The document discusses the phylum Nematoda, which includes roundworms. It notes that nematodes are one of the most abundant animals on Earth and can be found in nearly every habitat. They cause some of the most debilitating human diseases. Several examples of parasitic nematode genera are described in detail, including their life cycles, hosts, geographic distribution, symptoms caused, and methods of diagnosis and treatment.

1. Phylum Phylum Nematoda
Nematoda • Pseudocoelom
– Fluid-filled cavity that forms hydrostatic skeleton
• Most numerous animals
on earth • Simple nervous system
– May include sensory organs called phasmids/amphids
– 90,000 in 1 rotting apple
Nematodes – 1074 in 6.7 ml of coastal • Complete digestive system
mud • Four juvenile stages which all look similar
– Estimated 9 billion per – Separated by a molt of the cuticle
acre in good farmland – Called J1, J2, J3, J4
– Parasitic infections can be • Most juvenile stages are free-living
enormous – J3 is usually the stage that gets into the definitive host
Nematodes Phylum Nematoda
• “White worms” Phylum • More species than any
– Not segmented other phylum
– Covered with a cuticle Nematoda • Many species show eutely
– More insects have been
• Secreted by hypodermis – After embryogenesis, the nuclei of the cells
described
• Grows as worm grows do not divide
– Every insect studied has at
• Sexes are separate – The number of cells remains constant for the
– Find each other with pheromones
least one nematode parasite
rest of worm’s life
– Male sperm lack flagellum • Live in every habitat
• move by pseudopodia (Major sperm • The cells simply grow larger
protein)
– Free-living in marine,
• Exception is the ovary/testes
freshwater, terrestrial
• Most are slender with few – Number of cells varies by species
distinguishing characteristics. • Even between grains of sand
on a beach • Two classes
• Cause of some of the most
debilitating and disfiguring diseases – Parasitic on almost every – Enoplea
in humans animal
– Rhabditea
– Parasitic on plants
1

2. Class Enoplea Trichuris trichiura Trichuris trichiura
• Location: large intestine from • Diagnosis: bipolar eggs
• Amphids (sense organs) well developed
caecum and appendix to rectum in feces. Colonoscopy
• Most are non-parasitic – Burrows head into mucosa can also uncover worm
• Order Trichurida • Transmission: Ingestion of infections
– Trichuris, Capillaria, Trichinella embryonated eggs, usually in • Treatment:
contaminated food Mebendazole or
• Order Dioctophymatida
– Requires high humid, warm albendazole. Rectal
– Dioctophymata (Kidney worm) climate and shade to develop
prolapse treated with
• Order Muspiceida properly.
surgery
• Order Mermithida
– Parasite of insects
• Pathology and Symptoms:
Trichuris trichiura Low-level infections (<100 Trichuris • Females may lay 3,000 to
• Whipworm Trichuris worms) are asymptomatic 20,000 eggs a day for
• Definitive Host: Humans trichiura • Large infections can result in
trichiura many years.
– Dogs possibly diarrhea, bloody stool, • There are 60-70 species in
• Intermediate Host: None abdominal pain and rectal this genus, all live in large
– Pigs and chickens are transport prolapse
intestine
hosts • Chronic infections in children
– Flies will transport eggs on legs – T. felis – cats
can lead to growth retardation
• Geographic distribution: and finger and toe clubbing. – T. discolor – cattle
Cosmopolitan • In Phils – 80-84% prevalence – T. muris – rodents
– Warm Climate – T. vulpis – canids
• Often associated with Ascaris
– High rainfall • Occasionally infects
lumbricoides infections.
– Unsanitary conditions humans
– Mode of transmission same
– T. suis – pigs
2

