BIO258 Parasitology - NEMATODA .pdf

MEDICALLY IMPORTANT METAZOAN HELMINTHS Phylum Nemathelminthes: Class Nematoda 1 Ascaris lumbricoides 2 Trichuris trichiura 3 Strongyloides stercoralis 4 Hookworms 5 Enterobius vermicularis 6 Trichinella spiralis 7 Capillaria philippin...

MEDICALLY IMPORTANT METAZOAN HELMINTHS Phylum Nemathelminthes: Class Nematoda 1 Ascaris lumbricoides 2 Trichuris trichiura 3 Strongyloides stercoralis 4 Hookworms 5 Enterobius vermicularis 6 Trichinella spiralis 7 Capillaria philippinensis PHYLUM NEMATHELMINTHES also known as roundworms nematos = thread; helminths = worm 1 Ascaris lumbricoides BACKGROUND primary species involved in human infections globally ○ A. suum – ascaris from pigs; can also 1. Adult worms live in lumen of small intestine infect humans females produce 200,000 eggs per day causes Ascariasis passed to feces known as Giant Roundworm 2. Unfertilized eggs may be ingested; not infective infective stage: L3 larvae 3. After 18 days to several weeks, L3 larvae diagnostic stage: fertilized and unfertilized eggs develop from fertile eggs natural infections sometimes occur in monkeys depending on environmental conditions and apes optimum: moist, warm, shaded soil Ascaris spp. eggs may be found in dog feces 4. Ingestion of embryonated eggs ○ does not indicate true infection 5. Larvae hatch ○ indicates passage of eggs through invade intestinal mucosa (intestine) → coprophagy carry via portal circulation → systemic eating of feces circulation → lungs Ascaris spp. eggs require weeks in the 6. Larvae mature further in lungs environment to develop to an infective stage 10 to 14 days ○ infectious eggs are not likely to be penetrate alveolar walls → ascend encountered in clinical specimens bronchial tree → throat and swallowed 7. Re-enters small intestine MORPHOLOGY develop into adult worms very large nematodes that parasitize human 2-3 months – ingestion of infective intestine eggs to oviposition by adult female ○ adult female: 20-35 cm adult worms can live 1-2 years ○ adult males: 15-30 cm A. lumbricoides fertilized eggs CLINICAL PRESENTATION ○ rounded, thick shell with an external adult worms cause no acute symptoms mammillated layer that is often stained heavy infections by brown bile ○ in children: stunted growth via ○ decorticated eggs: outer layer is absent malnutrition ○ 45 to 75 μm in length ○ abdominal pain A. lumbricoides unfertilized eggs ○ intestinal obstruction ○ elongated, larger than fertile eggs, shell ○ potential perforation (high intensity) is thinner and mammillated layer is migrating adult worms variable ○ symptomatic occlusion of biliary tract with large protuberances or obstruction; loss of appetite, practically none vomiting, nausea ○ 90 μm in length ○ appendicitis ○ contain mainly a mass of refractile ○ nasopharyngeal expulsion granules esp. single female worm A. lumbricoides adult infections ○ females: straight tail DIAGNOSIS ○ males: curved tail microscopic identification of A. lumbricoides ○ possess three lips at anterior end of eggs in stool body ○ collect stool specimen LIFE CYCLE ○ preserve in fixative ○ concentrate using formalin-ethyl acetate sedimentation technique ○ examine wet mount of sediment direct wet mount examination: when concentration procedures are not available for quantitative assessments of infection ○ Kato-Katz ○ quantitative fecal flotation larvae can be identified: ○ sputum  ○ gastric aspirate during pulmonary migration phase adult worms are occasionally passed in: ○ stool ○ mouth or nose adult worms are recognizable by macroscopic characteristics (e.g. presence of three lips) molecular methods for detection of worm/egg DNA in human stools are used in research setting TREATMENT DRUG DOSAGE Albendazole* 400mg orally once; take w/ food 100mg orally 2x daily for 3 days or Mebendazole 500mg orally once 150-200mcg/kg orally once; take w/ Ivermectin water on empty stomach *not FDA approved 2 Trichuris trichiuria BACKGROUND 1. Unembryonated eggs are passed in stool known as Human Whipworm 2. 