Worms Nematodes/ Roundworms Trematodes/ Flukes Cestodes/ Tapeworms
Nematodes: roundworms • Ascaris lumbricoides – large, pink, cylindrical, un-segmented
• Ascaris suum from pigs: – almost identical species, also can affect humans
• Epidemiology: – M/C helminthic infection worldwide
• Affects food/ water: – especially poor sanitation and if human feces used as fertilizer
• Eggs are very hardy: – survive extreme temperature • months in feces/ sewage; contaminated soil for > 3 years
Ascaris lumbricoides pathogenesis • Ingested infected egg: – develops into larval worm that penetrates duodenal wall • enters blood--- to LV/ HT---enter pulmonary circulation and alveoli--- larvae proliferate
– after 3 weeks incubation they are coughed up and swallowed and returned to SI • adults now develop in lumen of SI – can lay up to 200,000 eggs per day for 1 year
• Infectious after 2 weeks in soil: – eggs in feces • Infective larvae develops 60 – 75 days after initial infection
Ascaris lumbricoide clinical syndromes • 1) Asymptomatic • 2) Symptomatic: – Migration (triggered by fever, drugs, anaesthetics) to damage tissue – eg. into bile duct/ LV and occasionally will perforate intestine: peritonitis with secondary bacterial infection
• can cause bowel obstruction/ appendicitis – tangled bolus of mature worms
• LU (potential Loeffler’s syndrome)
– pneumonitis (asthma- like attack) » worse if previous exposure/ hypersensitivity » eosinophilia and oxygen desaturation • Iff many larvae: – vomiting, fever, abdominal tenderness/ distension
A. lumbricoides lab dx./ Tx • Lab diagnosis: – Concentrated stool • knobby coated, bile stained, oval egg
– Adult worm in feces (20- 35 cm long) – Diagnostic imaging: filling defects – Pulmonary: larvae/ eosinophils in sputum
• Treatment: – If mixed infection: • tx. Ascaris first or worms migrate/ GIT perforation
• Control: – Hygiene, education, sanitation • No human feces as fertilizer
Nematodes: pinworms • Parasitic adult worms in GIT • Detect eggs in feces: – specific size/ shape, thickness of shell, specialized structure (polar plugs, knobs, spines etc.), +/- larvae present • Eg. Enterobius vermicularis: – pinworms (small, white)
Pinworm pathogenesis • Ingest embryonated eggs: – hatch in SI to become infective within hours penetrate LI and develop for 2-6 weeks in intestinal mucosa • adult worms migrate and females lay eggs in perinanal folds (> 20, 000 eggs)
• Characteristic egg shape: – thin walled and asymmetrical • flattened on one side
Pinworm epidemiology • M/C in temperate zones • Many types of transmission: – Person- to- person: • daycares, schools, mental institutions
– Fecal-oral, fomites, inhaled/ swallowed with dust, food- handlers, autoinoculation • eggs hatch in peri-anal folds and migrate into rectum and LI
Pinworm clinical disease • M/C’ly asymptomatic carriers • Iff allergic to worm secretions: – Enterobiosis (oxyuriasis): severe pruritis, loss of sleep/ fatigue, excoriation (20 bacterial infection)
• Iff migrate to GTU/ vagina: – genitourinary problems/ granulomas
• Possible link to appendicitis and bowel perforation
Pinworm diagnosis • Clinical signs and symptoms • Detect characteristic eggs – Anal swab/ tape with sticky surface • for 3 consecutive days when child arises and before bathing and defecation
– Rarely see eggs in stool
Pinworm treatment and prevention • Treatment: – Pyrantel pamoate or melenazole • Treat whole family simultaneously to prevent re-infection, repeat after 2 weeks
• Prevention: – Personal hygiene, clip fingernails,wash bed clothes and prompt, aggressive treatment
Hookworm • Ancylostoma duodenale (Old world) and Necator americanus (New world): – differ only in relative size, geography and mouth part structure
• Epidemiology: – Worldwide • need tropical, warm, humid conditions with shady, well drained soil
• Transmission is direct contact with contaminated soil or ingestion – fecal matter containing eggs
Hookworm pathogenesis • Filariform stage is infective: – penetrates intact skin (eg. bare feet/ legs) using shearing, chitinous plates
• Enters systemic circulation and then pulmonary circulation: – proliferates and then is coughed up and swallowed • (like A. lumbricoides)
• Develop to adult hood in the SI: – after 4-8 weeks female starts to lay eggs • (10,000 to 20,000 eggs per day for up to 5 years!!!!)