3. Life Cycle of Trichuris trichiura Capillaria Capillaria sp.
• Pathology: ulcerative and
• Very large genus
Adults in Eggs go
philippinensis degenerative lesions in the – Infect every organ and tissue of all classes of
Embryonate intestinal muscosa; disruption vertebrates.
large out in in soil to electrolyte balance leading • C. hepatica zoonotic human parasite but
intestines feces to heart failure normal host unknown
Eggs eaten • Symptoms: abdominal – Rat intermediate host
Emerge by humans pains, gurgling stomach and • C. aerophila live in lungs of carnivores
into lumen diarrhea • C. annulata esophagus and crop of birds
• Diagnosis: Eggs may be – Uses earthworm as intermediate host
Juvenile Juvenile found in feces • C. plica kidneys and urinary bladder of canids
Eggs
mature penetrate • Treatment: Albendazole • C. linearis in cats
hatch
mucosa • C. procyonis lives in the tongue of raccoons
Life Cycle of C. philippinensis Anatrichosoma
• Definitive Host: migratory
Capillaria fish-eating birds Eggs laid and Ingested by
ocularis
– mammals including humans embryonate in
philippinensis FW fish • Lives in the corneal
• Intermediate Host: None. freshwater epithelium of tree
• Geographic Distribution: Man ingests shrews, Tupaia glis
Philippines (1967- infected fish • Other Anatrichosoma
68:epidemic) and other Female sp. are parasitic in
Bird ingest
parts of Asia worms lay various tissues of many
infected fish
• Mode of Transmission: eggs mammals
Ingestion of infected fish • Closely related to
• Location in D.H.: small Juvenile in Trichuris and Capillaria
Adult in the
intestine small int
small int.
3

4. • Hosts: swine, rats,
Trichinella spiralis • Disease is trichinosis • Diagnosis: Antigenic and
Trichinella humans, bear, walrus, and – Pathology and – A.K.A. Trichiniasis or trichinelliasis
Trichinella serological tests, muscle
other carnivores. Symptoms • The Great Mimic biopsy plus case history.
spiralis – Individual is the D.H. for the – Mimics many other conditions spiralis
adults and I.H. for Juvenile • Treatment: No effective
– Rarely exhibits a set of symptoms
• Geographic Distribution: • Symptoms depend on location, treatment.
number and age of larval worms – Thiabendazole has worked in
Cosmopolitan. More
common in temperate • Most cases are asymptomatic experimental animals but
areas than tropics. • Initial phase: flu-like symptom results in human mixed
– There are at least seven – Caused by females penetrating – Steroids reduce inflammation
mucosa – Bed rest and analgesics help
sibling species and at least
3 strains • As worms mature, symptoms relieve pain and discomfort
• Different hosts, ribosomal may include nausea, vomiting,
DNA, gene sequences, and sweating and diarrhea for five
allozymes
to seven days.
– Look identical – Body’s reaction to worm waste
Trichinella spiralis Trichinella spiralis • Migration of larva causes
• Location: Adults in wall many symptoms Trichinella spiralis
– symptoms and – Including pneumonia,
of small intestine. • Prevention: Cook meat well.
Juvenile in striated pathology pleurisy, encephalitis,
meningitis, nephritis, – Most cases are from undercooked pork
muscles and organs.
deafness, peritonitis, brain – Includes processed meats, chops, sausages,
– Favorite are eye, tongue and eye damage, muscle
and masticatory muscles ham, etc.
stiffness, weak pulse,
– Then diaphragm and difficulty breathing,
intercostal
– Can also occur in bears, walrus, fox, etc.
hallucinations
– heavy muscles of arms and • Rarely occurs in cattle and horses
legs • Death is rare – How they get it is unknown
– Why they prefer certain – Usually due to
muscles is are unclear inflammation of heart • Can survive freezing down to –15oC
• Transmission: Ingestion muscle, respiratory
of Juvenile in under complications or kidney
malfunction
cooked meat.
4

5. Trichinella • Largest intracellular parasite Adults inside Female Juvenile
Enter
– Juvenile invade a muscle cell and converts it into intestinal release migrates to
spiralis - a nurse cell muscle
mucosa cell Juvenile striated
• Alters the metabolism of the cell to do what it cell
muscles
Notes wants
– Alters gene expression so it doesn’t make
contractile proteins Life Cycle of Turns into
• Releases Vascular endothelial growth factor Four molts
(VEGF)
nurse cell
T. spiralis
– Stimulates formation of capillaries around
cell
• Nurse cell secretes collagen coating
Penetrate Reach Infective in
• Don’t understand how worm does it Juveniles
intestinal small 4-8 weeks
– Eventually the body walls off the nurse cell by swallowed
calcifying the walls mucosa intestine
– Immune system will eventually kill the Juvenile
• But they can live over 39 years
Trichinella spiralis - Notes Dioctophyma renale Order Mermithida
• Juvenile molt four times and become an adult in 30-32 • Order Dioctophymatida
hours from ingestion. • Kidney worm • All are parasites of insects
• Female gives birth to live Juvenile – Larval stages develop and grow in hemocoel of
– No egg stage • Definite host are aquatic birds and mammals insect
• Immunity has been demonstrated in mice – Can occur in dogs, cats, and humans
– When nematode is nearly mature, it ruptures out
– Can be passed to young from immune mothers • Adults take over one kidney of the definitive host of the body wall of the insect
• There are at least four variations of the life cycle which and leaves other kidney alone • Usually when the insect is near water
may be different species
• Kills the insect
– Domestic • Grows to several feet in length.
• Use pigs and rats • Adults live in the soil, mate and lay eggs
– Sylvatic – Temperate zone
• Diagnosis by eggs in urine; worms (and kidney)
should be removed. – Eggs may be eaten by host or juvenile may seek
• Fox, bears
out host
– Sylvatic – Torrid zone • Uses two intermediate hosts
• Hyenas, lions • May be used in future for biological control of
– Sylvatic Frigid zone – First: freshwater oligochaete worm
pests.
• Polar bears, walrus – Second: a fish.
5