2-cell stage eggs develop in soil causes Trichuriasis 3. Advanced cleavage stage third most common roundworm of humans 4. Embryonate infections frequent in: eggs become infective 15 to 30 days ○ areas with tropical weather ingested through soil contaminated ○ poor sanitation practices hands or food ○ children 5. Eggs hatch in the small intestines 800 million people infected worldwide ○ release larvae that mature and establish ○ occurs in South United States in the colon reside in large intestine, cecum, appendix 6. Adult worms live in cecum and ascending colon infective stage: embryonated eggs ○ worms are fixated in this location diagnostic stage: unembryonated eggs ○ anterior portions threaded into mucosa ○ females oviposit 60 to 70 days after MORPHOLOGY infection T. trichiura eggs ○ females in cecum shed 3,000 to 20,000 ○ 50-55 μm by 20-25 μm eggs per day ○ barrel shaped, thick shelled ○ life span: 1 year ○ possess polar plugs at each end T. trichiura adults CLINICAL PRESENTATION ○ long, whip-like anterior end freq. asymptomatic ○ males: heavy infections (esp. in children) 30-45 mm long ○ gastrointestinal problems coiled posterior end abdominal pain ○ females: diarrhea 35-50 mm rectal prolapse straight posterior end ○ growth retardation LIFE CYCLE DIAGNOSIS microscopic identification of whipworm eggs in stool eggs are difficult to find in light infections, concentration procedure is recommended quantification with Kato Katz technique examination of rectal mucosa by proctoscopy ○ during renal relapse TREATMENT DRUG DOSAGE 400mg orally once daily for 3 days; Albendazole* take w/ food Mebendazole 100mg orally 2x daily for 3 days 200mcg/kg/day orally for 3 days; Ivermectin* take w/ water on empty stomach *not FDA approved 3 Strongyloides stercoralis BACKGROUND  known as Threadworms 5. Rhabditiform larvae develop into infective causes Strongyloidiasis filariform or L3 larvae rhabditid nematode 6. Filariform larvae penetrate human host skin to rarer human-infecting species = zoonotic initiate parasitic cycle ○ S. fuelleborni subsp. fuelleborni second generation filariform larvae ○ S. fuelleborni subsp. kellyi cannot mature into free-living adults animal-associated ○ must find new host to continue ○ S. myopotami (nutria) cycle ○ S. procyonis (racoons) ○ may produce mild short-lived cutaneous Parasitic cycle infections in human hosts (larva 6. Filariform larvae in contaminated soil penetrate currens, “nutria itch”) human skin during soil contact ○ does not cause true strongyloidiasis 7. Migration to the small intestine via different infective stage: Filariform (L3) stage routes: diagnostic stage: Rhabditiform (L1) stage L3 migrate via bloodstream and host specific, human parasite lymphatics → lungs → coughed up → detected in primates swallowed ○ chimpanzees through abdominal viscera or ○ monkeys connective tissue ○ dogs 8. In small intestine, larvae molt twice and become ○ cats (experimentally susceptible, adult female worms unknown if they have role as natural 9. Females live embedded in submucosa of small reservoir) intestine S. fuelleborni subsp. fuelleborni produce eggs via parthenogenesis ○ parasite of apes, monkeys which yield rhabditiform larvae S. fuelleborni subsp. kellyi 1. Rhabditiform larvae can be passed in stool ○ humans only (identified host) 10. Can cause autoinfection broadly distributed in tropical and subtropical areas Autoinfection transmission during summer months in rhabditiform larvae in gut become infective temperate areas filariform larvae that can penetrate either infections common in: intestinal mucosa of skin of perianal area ○ areas with poor sanitation once filariform larvae reinfect the host, they are ○ rural and remote communities carried to lungs, pharynx, and small intestine, or ○ institutional settings disseminate throughout body ○ among socially marginalized groups untreated cases can result in persistent infection ○ even after many decades of residence in MORPHOLOGY a non-endemic area ○ contribute to the development of hyperinfection syndrome LIFE CYCLE impossible with S. fuelleborni alternates between free-living and parasitic cycles; also involves autoinfection CLINICAL PRESENTATION initial sign of acute strongyloidiasis ○ localized pruritic, erythematous rash at site of skin penetration larvae migration (lungs to trachea): ○ tracheal irritation ○ dry cough larvae swallowed in gastrointestinal tract: ○ diarrhea ○ constipation ○ abdominal pain ○ anorexia chronic strongyloidiasis ○ asymptomatic ○ gastrointestinal and cutaneous manifestations may occur ○ rarely developed complications: arthritis cardiac arrhythmias Free living cycle chronic malabsorption 1. Rhabditiform larvae are passed in stool of duodenal obstruction