. The clinical manifestations and complications are mainly due to the microfilarae and not the worms

3.3.3.9. DIAGNOSTIC PROCEDURES

3.3.3.9.1. Laboratory

3.3.3.9.2. Immunological: Detection of the specific antibodies using ELISA & IHA

3.3.3.10. TREATMENT

3.3.3.10.1. Ivermectin (The drug of choice)

3.3.3.10.2. Diethycarbamazine (DEC) (Hetrazan