6. Mermithid-
infected ant Familes Sterinernematidae and
on left, Order Rhabditida Heterorhabditidae (con’t)
normal ant • Most are free-living nematodes. • Worms reproduce for several generations
on right while feeding on the bacteria and the insect’s
• Includes several families that were
probably “pioneer parasites”. organs until they run out of nutrients
– then produce J3 which return to the soil
– Families Sterinernematididae and
• wait for the next host
Heterorhabditidae (insects)
– Family Rhabdiasidae (lung worms of frogs, • True mutualism between the worm and
Mermithid bacteria
snakes, cattle, and other animals)
from – Neither can survive alone
– Families Strongyloididae and
abdomen Ancylostomatidae (medical importance to • May be a way of controlling insect pests.
of ant humans)
Familes • Includes two genera
– Steinernema
Family Rhabdiasidae
Class Rhabditea Sterinernematidae • Rhabdias bufonis and R. ranae are lung
– Heterorhabditis
• Amphids (sense organs) are usually
and worms of toads and frogs.
• Important parasite of
Heterorhabditidae – Parasitic Adults are protandrous hermaphrodites
poorly developed. insects.
• J3 juvenile invade host
• Includes many free-living as well as • J3 juvenile invades • Male organs develop first and make sperm
insect and releases • Then female organs develop and make eggs
most parasitic round worms. – Use stored sperm to fertilize eggs
bacteria
• Some eggs leave in feces and hatch into free-living adult
• Bacteria kill insect but males and females
also retards growth of – Feed on soil bacteria
other bacteria • Some eggs hatch in utero and feed on female internal
organs until she is dead.
– Insect doesn’t rot • J3 juvenile leave body to invade an insect.
6

7. Family Adults in Eggs go Hatch and
• Well developed buccal Small Molt
out in J1 develops
Ancylostomatidae cavity with teeth. Intestine feces in soil
- Hookworms • Four Larval stages. J2
– J1and J2 are free-living Molt
– J3 burrows into definitive Molt
J4
host skin and migrates to Hookworm
intestine
Molt Life Cycle J3 juvenile
• Require warm, wet burrows into
climate and shady areas Reach skin of host
– J1 and J2 can’t tolerate intestine
Family Rhabdiasidae drying, freezing, or Enters blood
• Many other species of Rhabdias spp. are exposure to sun. Up or lymph
Coughed Lungs Heart
lung worms of frogs, snakes, cattle, and • Adults actively graze on up then trachea vessel
other animals. intestinal mucosa swallowed
• Many different species.
Family • Definitive Host: Humans
– S. stercoralis and S. fuelleborni • Symptoms of hookworm Necator
Family in humans and primates – Most common human
– S. ratti in rats Ancylostomatidae infection vary by species americanus hookworm
Strongyloididae – S. ransomi in swine and number of worms.
– Many other species parasitize - Hookworms – Most infections are • Intermediate Host: None
- Strongyloides birds, reptiles and amphibians • Geographic Distribution:
asymptomatic.
sp. • Free-living stages mixed with Indigenous to Africa, India,
parasitic stages. – A. duodenale causes more
– Random mix damage than N. americana southeast Asia, China, islands
– Free-living worms are male or – Nutrition of host also of sw Pacific.
female. important in determining the – First found in Brazil and Texas
– Parasitic worms are all degree of symptoms
parthenogenic females – Brought to New World with slave
• No sperm has been found in – Race also affects symptoms trade
parasitic forms • Blacks are more resistant to
– Autoinfection may also occur infection than whites
• Transmission: J3 burrows
into skin.
7