infected definitive host nephrotic syndrome 2. Develop into either: recurrent asthma infective filariform larvae (direct ○ 75% have mild peripheral eosinophilia or development) elevated IgE levels free living adult males and females ○ mate and produce eggs DIAGNOSIS 3. Eggs are produced by fertilized female worms microscopic identification of Strongyloides 4. Rhabditiform larvae hatch from embryonated stercoralis larvae (rhabditiform and occasionally eggs filariform) in: ○ stool  ○ duodenal fluid ○ urticarial dermal reaction (“ground itch”) ○ biopsy specimens larval pulmonary migration ○ possibly sputum in disseminated ○ respiratory involvement including infections eosinophilic pneumonia Antibody Detection ○ second urticarial rash Molecular Detection vague gastrointestinal disturbances and eosinophilia (Wakana syndrome) following 5 Hookworms peroral infection BACKGROUND DIAGNOSIS Intestinal hookworm disease in humans is microscopic identification of hookworm eggs in caused by: stool ○ Ancylostoma duodenale, A. ceylanicum, ○ collect stool specimen and Necator americanus ○ preserve in fixative ○ concentrate using formalin-ethyl LIFE CYCLE acetate sedimentation technique ○ examine wet mount of sediment direct wet mount examination: when concentration procedures are not available for quantitative assessments of infection ○ Kato-Katz ○ FLOTAC ○ mini FLOTAC 5 Enterobius vermicularis BACKGROUND “human pinworm” due to female’s long, pointed tail; also called “threadworm” or “seatworm” another pinworm species: E. gregorii ○ reports from Europe, Africa, and Asia ○ immature form of E. vermicularis rat pinworm: Syphacia obvelata 1. Eggs are passed in the stool causes Enterobiasis under favorable conditions (moisture, Infective Stage: Embryonated eggs warmth, shade), Diagnostic Stage: Eggs in perianal folds; Adult 2. Larvae hatch in 1 to 2 days and become worms if grossly found in perianal area (during free-living in contaminated soil anorectal exam.) released rhabditiform larvae grow in the Humans only host feces and/or the soil ○ sometimes captive chimpanzees 3. Development to infective filariform larva occurs usually in school or pre-school children after 5 to 10 days (and two molts) and crowded envi. infective larvae can survive 3 to 4 weeks in favorable environmental conditions MORPHOLOGY Eggs: 4. Filariform penetrates skin ○ 50-60um x 20-30um larvae penetrate the skin → blood ○ transparent, elongate to oval shape vessels to the heart → lungs ○ slightly flattened on one side ○ penetrate into the pulmonary Adult worms: alveoli, ascend the bronchial ○ both have cephalic expansion tree to the pharynx, and are ○ Males: swallowed 2.5mm long x 0.1-0.2mm wide 5. larvae reach the jejunum of the small intestine blunt posterior end w/ single reside and mature into adults spicule Adult worms live in the lumen of the ○ Females: small intestine, typically the distal 8-13mm long x 0.3-0.5mm wide jejunum, where they attach to the long pointed tail intestinal wall with resultant blood loss by the host LIFE CYCLE most adult worms are eliminated in 1 to 2 years CLINICAL PRESENTATION asymptomatic attachment of hookworm to intestinal walls: ○ abdominal pain, nausea, anorexia heavy infections ○ iron deficiency anemia ○ Occult blood in the stool severe cases ○ protein malnutrition from chronic plasma protein loss filariform larvae penetration  6 Trichinella spiralis BACKGROUND “pork worm” found worldwide in many carnivorous and omnivorous animals other T. spp.: ○ T. pseudospiralis (mammals and birds) ○ T. nativa (Arctic bears) ○ T. nelsoni (African predators and scavengers) ○ T. britovi (carnivores of Europe and western Asia) ○ T. papuae (wild and domestic pics in Papua New Guinea and Thailand) Infective Stage: encysted larvae in undercooked meat Diagnostic Stage: encysted larvae in muscle tissue biopsy 1. Gravid (pregnant) adult female deposit eggs on perianal folds 2. Infection via self-inoculation (transfer of eggs to mouth w/ hands that have scratched perianal area) or exposure to eggs in environment 3. Larvae hatch in small intestine 4. Adults settle in colon (in cecum) 5. Gravid females migrate nocturnally outside anus and oviposits while crawling on skin of perianal area ○ 1 month: from ingestion of eggs to female’s oviposition (lay eggs) ○ At full maturity: i. Females: 8-13 mm ii. Males: 2-5mm ○ Life span: 2 months 6. [back