parasitology exam 2

phylum nematoda

• highly abundant

• 80,000 spp.

  • 75% free living

  • ~18,000 parasitic: cause disease of medical, veterinary importance

• bilaterally symmetrical, elongated and tapered at both ends

• pseudocoel: fluid filled body cavity that is not lined by peritoneum, functions as a hydrostatic skeleton

• exhibit eutely: entire body or parts have a fixed number of cells

• separate sexes = dioecious

• few spp. hermaphroditic, some show sexual dimorphism (females usually longer than males in length)

• possess only longitudinal musculature = operate antagonistically against the pseudocoel = lashing back and forth motion from using one muscle

• one way gut with mouth and anus

• muscular esophagus = help pump blood or body fluids from host inward

• size variable = 1mm (most free living are tiny) to 8-9m (mostly para.)

• tough/flexible outer cuticle that covers the body

• grow by molting or ecdysis = molt the culticle 4 times to adulthood from the time they hatch

largest nematode ever observed:

Placentonema gigantisma

• discovered in the placenta of a sperm whale

• 9m in length with 32 ovaries

hookworms

• order: strongylida

• commonly reffered as geohelminths

• distributed in warm, moist climates

• infect over a billion people

hookworm general features

• males posses copulatory bursa = at posterior end, composed of muscular rays which grabs onto the female for copulation

• large buccal capsule with cutting plates, designed to penetrate and feed on tissue of the host

• esophagus is muscular, adapted to sucking blood

• anterior portion of the worms are bent dorsally = giving them a hook like appearance

hookworm lifecycle

• in the small intestine

• separate sexes mate

• eggs of female get fertilized then pass with host feces

• worm hatches out of egg into soil (J1) then molt into J2, eventually to J3

  • J3 = non feeding period, lives in upper few mm of the soil and penetrates hosts skin

• once in skin they enter circulatory system and eventually end up in lungs (filaform juveniles)

• juveniles break out into the alveoli → molt → then migrate to small intestine via trachea

• J3 will molt to J4 after being swallowed or when it arrives in the small intestine

• molts into the adult which then grows and mates and reproduces (cycle repeats)

2 hookworm species of medical importance

1. Necator americanus

2. Ancylostoma duodenale

Necator americanus characteristics

hookworm

• distribution: southern US, africa, india, china, parts of SA and SE asia

• responsible for 95% of hookworm infections in the US

• morphology: males are 5-9mm, females are 9-11mm which produce 5-10,000 eggs per day and lives 3-5 years in host

  • adults have dorsal and ventral pair of cutting plates

  • spicules of copulatory bursa are fused distally (at the tips)

Ancylostoma duodenale characteristics

hookworm

• distribution: europe, N Africa, india, china, southern asia

• morphology: males are 8-11mm and females are 10-13mm which produce 10-30,000 eggs per day and live one year in host (b/c they put in alot of energy towards reproduction)

  • adults have two ventral cutting plates each with two large ventral teeth

  • spicules of the copulatory bursa have simple tips and are not fused

  • sucks more blood than Necator → blood loss per worm is 0.03ml per day for necator but 0.26 for A. duo

  • kills 65,000 people annually

hookworm pathology

• infection does not equal disease, most are asyptomatic

• severity of infection depends on worm intensity, hookworm species, and nutritional state of infected person

• worm intensity:

  • <25 worms = little pathology

  • 25-100 = light symptoms

  • 100-500 = moderate pathology

  • 500-1000 = severe pathology

• between both species above: both secrete anticoagulant (permits blood clotting)

• nutritional state of host = hookworm disease is intensified by the degree of malnutrition

signs of hookworm infection

• skin penetration causes a slight lesion which may cause itching

• minor chest pain and inflammation of pulmonary tissues as worms break out of alveoli

• minor sore throat, coughing, sometimes occurs after swallowing juvenilles

• abdominal pain and loss of appetite

• some people exhibit geophagy = eat soil, to increase penetration

• in long standing infections, anemia may occur

  • depletion of iron and inability to maintain a normal amount of hemoglobin

• dry skin and hair, metal dullness or low IQ is often accompanied by heavy hookworm infection

hookworm epidemiology

• poor sanitation

• warm, moist, well drained soils favor the development and survival of juveniles; freezing and direct sunlight kills juveniles