8. • Pathology: Due to • Pathology: Due to damage
Necator damage of tissue during Hookworm • Hookworm infection does not
Ancyclostoma of tissue during migration of always lead to hookworm
americanus migration of J3 juvenile and J3 juvenile and ingestion of Disease
ingestion of intestinal duodenale disease.
intestinal mucosa by J4 – Most infections are
mucosa by J4 juvenile and juvenile and adults asymptomatic
adults
• Symptoms: Usually • Development and severity of
• Symptoms: Usually asymptomatic. May cause
asymptomatic. May cause Hookworm disease depends
hookworm disease. on three factors.
hookworm disease. – We will discuss Hookworm – Number of worms present
– We will discuss Hookworm disease later.
disease later. – Species of hookworm
• Diagnosis: Eggs in feces – Nutritional status of the host.
• Diagnosis: Eggs in feces
• Treatment: Mebendazole
• Treatment: Mebendazole
• Definitive Host: Humans • Number of worms
Ancyclostoma• Notes: First hookworm the – Less than 25 N. americanus are
Ancyclostoma • Intermediate Host: None life cycle was determined
Hookworm asymptomatic
• Geographic Distribution: duodenale – 25-100 light symptoms
– In 1896 Arthur Looss was Disease
duodenale southern Europe, northern Africa,
dropping cultures of worm into – 100-500 moderate symptoms
India, southeast Asia, China.
mouth of guinea pigs – 500-1000 severe symptoms
– Scattered locations in United States,
Caribbean Islands, and South – He accidentally dropped a drop – >1000 are frequently fatal.
America. • Species of worm
on his hand.
– Found in 1000 year old mummy in
• The area began to itch and turned – A. duodenale sucks more blood so fewer
Peru
red. worms required to cause symptoms
• May not have been brought over
with slave trade. • He wondered if the worm could • Nutritional status of Host
– Frequently found in mines well north have penetrated skin – Poor nutrition leads to worse symptoms.
of freeze line – He then started sampling his – Suppresses immune system
• Provides stable climate, no own feces – Fewer nutrients to repair damage
freezing, no sun.
• Found hookworm eggs in feces a
• Transmission: J3 burrows into few weeks
skin.
8

9. Incidence of Hookworm Disease Incidence of Hookworm Disease Phases of Hookworm Disease
• Unsanitary conditions: feces released into soil • Race • Intestinal Phase
• Repeated contamination of soil – In general, whites are 10 times more susceptible – juvenile and adults suck blood from intestinal
– Repeated visit to same area to defecate increases to hookworm disease than blacks. lining
transmission • Exact mechanism isn’t clear • 0.03 ml/day for N. americanus
• Environmental conditions: Warm, humid, – Gave rise to image of “poor white trash” in • 0.26 ml/day for A. duodenale
climate without freezing, proper soil
southern U.S. – Bleeding into intestines can occur
– Must have loose, aerated soil, with lots of humus.
• Whites were frequently victims of high hookworm • Most iron is reabsorbed in intestines
– Warm, humid climate necessary for the worm to
develop in soil in shady areas loads – Worms do not use the iron
– Made them weak, apathetic, and lethargic
• Exposure of skin to soil – Anemia can result if dietary intake isn’t
• Blacks of the same socioeconomic situation were sufficient to replace the iron lost
– Must have access to skin so it can burrow into the
resistant to hookworm disease
skin. • Severity depends on worm load and dietary intake.
– They were industrious and hard-working
Incidence of Hookworm Disease Phases of Hookworm Disease
• Longevity of worm Phases of Hookworm Disease
• Cutaneous Phase
– Juveniles can live is soil for several weeks • Intestinal Phase
• Up to a year in a mine.
– Occurs when juvenile burrow into skin and enter vessels
– Localized allergic reaction
– Most common symptoms
– Adults can live 5-15 years • Slight, intermittent abdominal pains
• N. americanus lives up to 15 years, making 9,000 eggs/day. • Pulmonary Phase
• Loss of normal appetite
• A. duodenale lives up to 5 years but releases 25-30,000 – Caused by larval migration through lungs and up trachea
eggs/day • Geophagy – desire to eat soil
– Usually asymptomatic but can cause dry coughing and
– Adults travel with host when host moves – Reason is unknown
sore throat – Many areas of the southern U.S. have clay soil that
• Paratenic Host – May allow for secondary bacteria infections seems to relieve symptoms
– Recently discovered A. duodenale juvenile can – Pneumonitis can occur in very large infections » In 1920’s, a business person began to ship the
burrow into “wrong” species and survive in muscle clay to people around the country.
– Human infected when food is eaten
9