to 1]: ○ 4-6 hours: larvae in eggs develop; eggs become infective CLINICAL PRESENTATION freq. asymptomatic perianal pruritus at night; leads to: 1. Ingestion of undercooked meat containing ○ excoriations (scraped and abraded skin) encysted larvae ○ bacterial superinfection (second 2. Larvae released from cyst after exposure to infection or reinfection w microbial gastric acid and pepsin agent) 3. Invade small bowel mucosa and develop into vulvovaginitis (inflammation/irritation of vagina adults or vulva) Females: 2.2mm pelvic or peritoneal granulomas Males: 1.2mm teeth grinding, enuresia (bed-wetting), Life span: 4 weeks insomnia, anorexia, irritability, and abdominal 4. After 1 week, females release larvae pain [mimics appendicitis] 5. Larvae migrate to striated muscles, where they larvae found w/in appendix on appendectomy cyst rare instances of eosinophilic colitis CLINICAL PRESENTATION DIAGNOSIS Light infections: asymptomatic Scotch test, cellulose tape slide test Intestinal invasion —> GI symptoms ○ applying cellulose tape to anus ○ diarrhea ○ morning; before 1st poop ○ abdominal pain ○ eggs will adhere to tape ○ vomiting ○ seen microscopically Larval migration to muscles (1wk after infection) Anal swabs or “Swube tubes” (paddle coated w ○ periorbital and facial edema adhesive material) ○ conjunctivitis (pink eye) ○ eggs can be found but less frequently in ○ fever stool ○ myalgia (muscle pain) ○ urine & vaginal smears ○ splinter hemorrhages (capillaries in nail If ectopic infection: bed burst) ○ eggs seen in urine or in cervicovaginal ○ rashes Papanicolau smears ○ peripheral eosinophilia Life-threatening symptoms (occasional): ○ myocarditis (inflamm. of heart muscle) ○ CNS involvement  ○ pneumonitis (inflamm. in lung tissues w/o infection) 1. Unembyonated, thick-shelled eggs passed in Larval encystment in muscles feces ○ myalgia and weakness 2. In 5-10 days —> embryonated in ext. environment DIAGNOSIS 3. Ingestion of freshwater fish —> larvae hatch —> Antibody detection penetrate intestine —> migrate to tissues ○ enzyme immunoassays (EIA) detect 4. Ingestion of raw fish of human host Trichinella-specific antibodies 5. Adults reside in human small intestine, burrow use TSL-1 antigens in mucosa ○ 3-5 weeks after infection Adults are very small ○ IgG, IgM, and IgE ○ Females: 2.5-4.3mm Muscle Biopsy ○ Males: 2.3-3.2mm ○ larvae in muscle tissues 6. Females can produce eggs lacking shells (only Microscopy vitelline membrane) ○ direct examination of tissues and embryonated w/in female’s uterus or samples intestine 7. Released larvae re-invade intestinal mucosa and TREATMENT cause internal autoinfection lead to hyperinfection (high # of adult 7 Capillaria philippinensis worms) BACKGROUND CLINICAL PRESENTATION “pudoc worm” or “mystery disease” abdominal/GI disease causes human intestinal capillariasis ○ serious if not treated; autoinfection Unlike C. hepatica, humans = definitive host (reinfection of agent already present in Transmission: eating undercooked fish body) Piscivorous birds (fish-eating birds) protein-losing enteropathy (proteins lost in dig. ○ alleged wildlife reservoir of C. system, part. intestine) leads to: philippinensis ○ cardiomyopathy Intermediate Host: Freshwater fish ○ severe emaciation (extremely thin) endemic to Philippines ○ cachexia (wasting syndrome) ○ Northern Luzon region ○ death! also endemic to Thailand; sporadic cases from case fatality = >10% East and Southeast Asian countries also northern Egypt DIAGNOSIS Infective Stage: Larvae in intermediate host and finding eggs, larvae, and/or adult worms in stool small intestinal mucosa of definitive host or intestinal biopsies Diagnostic Stage: Unembryonated, thick-shelled ○ unembryonated eggs: typical stage in eggs in feces feces severe infections: embryonated eggs, larvae, MORPHOLOGY and even adult worms in feces Eggs: 35-45um (length) x 20-25um (width) NO VALID SEROLOGICAL TESTING ○ smaller than C. hepatica EGGS NOT INFECTIOUS TO HUMANS ○ two flat polar prominences ○ striated shell TREATMENT Adult males: 2-3.5mm (l) DRUG DOSAGE Adult females: 2.5-4.5mm (l) Albendazole* 400mg/day for 10 days ○ may contain embryonated or Mebendazole 200mg x 2/day for 20 days unembryonated eggs in utero PREVENTION LIFE CYCLE Sanitation and hygiene precautions ○ use sanitation toilets out of reach from animals and no leakage for feces ○ Wash hands