• white people are 10x more likely to be infected than black people

• a study in 2017 found that 35% of indivs. tested positive for hookworm in rural communities in alabama → lack of sewage infrastructure, sewage that drain homes end up in nearby ditches, which become easily flooded, spreading feces and eggs

hookworm diagnosis/control/treatment

• diagnosis: identification of hookworm eggs in feces

• treatment: mebendazole (single dose) or albendazole (if theres resistance against the first); dietary supplements

  • topical ointments

• control: proper sanitary disposal of fecal waste; wear shoes and gloves when gardening

cutaneous larval migrans

aka creeping eruption

• juvenile hookworms of another species that normally matures in other animals infect the skin of humans (ex. Anclyostoma canium = dog worm)

• juveniles penetrate epidermis but are unsuccesful in migrating to the intestine and so they wander under the skin

• wandering leaves behind a red, itchy wound that may become infected with bacteria → wander for several weeks to months

• topical ointments are often used as treament

Large intestinal roundworms

• Order Ascarididia

• typically large, stout, with 3 lips, some are longer than 45mm

• adults live in the intestine and many species are of medical and veterinary importance

Ascaris lumbricoides

large intestinal roundworm

• causes ascariasis in humans

• cosmopolitan distribution

• recorded by early civilizations

• may originally have been a parasite of pigs

• ~800m-1.2B infections, mostly children

• >60k annual deaths

• morphology:

  • three prominent lips

  • males are 15-30cm which are smaller than females = 20-50cm, and have a slight curvature at posterior end; uterus may contain up to 27 million eggs with 200,000 laid per day

• egg morphology: fert. eggs are oval and have a thick/lumpy outer shell layer made of lipids and proteins

  • resistant to chemicals such as 2% formalin, chlorinated water, and 50% solutions of hydrochloric acid, acetic acid, or sulfuric acid

  • long lived (up to 10 years)

• (ex. mueller put eggs on strawberry plot to see infection rate)

roundworms lifecycle

• adults live in small intestine where females lay hundreds/thousands of eggs daily

• eggs passed in feces, develop in soil/water to infectious L3 stage

• infection occurs through ingestion of contaminated fruits and veggies

• L3 larvae hatch in small intestine and penetrate intestinal lining

• enter hepatic portal system → migrate to lungs → molt in lungs

• break out of alveoli, travel up respiratory tract to esophagus

• return to small intestine where they mature to adults

• migration pathway poorly understood, possibly evolutionary from pig parasties

roundworms epidemiology

• over 1 billion people infected globally

• infection occurs by ingesting contamintaed soil, fruits, veggies

• areas that are seeded that perpetuate infections for very long periods

• using human feces as fertilizer facilitates transmission

• wind can carry eggs = very small and wind borne

• cockroaches found with eggs attached to bodies

• eggs survive on monetary notes due to poor hand hygeine

roundworm pathology

• minimal with intestinal infections

• adults suck blood and intestinal contents while in intestine

• wandering juveniles that get lost in major organs (liver, spleen, brain) cause inflammatory response

• lung pathology form larvae breaking out of alveoli

  • damage to air sacs/respiratory symptoms possible with heavy infection

• upstream wandering of adult worms: can enter trachea and block breathing, may crawl into ears or nasal cavity

• downstream wandering: can block appendix or exit through anus, heavy infections can cause intestinal blockage from entangled worms

roundworms treatment and diagnosis

• diagnosis: through identifying characteristic eggs in fecal smear

  • can identify whole worms if vomited or extracted from body

• treatment: mebendazole

  • affects microtubules, binds and kills worms

  • dead worms passed in feces (dont dissolve)

• prevention: wash fruits and veggies esp when traveling

  • iodine tablets ineffective against these eggs

Toxicara canis

• dog intestinal roudnworm

• cosmo. roundworm parasite of domestic dogs

• prevalence: 98% of puppies, 20% of adult dogs in US
  found everywhere dogs are present