10. Phases of Hookworm Disease Ancyclostoma • • A.K.A. Creeping eruption
Definitive Host: Dogs and
• Chronic Heavy Infections Cutaneous • Hookworm juvenile
caninum cats penetrates skin of the
– Patient suffers from severe protein deficiency • Intermediate Host: None larval migrans wrong host
• Can cause dry skin and hair, spoon nail, edema, • Distribution: Cosmopolitan • Juvenile dies during
potbelly, delayed puberty, mental dullness, heart migration
failure and death. – but particularly common in
northern hemisphere – Body reacts to worm and
– Hookworms don’t block absorption of nutrients creates nasty skin irritation
• Transmission: J3 juvenile where every the worm went.
• Disease complicated by malnutrition
burrow into skin • Treat with thiabendazole
• Loss of protein and iron to worm is catastrophic to
• Location in definitive Host: • A. braziliensis most
those subsisting on minimal diet
common cause
– Prolonged exposure during childhood can lead small intestine
– A. caninum as well.
to lower intelligence and “laziness” – Many other hookworms can
cause it.
Hookworm Disease Family
• May explain the lower economic status in many Ancyclostoma
• Pathology: damage to Strongylidae
developing countries.
– Lethargic population can’t produce as many goods as
caninum intestinal mucosa by • Very important parasites of
healthy population grazing and sucking horses.
• Proper sanitation has eliminated it from most of blood.
U.S., Caribbean, and many other areas. • Many species
• Symptoms: – Large species – Strongylus
– Latrines and treatment was provided by J.D.
Rockefeller and lead to formation of Rockefeller Asymptomatic in most • Particularly S. vulgaris
Foundation dogs and cats – Smaller species Cyathostomum
• Incidence worldwide has increased in last 50 • Diagnosis: Eggs in
years • J3 juvenile is ingested
– 25% of world population still infected. feces. • Oesophagostomum sp.
• Hookworms have evolved many ways to evade or • Treatment: – Important parasite of ruminates,
suppress the immune system. Thiabendazole primates, and swine
10

11. Family Trichostrongylidae Haemonchus • Pathology: Use lancet
S. on anterior end to
• Very large family with many genera and
vulgaris species contortus pierce stomach lining
in horse • Found in all classes of vertebrates. • Ingests blood
intestine – Females have intestines
• J3 are ingested – direct life cycle intertwined with ovaries
– Heavily grazed pastures can have large • Gives the female the
accumulation of juvenile alternating pattern similar
to a barber pole
• Very important parasite of domestic live
stock. • Symptoms: anemia,
– $222 million in annual cost to Australian sheep emaciation, edema, and
industry intestinal disturbances.
S. vulgaris ingesting – Controlled by Ivermectin. However, resistance is – Heavy infections can be
becoming a problem. fatal.
intestinal lining.
– Also some resistance to the benzimidazole drugs – Survivors frequently
has been reported. develop immunity
Family Sygamidae • Barberpole worm
Haemonchus Haemonchus • Diagnosis: Eggs in
• Gapeworm of poultry • Definitive Host:
feces.
• Lives in the trachea contortus ruminants, including contortus
– Trachea becomes blocked by cattle, sheep, goats. • Treatment:
worms and mucus Mebendazole or
– Causes bird to gasp for air
– Human cases have been
reported Ivermectin
• Many species in Syngamus
found in wild and domestic • Intermediate Host: None • Male do not show
fowl the stripes of the
• Geographic distribution:
• Male is permanently barber pole but have
attached to female. Cosmopolitan
an unusual
• J3 are ingested • Location: Abomasum
– Use earthworms and
asymmetrical
(fourth stomach)
terrestrial mollusks as copulatory bursa
paratenic hosts • Transmission: ingestion
of J3 juvenile
11