• Eggs hatch in body and are released into soil as rhabditiform larvae (non-infective): – after 2 weeks in soil they develop to the infective filariform larvae
Hookworm clinical disease • Possible allergic skin reaction/ rash at site of entry • If progress to LU – pneumonitis, Loeffler’s syndrome
• Iff large amount of adult worms present:
– nausea/ vomiting and microcytic hypochromic anemia (blood loss from feeding worms)
• Iff severe chronic infection:
– emaciation, mental and physical retardation, metabolic dysfunction
Hookworm lab dx./ Tx/ prevention • Lab diagnosis: – Characteristic eggs in stool • Develop into larvae iff left at RT for > 1 day
• Treatment: – mebedazole/ pyrantil pamoate • Iff anemic: iron therapy • Iff chronic, severe: blood transfusion
• Prevention: – education, improved sanitation, controlled disposal of human waste, wear shoes in endemic areas
Filariasis • Bancroft’s filariasis – Wuchereria bancrofti • no animal reservoir
• Malayan filariasis – Brugi malayi • cat/ monkey reservoir
• Epidemiology: – tropic/ subtropical countries
Pathogenesis • Infective larvae enter via bite from infected mosquitoe: – migrate to lymphatics of arms/ legs/ groin: – grow to adulthood in 3-12 months • male fertilizes female:
– female gives birth to sheathed larval microfilarie
• most acute symptoms are due to: – molting adolescents and dead/ dying adults in lymphatic vessels
• chronic symptoms are due to: – physical blockage of lymphatic vessels
• adults can persist in human body for up to 10-17 years
Clinical disease • Can be asymptomatic even if blood smear + • Acute: – fever, lymphadenitis with chills, lymphangitis, recurrent febrile attacks
• Chronic: – enlargement of LNs especially in extremities, scrotum and testes
• Recurrent bacterial infections and host reaction contribute to pathogenesis • rarely: – ascites and pleural effusions secondary to rupture of enlarged lymphatic vessels in peritoneal/ pleural cavity
• Elephantiasis: – chronic thickening/ enlargement of tissues • especially in extremities
Lab diagnosis • 1) Definitive: – microfilariae in Giemsa stained blood smear • characteristic sheath and head/ tail structures
– Nocturnal periodicity: • collect blood between 10 p.m. and 4 a.m.
• 2) Other: – marked eosinophilia • increased filarial Ags: Direct ELISA
Treatment and prevention • Treatment: – for acute only (little use if chronic) • diethylcarbamazine, ivermectin – supportive/ surgical therapy for lymphatic obstruction
• Prevention: – education • mosquitoe control – protective clothing/ insect repellants etc.
– more difficult to control B. malayi • (animal reservoirs)
Trichinella spiralis epidemiology • Adults: – live in duodenual/ jejunal mucosa of flesh eating mammals
• Larvae (infectious); – live in striated muscle of carnivores and omnivores
• Epidemiology: – Worldwide • Can live in pork, horses, polar bears and walruses etc. (resist freezing) • Very common to have cysts in musculature – eg. > 1.5 million Americans have cysts
T. Spirales pathogenesis • Ingest infected meat (encysted larvae): – enter SI and larvae leave meat
• 2 day incubation to develop to adults: – females lay 1500 larvae in 1-3 months • leave intestinal mucosa and enter bloodstream – enter many different new muscle sites » eg. gastrocnemius, diaphragm, extraocular muscles of eye, tongue, deltoid, pectoral, intercostal
• coil in striated muscle as encysted larvae – viable for many years • infectious when ingested by new host
T. spirales clinical syndrome • M/C’ ly asymptomatic – especially if <10 larvae/ gm
• Iff > 100 larvae/ gm tissue: – a) if few migrating: • flu-like syndrome, slight fever, mild diarrhea
– b) if many migrating: • Persistent fever, GI distress, marked eosinophilia, muscle pain, periorbital edema • splinter hemorrhages – common due to vasculitis from toxic secretions of migrating larvae
• Decrease in clinical symptoms after 5-6 weeks
T. spiralis clinical syndromes • Iff >1000 to 5000 larvae/ gm tissue: – severe neurological symptoms, psychosis, meningoencephalitis, CVA
• Can be lethal: – myocarditis, encephalitis, pneumonitis • death 4-6 weeks after infection
T. spiralis lab diagnosis/ Tx/ prevention • Lab dx: – encysted larvae in implicated meat or in muscle biopsy from patient • Marked eosinophilia • Significant Ab titre – >3 weeks after onset of illness
• Treatment: symptomatic only • Prevention: – cook pork/ polar bear until interior is gray –
• Microwave cooking, smoking/ drying meat does not kill all larvae Freezing kills larvae iff quick freeze (-400C) or low temperature storage (-150C for > 20 days)
– No feeding garbage to pigs • decrease foraging of bears in garbage pits and public parks
Cestodes (Tapeworms) • Flat ribbon-like body • Heads (scolex) contain organs of attachment: – 4 muscular shaped suckers and crown of hooklets (exception is D. latum) • Proglottids: – individual segments of worms that join together to form long chains (strobila) • All are hermaphroditic • Eggs – most are non-operculated with 6 hooked hexacanth embryo (exception is D. latum) • No digestive system: – nutrients from host intestine diffuse across soft body wall
• Complex life-cycle with intermediate hosts
Tapeworms
Taenia solium (pork tapeworm) • Pathogenesis: – person ingests pork muscle containing a larval worm (cystericercus) – head attaches to SI and produces proglottids: • divide and replicate into long chains (strobila)
– sexually mature proglottids produce eggs: • leave host in feces: – contaminate water/ vegetation ingested by swine
– eggs develop to 6 hooked larvae (oncosphere) • penetrate intestinal wall and travel via circulation to tissues to develop into cystericercus
Tapeworms
Epidemiology and clinical disease • Insufficiently cooked pork • infrequent in N.A. – (more common in Africa, India, SE Asia etc.)