• adult males = 4-5cm / females 7-15cm in small intestine

life cycle of Toxicara canis

• eggs passed with feces

• develop L3 stage in soil

• young puppies with no prior infection: hepatic portal migration → lungs → small intestine (like A. lumbricoides)

• older dogs with prior infection: no lung migration occurs, larvae wander through body tissues and undergo developmental arrest

• pregnant dogs: dormant juveniles reactivated by pregnancy hormones; larvae cross placenta and infect unborn puppies

  • complete migration in fetal puppy (lungs → intestine)

  • pups born with adult worms in intestine

• eating infected rodents: rodents with developmental arrest larvae in tissues, migration pattern depends on dogs prior exposure history

visceral larval margins

• occurs when humans accidentally ingest Toxicara canis eggs

• most common cause of visceral larval margins, though other nematodes can cause it

• children most commonly affected due to playing in contaminated areas

• larvae hatch and wander throughout body organs

  • commonly end up in liver and brain

  • all organs susceptible (lungs, kidneys, muscles, eyes, nervous tissues)

• juveniles become encapsulated in host fibrous tissue (granuloma)

  • exception: brain tissue cannot form granulomas

• symptoms include fever, neurological issues, tissue inflammation

roundworm treatment and control

• mebendazole

• control measures: deworm household pets regularly, proper disposal of dog feces, separate dogs and playgrounds (difficult to implement), prevent fecal contamination of play areas

whipworms

Trichuris trichiura

• distrib: cosmopolitan, infectio 800m globally

• prevalence: up to 25% in some US areas, usually 1-2%

• found mostly in warm, subtrop/tropical areas

• morphology: sexual dimorphism → females longer than males, “whip and handle” appearence means thick posterior section (handle) contains reprod. organs with a thin anterior sectiom (whip)

• life cycle simpler than hookworms (direct, one host cycle)

• no hepatic migration required

• females lay 3,000-20,000 eggs daily

• development: 21 day embryonation in shady, moist soil

• infection pathway: eggs ingested → larvae penetrate intestinal cells → travel through epithelium

• location: lower epithelium, rectum, colon (often affects appendix)

• female morphology: thin anterior half embedded in intestinal tissue, thick posterior half visible during scoping

whipworm pathology and symptoms

• adults feed on blood and epithelial cells causing hemorrhaging and anemia

• asymptomatic: <100 worms

• severe infections: 200-1000 worms, dysentery, anemia, growth, retardation

• heavy infections: prolapsed rectum, rectum collapses through anus - unique to whipworms

whipworm epidemiology

• endemic in areas with poor sanitation and human feces used as fertilizer

• optimal conditions: warm climate, moderate rainfall, moisture retaining soil

  • over 1billion people infection globally

• common in subtrop/tropical agriculture areas

whipworm diagnosis and treatment

• diagnosis: distinctive lemon shaped eggs in feces with bipolar plugs at each end

• treatment: mebendazole (attacks tubulin/microfibers, kills adults but not eggs)

• reinfection if possible - control measures critical

Trichinella spiralis

whipworm

• economic and social history since 1835 discovery

  • 1870s: US shipped infected pork to europe causing international strain

  • 1879: europe placed emargo on all US meat products

  • 1906: meat inspection act established - USDA inspection requirements

  • france maintains embargo on US horse meat due to contamination

• distrib/hosts: originally arctic/northern lats, now cosmopolotan through human activity

  • primary hosts are carnivores (pigs, bears, wild cats)

  • mexico identified as high risk area (20-24% prevalence in some regions)

  • humans are dead end hosts (zoonotic disease)

Trichinella spiralis morphology and life cycle

morphology:

• worlds largest intracellular parasite

• females are 3mm

• males are 1.5mm

• lives inside muscle cells

life cycle:

• unique, same host serves as definitive and intermediate

• adults in intestinal epithelium, larvae in muscle cells

• infection: ingest larvae in muscle → molt 4 times in intestine → adults in epithelium

• females gives live birth to juveniles (no eggs, then die)

• juveniles enter circulation → travel to heart, lungs, throughout body

• penetrate skeletal muscle cells and take control

parasite-nurse cell complex formation:

• parasite alters host cell gene expression

• cell changes: microfibers lost, smooth ER increases, collagen increases, mitochondria degrade

• cell size increases, parasite enters developmental arrest

• network of blood vessels forms around infection cell for nutrition

• can remain viable for years, eventually calcifies

Trichinella spiralis pathology

• symptoms vary by location of larvae, can cause heart failure if larvae reach heart muscle

• diagnosis: tissue biopsy only

• no treatment available; symptom management only

• prevention: cook pork to 160 degrees, avoid raw/undercooked

pinworms

Enterobius vermicularis

• human pinworm

• disribution: cosmo, >400m infections globally, very common in the US, esp in daycare centers; more physiological discomfort than pathogenic threat

• morphology: females are 8-13mm, males are 1-4mm

  • named for the sharply pointed posterior end in females

  • females are the primary cause of symptoms and discomfort

• life cycle: adults in lower part of the intestine, females migrate to the perianal skin and leave a trail of eggs then die

  • eggs with J3 swallowed by host

  • J3 hatches in small intestine, molts twice into an adult

• pathology: 1/3 infections are asymptomatic

  • movements of gravid female to deposit eggs occurs at night (tickling sensation, itching)

  • itching can lead to bleeding, bacterial infection and discomfort

  • worms wander into vulva, vagina and uterus

• epidemiology: clothing and bedding becomes contaminated with eggs → also on curtains, walls, carpets

  • schools and daycare centers

  • eggs are light and carried in air currents then swallowed

  • entire home must be sanitized for drug treatment

guinea worm

Dracunculus medinensis

• distribution: specific countries; formally in 20 countries including middle east, central and west africa, india and pakistan

  • 3million infections since 1980s

  • in 2016 25 cases in chad, ethiopia, S. Sudan, due to who eradication program

  • in 2024 15 cases

Dracunculus medinensis morphology and life cycle

morphology: longest parasite nematodes in humans

• females = <800mm

• males = <40mm

• worms are viviparious, giving live birth to juvenilles

life cycle: when females become gravid, tension within uterus increases, stimulates female to migrate to skin

• muscular contractions (stimulated by water) force juveniles out of uterus; half million ejected

• juveniles elicit an allergic rxn → blister (ruptures and juv. escape)

• 1. L1 released into water from broken blister 2. copepod eats L1 3. molt twice into the J3 4. person drinks the water that has the copepod with the larvae in it 5. molt until get to the adult stage in human (10-14 months for female to release larva after host becomes affected

Dracunculus medinensis pathology and epidemiology

pathology: blister forms from allergic reaction to metabolic waster products

• blister ruptures = painful, can become infected with bacteria

• worms that do not reach the skin during migration are often calcified

epidemiology: endemic in areas of drought

• infections near water holes that are usually stagnant and deep as copepods thrive in such environments

diagnosis: appearence of the blister, release of juveniles from uterus

treatment: winding the female around a stick one day at a time (three weeks) = only treatment

control: filter water to remove infected copepods

• winding of the serpent carried by Roman God of Medicine similarity

Filarial Nematodes

• includes many species

• thread-like parasitic nematodes transmitted by arthropod vectors; adult worms product microfilariae (tiny thread like larvae), infect vector arthropods, which mature into infective larvae (J3)

• Wuchereria bancrofti, Loa loa, Dirofilaria immitis

Wuchereria bancrofti

• diseases: lymphatic filariasis and elephantiasis

  • distressing, lead to disfigure of body

• distrib: world helath organization est. that 1/5 of worlds population live in at risk areas

  • >173 countries, 120 million infections at one time

  • widespread in tropical and subtropical climates: SE Asia, islands of the south pacific, southern arabian peninsula, subsaharan africa, india, south america

• life cycle: adults in lymphatic vessels and lymph nodes, females give live birth releasing thousands of microfilariae for 15 yrs or more

  • adult worms mate → gives birth in lymph. system → MF make way and circulate in the peripheral blood (most abundant in the blood b/w 10p-2a → MF migrate from gut of mosquito (after mos. takes blood from human) into hemocoel and penetrate thorax muscle cells, transform into sausage shaped forms then grow and molt into J3 → mos. takes another blood meal from a human which J3 penetrates bite wound after mos. mouthparts are removed → enter lymph and carried to lymph nodes