12. Adults in Eggs go out Metastrongyloids Angiostrongylus cantonensis
Hatch
Abomassum in feces • Transmission: J3 juvenile ingested
• Lung parasites of many mammals.
• Location: Pulmonary Artery and heart
• Most require an invertebrate
J1 and J2 • Pathology: Generally asymptomatic in rats.
Life Cycle of intermediate host In all hosts, it undergoes a migration from
Mature in develop in
3 days Haemonchus soil • May use several transport hosts. intestines to blood vessels near the brain. In
• Metastrongylus apri important swine humans, it leaves vessels to wander through
contortus brain and spinal cord.
parasite
J4 in Molts as it passes J3 ingested • Symptoms: None in rats. Causes
– Uses earthworm intermediate host
abomassum through first three with forage Eosinophilic Meningoencephalitis in humans
stomachs – Cause pneumonia in pigs – Headache, fever, stiff neck
– Vector/reservoir of swine influenza virus – Paralysis of fifth cranial nerve
– Coma and death
Other Trichostrongylids • Definitive Host: Rodents Angiostrongylus cantonensis
• Trichostrongylus sp. are very small intestinal Angiostrongylus – Recently discovered in humans
• Diagnosis: High eosinophil count in
parasites of many animals • Intermediate Host: Snails,
– T. colubriformis in sheep
cantonensis spinal fluid. Sometimes worms are
slugs,
– T. tenuis in poultry collected in spinal fluid.
• Paratenic hosts: terrestrial
– T. axei in a variety of mammals planarians, freshwater – Symptoms similar to hydatidosis,
• Ostertagia sp., particularly O. ostertagi, cause shrimp, land and freshwater cysticercosis, flukes, and other parasites
$600 million in losses to U.S. cattle industry crabs, frogs, maybe clams – Symptoms also similar to bacterial or viral
and oysters meningoencephalitis.
• Dictyocaulus filaria is a lung parasite of sheep
and goats. • Geographic Distribution: • Treatment: Thiabendazole treats the
Human infections from SE
• Nippostrongylus brasiliensis uses rats as Asia, East Indies,
larval stages but no treatment is known
definitive host. Madagascar and Oceania for adults. Spinal tap may relieve some
– Easy to keep in lab so used to study nematode symptoms. Dead worms also present
infections.
problems.
12

13. Adults in Eggs laid Eggs break • Ingestion of eggs in
J1 migrate • Largest of the nematode Ascaris contaminated food or water.
pulmonary and carried into alveoli up trachea
Ascarids
artery to capillaries and hatch parasites – Use of night soils on crops
– Some are over a foot long
lumbricoides - increases transmission
Molt • Stout, big worms Transmission • Require shade and mild
Life Cycle of A. Swallowed temperatures
and out in • Mouth surrounded with
J4 migrates to • Eggs are very resistant
cantonensis feces large lips, usually 3
pulmonary – Eggs can embryonate in very
artery • Most are intestinal strong chemicals
J2 survives J1 eaten parasites • 2% formalin
if I.H. eaten by I.H. • Potassium dichromate
Molt by P.H. • Infections are usually very • 50% hydrochloric, nitric, acetic,
heavy and sulfuric acid
J2 – Very long life
Migrate to J3 ingested
develops • At lest 10 years
brain by D.H.
in I.H.
• Eggs can splash up onto
Ascaris • Definitive Host: Humans Ascaris vegetables
Intermediate Host: None Eggs can be picked up and
lumbricoides • lumbricoides - • transported by cockroaches.
• Geographic Distribution:
Cosmopolitan Transmission • Wind borne dust may carry the
– 25% of world population is eggs
Nematodes II infected – Trapped on mucus membranes
then swallowed
– Has been known as human
• Eggs have been found on
parasite for over 2000 years
German bank notes!
• Found in writing of ancient Greeks
• Children in infected much more
• Location: small intestines frequently than adults
– Dig in soil and put fingers in
mouth
13

14. • Ascariasis
Ascaris • Depends on the number of A. lumbricoides – Pathology Ascaris
worms and Symptoms
lumbricoides – • Worms subsist on liquid
lumbricoides
• Wandering adults are dangerous. • Sperm does not
Pathology and content of small intestines
– Overcrowding can lead to wandering have a flagellum!
– Do not suck blood or graze on
Symptoms • Upstream to pancreatic or bile ducts • Crawls around like
mucosa.
– May cause liver damage
• Small to medium infections an amoeba
– If reaches stomach, causes vomiting of worm
are usually asymptomatic – Unusual contractile
• Downstream to appendix or out anus
protein allows them
– May cause “sensitization – Females like to crawl through small spaces to move.
phenomenon” • Looking for curly tail of male
• Allergic reaction to worm waste. • Females can lay
• She may crawl through nose, ear, or any other opening
• Rashes, eye pain, asthma, – Image the surprise as a 1.5 foot worm crawls out the nose
200,000 eggs a day
insomnia, restlessness or ear! and have 27 million
• Aspiration of worm can cause death eggs in uteri
Ascaris • Diagnosis:
Ascaris • Heavy infections can block
– Eggs in feces.
intestines. lumbricoides
lumbricoides – – Juveniles in sputum.
– Sometimes fatal • Difficult to identify to
Pathology and species.
• Juveniles migrate through
– Dead adults may be found
Symptoms the lungs in feces
– Causes Ascaris pnuemonitis
• Treatment:
– Fatal in heavy infections Mebendazole will kill the
• Penetration of intestine or adults but not the
appendix may occur migrating larvae
– Frequently fatal – May need to repeat
treatment
• Dead adults usually pass
out through the anus
14