• Clinical disease: – rarely symptomatic – or mild: • irritation at site of attachment – chronic abdominal discomfort, chronic indigestion, diarrhea
• M/C’ly only aware of infection when proglottids or strobila of proglottids are seen in feces
Lab diagnosis • Stool: – characteristic proglottid structure: • T. solium (pork)---smaller, 7- 13 lateral uterine branches • T sanginata (beef)--larger, 15-30 lateral uterine branches • D. latum (fish)--rosette structure in uterus
• Eggs: – spherical, thick, radially striated shell with 6 hooked hexacanth embryo • (similar in T. sanginata and T. solium)
– D. latum--bile stained, operculated egg with knob-like structure at bottom
Treatment and prevention • Treatment: – niclosamid, praziquantil, paromomycin, quinacrine
• Prevention: – cook pork until interior is gray • freeze at -200C for at least 12 hours
• Sanitation: – keep contaminated feces out of water and vegetation ingested by pigs
Cisterocercosis • Human infection with larval stage of T. solium – (normal intermediate hosts are pigs)
• fecal-oral transmission – eggs transferred---hatch in ST • release hexacanth embryo or oncosphere – penetrate intestinal wall---circulation to tissue » develop over 3-4 months into cysticercus in muscle, connective tissue, brain, lungs and eyes » can remain viable in human flesh for up to 5 years
Cisterocercosis epidemiology • Only in areas where T. solium is found • M/C’ ly fecal- oral transmission but also auto-infection – proglottid containing eggs is regurgitated from SI into ST: eggs hatch and release infectious oncosphere
• Prevent infection by rapid, aggressive treatment of T. solium infections – decrease egg transmission
Cisterocercosis clinical disease • 1) asymptomatic iff few larvae in non-vital tissues • 2) iff in brain (hydrocephalous, meningitis, CN damage, seizures, increased DTRs, visual defects) or in eye (decreased visual acuity and visual fields) • Iff viable larvae: – host reaction is minimal
• Iff death of larvae: – release increased Ag material • marked inflammatory reaction – (fever, myalgia, eosinophilia)
Cisterocercosis lab diagnosis and treatment
• Lab diagnosis: – appearance of calcified cysticerci in soft tissue • CNS lesions detected by CT scan, US, radioisotope scanning
• Treatment: – praziquantel, albendazole, concurrent corticosteroids • surgical removal of cerebral or ocular cysts
Taenia sanginata • Ingest insufficiently cooked beef containing cysticeri – develop to adults in SI • egg production in maturing proglottids
• adults can parasitize jejunum/ SI for up to 25 years (reach a length of up to 10m) • Will not cause Cisterocercosis (unlike T. solium)
Beef tape worm lifecycle
Epidemiology • Worldwide – one the M/C cestode infections in the USA
• Human feces contaminate water/ vegetation with eggs: – ingested by cattle • develop to cystericeri in cattle and then into adult tapeworms
• Adult tapeworms are ingested by humans in rare/ insufficiently cooked beef
Lab diagnosis and treatment • Treatment: – single dose of nicloscimide will eliminate most adult worms
• Prevention: – cook beef fully • control disposal of human feces
Diphyllobothrum latum • Fish tapeworm: – unlike other cestodes: • scolex is lance shaped with long, lateral muscular grooves (bothria) but no hooklets • egg is unembryonated and is operculated
• one of the longest tapeworms – (up to 20 to 30 feet)
Life cycle • humans eat raw, undercooked, fresh water fish containing ribbon-like larval worm (sporganum) in flesh – broad shaped proglottids
• after 1 month reach sexual maturity and lay eggs (>1 million per day) – reach fresh water and 2-3 weeks later hatch into ciliated free swimming larvae (coracidium) • ingested by tiny, fresh water crustaceans (Cyclops and Dioptomus)---develop into procercoid larvae – crustacean eaten by freshwater fish » infectious plerocercoid sporganum develop in musculature of fish
Epidemiology • Worldwide: – especially in cool lake regions where people eat a lot of raw or pickled fish or undercooked, campfire-cooked fish or geifilte fish
• reservoir: – bears, minks, walruses, dogs, cats
• Increased risk with dumping raw sewage in to fresh water lakes