• pathology: depends on length and intensity of exposure

Wuchereria bancrofti life cycle and pathology

• life cycle: adults in lymphatic vessels and lymph nodes, females give live birth releasing thousands of microfilariae for 15 yrs or more

  • adult worms mate → gives birth in lymph. system → MF make way and circulate in the peripheral blood (most abundant in the blood b/w 10p-2a → MF migrate from gut of mosquito (after mos. takes blood from human) into hemocoel and penetrate thorax muscle cells, transform into sausage shaped forms then grow and molt into J3 → mos. takes another blood meal from a human which J3 penetrates bite wound after mos. mouthparts are removed → enter lymph and carried to lymph nodes

• pathology: depends on length and intensity of exposure to larvae; response of indiv person

  • disease progresses through 4 stages:

    • 1. incubation

    • 2. some symptoms

    • 3. acute (bloackage of lymph vessels, swlling; obstructed lympth ducts causes milky urine called Chyluria

    • 4. chronic (changes in extremities and genitalia due to blockage of lymph vessels; skin thickens, lose elasticity

Wuchereria bancrofti diagnosis/epidemiology

• diagnosis: take blood sample (take during time MF is in blood)

  • not found in peripheral blood during the day, they hide in capillaries and tissue space

  • peak microfilarameria (mf in blood) is b/w 10p-2a

  • antigen test is sensitive to infection; detects antigens released from adult worms or MF

• epidemiology/control: circadian periodicity of MF; during peak, mosquitos are activley feeding

  • two controls:

    • 1. vector control: DDT to control mosquitos; DDT is banned in the USA but is the biggest producer in the world

    • 2. chemotherapeutic drugs: (diethylcarbamazine or DEC); it eliminates MF in blood and kills 40% of adults; works by sensitizing worms to phagocytosis; side effects are digestive tract issues, fever

Loa loa

• distribution: specific areas around the world like tropical forests of west central africa (ex. gabon, cameron, congo)

• life cycle: adults live in subcutaceous connective tissues of back, chest, axilla, groin, penis, scalp, and eyes

  • intermediate hosts are deer flies that feed on the skin picking up MF → develop into J3

  • MF exhibit periodictiy in the blood; most abundant during the day

  • humans infected with J3 during deer fly bite, worms wander throughout subcutaceous CT and eye

• diagnosis: demonstrating MF in blood, take sample during day

• treatment; surgical removal of the adults is simple and effective

  • drug of choice: ivermectin, but only affects MF and not adults

• control: deer flies live in swamp areas, proven to be difficult to control (associated with vegetation)

Dirofilaria immitis

dog heartworm disease or dirofilariasis

• main host is the domestic dog, other canids are good hosts

• the domestic cat is also infected with lower prevalence

• humans are rarely infected

distribution: current prevalence in SE US ranges from 10-70% whereas in the N part of the country it ranges from 1-8%

• dirofilariasis is considered to be a major disease of dogs in N and S america, japan, china and AU

Dirofilaria immitis lifecycle and pathology

• J3 enters dog via bite wound made by mosquito and larvae migrate to sub. C and musculature tissue

• 90 days later it migrates to the heart where they live as adults producing MF

• MF are picked up by mosquito during feeding

• MF migrate to the gut and enter malpighian tubules where they become sausage shaped larvae

• J3 migrate to head of mosquito

• pathology:

  • clinical signs appear in dogs that become sexually mature

  • adults in right heart and pulmonary artery; blood flow is impeded, heart valves cannot close properly

  • this increases back pressure from the lungs to the liver

  • heart has to work harder, liver becomes enlarged, insufficient oxygenated blood for the animal to maintain activities

  • avg. # worms per infection = 20-30

Dirofilaria immitis symptoms and epidemiology

symptoms: respiratory insufficiency, vomiting, chronic cough, exercise intolerance

• death from cardiopulmonary failure

epi.: mosquito abundance and control

• dogs taken along family vacations spreads disease, adult worms may be killed with arsenic drugs → dead adult worms carried downstream can damage lung = dog may die