15. Adults in Molt into • Pathology in humans:
Eggs out Embryonate Toxocara • Definitive Host: Dogs and
small in feces in soil J1 Toxocara Causes visceral larval
intestine canis other canids migrans (VLM)
Molt into • Distribution: Cosmopolitan
canis – Juveniles are in wrong host
Coughed up J2 • They wander and some times
and swallowed • Location: Small Intestines go dormant
Life Cycle of • Transmission: Ingestion of • Body walls them off in a
Shelled granuloma
Move up larvae is
Ascaris embryonated egg in – Pathology depends on
trachea swallowed contaminated food and water. where they wander
lumbricoides There is also fetal – Other species of nematodes
Molt twice Hatch from
transmission from mother to can cause VLM
egg
puppies. If rodent eat eggs, – Good reason to de-worm
Break out Enter lymph dogs regularly
into airspace Right side Penetrate becomes paratenic host.
or blood
of lung of heart mucosa
vessel
• Uses pigs as definitive host. • Pathology in dogs: Depends • Symptoms: Canine infections
• Frequently considered the Toxocara on age and immune status of Toxocara are usually asymptomatic.
Ascaris suum host. VLM can cause fever,
same species as A. canis canis pulmonary symptoms,
• If host is naïve, goes on lung
lumbricoides migrations like Ascaris, returns hepatomegaly, and
– Differences in DNA to intestine and lives on fluids eosinophila
– Different lip morphology • If host is immune, juveniles – Depend on number of worms
– Probably a recent split migrate but eventually go into – Can cause death when brain is
developmental arrest infected.
• Less gene flow between the two
species. • When female dog becomes • Diagnosis: For dogs, eggs in
pregnant, worm “wakes up” and feces. ELISA test for humans
• Biology is exactly the same cross placenta • Treatment: None listed for
as A. lumbricoides. – Almost all puppies born in the U.S.
are infected dogs (deworming medicine).
• Can also be transmitted in For humans, Mebendazole but
mother’s milk. only in most severe cases.
15

16. T. canis • Prevention: Frequently de- Other • Toxocara cati - cats • Pathology and Symptoms:
worm pets. • Toxocara vitulorum – cattle Anisakis sp. Usually asymptomatic. If juveniles
– Cover sandboxes when not in Ascarids • Toxocara pteropodis – Australian fruit penetrate stomach, can cause
use bats abdominal pain, nausea,
– Keep animals from defecating • All three can infect young through sometimes vomiting. If juveniles
where children play. mother’s milk but not through placenta wander, mimics other diseases.
• Notes: Children are more • Toxoascaris leonina – dogs and cats • Diagnosis: Frequently seen with
frequently infected than – Doesn’t cause visceral larval migrans endoscope. Immunodiagnosis.
adults • Parascaris equorum is the only large
• Treatment: Removal with biopsy
– 4.6 to 7.3% of children in U.S. ascarid in horses
forceps. No drug treatment.
test positive • Baylisascaris procyonis in raccoons
– May cause pathology in humans • Prevention: Don’t eat
– Rates as high as 30% in undercooked, raw, salted, or pickled
African American children • Lagochilascaris minor found in
pharynx of wild cats in South America, fish. Can be prevented by blast
– In developing countries, 50 to freezing or cooking.
80% of children test positive. North America and Africa
– Has caused death in humans
Adults in Eggs out Develop in Egg eaten by: Anisakis sp. • Definitive Host: wide variety of • Definitive host is birds,
small in the egg to J2 marine fish, birds, and mammals Heterakis particularly poultry.
naïve immune
intestine feces larvae – Rarely humans
dog dog gallinarum • Intermediate host is an
• Intermediate Hosts: earthworm
Mature crustaceans
• Paratenic hosts: any marine • Eggs of the worm carry
J2 hatches
fish Histomonas meleagridis, a
Migrates through • Geographic Range: flagellate protozoan
lungs to small Life Cycle of Cosmopolitan – Causes blackhead disease in
intestine Wanders – Human cases are from Japan, turkeys
Europe, and Scandinavia. U.S. • Destroys the liver
T. canis infections are increasing • Losses on turkey farms
• Transmission: Eating infected – Has no effect on any other bird.
Enters Female Goes
Crosses crustaceans or fish
puppies becomes dormant – Nematode is the intermediate
placenta • Location: Stomach host for H. meleagridis
pregnant
• Eats the protozoan which multiples
in its intestines
16

