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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, auto-
inoculation
• 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
• 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
• 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
– Irish prayer
Quote of the day
– Theodore Roethke