• surgical removal involves cutting into major vessels which is risky and expensive

treatment: MF (not adults) may be killed by doses of ivermectin, used prophylactically once per month to kill J3 and J4 stages

Nematomorpha (aka gordian worms, horsehair worms)

• nematomorphs are one of 3 phyla completly parasitic, Dicyemida and Acanthocephala are the others

• hair worms often occur in highly tangled masses resembling the classical gordian knot

• general characteristics: pseudocoelomate (fluid filled without peritoneum)

  • long, cylindrical, filamentous rnaging from few cm-3m

  • dark color, dioecious, females longer than males

  • cuticle with numerous fibers organized in criss-cross parallel, creating stout body

  • longitudinal muscle only

  • digestive system reduced, absent in many species, non feeding adults

  • larvae are structurally different from adults = small (100mm), annulated cuticle, eversible proboscis with hooks, no molting

nematomorphs two main groups

1. nectonematids (marine)

• larvae parasitize marine inverts such as hermit crabs, adults in marine waters

2. gordiids (FW)

• larvae parasitize terrestrial arthropods, such as mantids, beetles, and crickets; adults in FW streams and ponds etc

• 300 species, majority occur in FW and 5 species are marine

-larvae in arthropods, adults are free living

• larvae is parasitic

• they can alter the behavior of their arthropod hosts

• infected insects are more likely to jump into a aquatic environment where adults reproduce

• research show that crickets infected by Paragordius tricussipidatus are more likely to jump into water than uninfected ones

• infected hosts display an erratic behavior which brings them closer to a stream

nematomorph life cycle

• adults begin molting after emergence, females deposit a million eggs on a string

• larvae develop 15-30 days after egg depositon

• larvae burrow into invert. host and encyst

• trophic transmission; larvae burrow through gut into hemocoel and mature

nematomorphs: phylum Acanthocephala (thorny headed worms)

general characteristics: thorn like hooks on proboscis (taxonomically important); 1,200 species but only 80 life cycles are known

• exclusivly parasitic

• adults are dioecious and females are usually longer than males

• pseudocoelomate

• lack digestive system, absorb nutrients through tegument

Acanthocephala morphology

• proboscis on top, neck, then trunk is the majority of the body (houses reproductive organs)

• male has testis, cement gland designed to produce sticky substance that when he mates he releases some of it, copulatory bursa as a penis, cement reservoir, genital ligament

• female has vagina, uterine bell, uterus, genital ligament

• when male releases sperm into vagina, he plugs her opening with his cement to keep other males from producing with her

  • cement eventually disentegrates after a few days

  • males can do the same plug act with other males to prevent them from mating with other females = homosexual rape = competition

Acanthocephala life cycle

• adult lives in the digestive system of the final host (Heron bird)

• egg with acanthor

• fiddler crab eats egg, larvae develops into acanthella

• acanthella develops into the next stage, becoming a cystacanth = larval stage infective to final host

• final host eats crab → life cycle repeats

• note**no free swimming larval stages, transmission is trophic between hosts

Avian schistosome (marine and FW)

• designed to get into birds and not humans

• life cycle: typical like a schistosome

  • venueles of female host, lays eggs, miracidium hatch and infect snail, reproduce in gonad, cercaria leave, they need to find bird host as final host BUT humans are accidentally penetrated by cercaria because they cant tell if its a bird, so it will still burrow into skin

    • produced atingens = immune system recognizes this and skin will become inflammed

Chlonorchis sinensis (human liver fluke)

• 30 million infected

• japan, korea, taiwan, china, vietnam

• adults (8-15mm) mature in bile ducts

• produce up to 4000 eggs a day

• trophically transmitted trematode = infection through ingestion

• association with bile duct cancer

• anatomy: highly branched testis, ovary, seminal receptacle, uterus, vitelline gland, excretory bladder, acetabulum (distome)

Chlonorchis sinensis life cycle

• adult worm found in bile duct of human, passed eggs through feces

• egg contains miracidium

• snail has to eat the egg, then miracidium hatches out within the snail

• reproduce sporocysts, which produce daughter and mother redia then lastly producing cercaria