Clinical disease • M/C asymptomatic • If symptomatic: – Epigastric pain, abdominal cramping, n/v, unexplained weight loss
• low serum levels of Vitamin B12 – rarely, 0.1%- 2%, develop to megaloblastic anemia, numbness and decreased vibration sense • diminished posterior column integrity)
Lab diagnosis/ treatment and prevention • Lab dx: stool: – bile stained, operculated egg with knob-like projection on posterior • proglottids with rosette uterine structure
• Treatment: – niclosamid, praziquantil, paromomycin
• Prevention: – avoid ingestion of insufficiently cooked fish • control disposal of human feces, proper sewage treatment – proper, aggressive treatment of infections
Schistosomes • M/C spp are Schistosoma mansoni, S. japonicum, S. heamatobium • Produce schistosomiasis (bilariasis or snail fever) • Differ from other flukes: – male and female (not hermaphroditic), eggs do not have an operculum, obligate intravascular parasites (not found in cavities, ducts and other tissues), infective forms are skin penetrating cercariae liberated from snails (not eaten on vegetables, in fish or in crustaceans)
• Similar to other flukes: – both sexes have oral and ventral suckers and incomplete digestive system; both sexes are cylindrical
Life cycle and pathogenesis • Ciliated, free swimming cercariae in fresh water penetrate intact skin and (depending on species) develop in intrahepatic portal system or in vesical, prostatic, rectal and uterine plexuses and veins • Defense mechanism in portal circulation: – coat themselves with host substances therefore, minimal host response---chronic infections for 20 to 30 years
• After developing in portal system, male and female pair up and migrate to final site – (eg. mesenteric veins, urinary bladder)
• Fertilization and egg production occur – (300-300 eggs daily for 4- 35 years)
Pathogenesis • Host response to adult worms: minimal • Host response to eggs: – intense, inflammatory reaction • (cellular infiltrates and microabscesses)
• Larvae inside eggs produce enzymes; – aide in tissue destruction and allow eggs to pass through mucosa into lumen of bowel and UB and eventually into feces and urine
• Eggs hatch once they reach fresh water: – release motile miracidia---invade snail host • develop into infectious cercariae – released into water and infectious for humans and other mammals
Schistosomiasis • 1) Immediate and delayed hypersensitivity reactions – intensely pruritic, papular skin rash • (reaction to parasite Ags as cercariae penetrate host skin)
• 2) Katayama syndrome (at onset of oviposition): – 1-2 months after primary exposure, persist for > 3 months • fever, chills, cough, urticaria, arthralgias, lymphadenopathy, splenomegaly and abdominal pain – due to massive release of parasite Ags and subsequent immune complex formation • get leukocystosis, eosinophilia, polyclonal gammopathy
Schistosomiasis cont’d • 3) Chronic phase: – granulomas and fibrosis due to presence of eggs in various tissues • retained eggs cause extensive inflammation and scarring – location and number of eggs affects type of disease
– eg. Intestinal schistosomiasis – (S. mansoni, S. japonicum)
• Vesicular (bladder) schistosomiasis – (S. haematobium)
Lab diagnosis • Characteristic eggs in • 1) stool: – S. mansoni: large golden eggs with sharp lateral spine – S. japonicum: small golden eggs with tiny spine
• 2) Urine: – S. haematobium: large terminally spined eggs
• Rectal (or bladder) biopsy: – egg tracts laid by worms in vessel
Treatment/ prevention • Treatment: – praziquantel, oxamniquine – for skin conditions: • antihistamines, corticosteroids
• Prevention: – education regarding lifecycles of worms – snail control with molluscacides – Improved sanitation, water purification and control of human fecal deposits
Quote of the day • • • • • •
“ May the road rise to meet you, May the wind always be at your back; May the sun shine warm upon your face, The rains fall soft upon your fields; And until we meet again, May (your) God hold you safely in the palm of His/ Her hand.” – Irish prayer
Quote of the day
• “ God bless the roots! • Body and soul are one.”
– Theodore Roethke