• cercaria swim out of snail and look for fish

• fish = 2nd inter host

  • penetrate and drop off tail then head makes way to muscle then forms into metacercaria

• when people eat raw fish they get infected

• once metacercaria hit gut, enzymes break down cyst wall, continue to move to bile duct

• 1 month of arrival in duct, egg production starts

Chlonorchis sinensis disease

• chlonorchiasis: disease in bile duct

• common where raw fish is eaten regularly

• grass carp = common fish in asia

• one way to kill metacercariae is high heat, to cook it well

Chlonorchis sinensis pathology/diagnosis

• erosion of lining of bile ducts leading to gradual thickening of the ducts

• eggs can cause backup = liver dysfunction

• eggs have little hatch door for metacercariae

• sample feces to diagnose

• drug is praziquantel

Paragonimus westermani

• lung fluke

• infects humans, felines, canids, rodents, pigs

• discovered in 2 bengal tigers who died in a european zoo

• japan, korea, philipines, manchuria, china, taiwan, popa new guinea

• trophically transmitted

• adults primarily live in the lungs but also in vicera and brain

• almost 300 million at risk

Paragonimus westermani life cycle

• adult worms in lungs of humans and cats

• eggs gets out of the body by 1. entrained in mucus and flem, coughed up but swallowed mucus going into digestive tract so it will go through feces 2. coughing up into atmosphere so leave orally

• miracidium hatches, swims around and finds snail

• penetrates, produces sporocysts, making redia, then cercaria that crawls out snail and into water

• cercaria tail is short and stubby = not designed for swimming → crawling on sediment more, not in water column (has stylet to help penetrate crab)

• 2nd intermediate host is a crab: cercaria penetrates soft spot around exoskeleton of crab, tail falls off, head transforming into metacercaria

  • found in mucus, body cavity, overall internal

• person eats crab that has meta cercaria

• hatches in gut, burrows up into the diaphram

• once in lungs, 6 weeks until eggs are produced

Paragonimus westermani anatomy/pathology/diagnosis

• weird overall shape, known for the ovary looking like a flower, testis hard to see and internal anatomy

• integument is covered in spines

• Paragonimiasis: high infection in lungs

  • occurs when humans eat undercooked or raw crusteceans

  • in asia, lives crabs are immersed in wine and eaten = unsafe

• adults in the lungs stimulate an inflammatory response → encapsulation of surrounding tissue

• chest pain, difficulty breathing

• identification of eggs in the spit you cough up or feces

• lung biopsy showing eggs encapsulated in lung tissues

• praziquantel is drug of choice, or triclabendazole

alteration of host behavior by trematodes

• makes host vulnerable to predation by their next host as parasites have complex life cycles

• this increases the probability of trophic transmission ensuring the life cycle continues

  • these alterations are not novel behaviors; rather parasites elicit “inappropriate behaviors that make them more conspicuous to a predator

• ex. cockroaches affected with thorny headed worms: cocks are nocturnal to avoid predation during the day, when infected, they come out in the midle of the day

three trematodes who hijack their host

• dirocoelium dendriticum

• leucochloridium paradoxum

• euhaplorchis californiensis

dirocoelium dendriticum

• adult worms live in bile ducts of sheep, cattle, pigs, goats, etc

• liver → digestive system

• life cycle: domesticated final host, eggs passed with feces from bile duct

  • miracidium developing in egg, egg on grassy area

  • land snail eats egg, mira. released, produced sporocyst then cercariae (no redia and castrate)

  • cercariae doesnt need water → escape snail through slime/mucus; escape in slime ball

  • ant is 2nd inter = eats slime w cercariae in it → tail drops off and becomes meta., develops in ant body cavity

  • some cercariae encyst very specific ganglia of ant (subesophageal ganglion, nerve cells), part of the nervous system that controls mouth parts (mandibles)

  • when ant is infected, if temp is low enough, ant becomes locked onto plant by its mandibles and stays = increased prob. that it will be eaten by grazers

leucochloridium paradoxum

euhaplorchis californiensis