17. Order • “Pinworms” • Transmission: Eggs are infective Enterobius vermicularis –
• Females have slender, sharp-
Enterobius stage. They are light and can float.
Oxyurida pointed tails. vermicularis 3 modes: Pathology and Symptoms
• Includes parasitic and free- – Hand to mouth (fecal/oral • Heavy infections may cause nervousness,
living species contamination)
restlessness, irritability, loss of appetite,
• Eggs are picked up on the fingers
• Uses invertebrates and nightmares, insomnia, bed wetting, vomiting
and transferred to mouth
vertebrates as definitive hosts
– Inhalation • Rarely fatal.
– No pinworms are found in dogs
and cats • Eggs float and are inhaled, trapped – Worms do attach to the mucosa, resulting in
by mucus membrane, then ulcerations
• Only endoparasite with
swallowed • Lead to secondary bacterial infections which can be fatal.
haplodiploidy
– Reinfection – Worms occasionally penetrate submucosa leading
– Females are diploid
• Develop from fertilized egg • Eggs hatch and larvae crawl back to death.
– Males are haploid through anus
– Worms may also wander up through the vagina, to
• Develop from unfertilized egg • Location in definitive host: uterus, up oviducts and lodge in peritoneum
– Also seen in rotifers, Intestines from stomach to anus • Causes peritonitis and granulomas around the worm.
hymenopteran insects, and Acari
– Most common in ileum-cecum region
mites
Enterobius vermicularis – Enterobius vermicularis –
Pathology and Symptoms Pathology and Symptoms
• Graze on epithelium cells and bacteria
– Cause very little damage • Pinworm Neurosis
– More of a mental condition
Enterobius vermicularis • Disease is called enterobiasis than a medical one.
• Definitive Host: Humans • 1/3 of cases are completely asymptomatic. – Female lays 15,000 eggs
• Distribution: Cosmopolitan but more common in • Most cases, the worst symptom is intense itching. – The eggs get into everything
temperate zones in industrialized countries. • Bedding
– Female migrates out of anus at night to lay eggs • Clothing
– Infects approximately 400,000,000 (10%) worldwide
• Second only to Ascaris lumbricoides (1,000,000,000 or 25%)
– Causes small breaks in skin which are invaded by • Curtains and drapery
bacteria • Stuffed animals
– Most common endoparasite in Europe and U.S.
• Incidence between 30-80% in Caucasian children – Host scratches area, results in more breaks in skin and – People spend time and
• Non-Caucasians seem to be more resistant more bacterial infections and more itching. money trying to eliminate the
– Big problem in institutional situations eggs from the house.
– Larvae may also invade the urethra, vagina, vulva
• Causing itching around those openings as well
17

18. E. vermicularis – Life Cycle
Enterobius vermicularis Adults in the Copulate Female Lays Spirurina: Acuariidae
• Diagnosis: Two preferred techniques: Intestines and goes to eggs
– Scotch tape technique Males die anus outside • All parasites of birds
• Early morning, pat the area around the anus with a piece of
anus – None infect humans
Scotch tape (or any other transparent tape) Mature
• Place tape on microscope slide with a drop of acetone. Eggs Eggs
• Live in stomach and gizzard
• Examine slide for eggs hatch become • Very unusual structures around head
J3 larvae
– Flashlight technique near airborne
craw back – Called cordons
• Shine a flashlight on the anus during the middle of the night anus
• You can see the adult females crawling out to lay eggs.
into anus – Function unknown
• Treatment: Mebendazole (Vermox). Must Eggs – Aids with identification
treat entire family and repeat after 10 days. coughed • Only Echinuria spp. are of economic
Molt twice as J3 larvae
Bedding, towels, and clothing should be up
move to Large hatch in importance
washed in hot water. Eggs
Intestine small – Infect geese, ducks, and swans
swallowed
intestine
Enterobius vermicularis Spirurina: Gnathostomatidae
• Short life span Order Spirurida • Includes several large genera
– Females die after oviposition – Tangqua sp. in reptiles
– Males die after copulation
• Divided into two suborders
– Echinocephalus sp. in elasmobranchs
• Infections become large, however, due to – Spirurina
– Gnathostoma sp. in carnivorous mammals
autoinfection and reinfection • Includes the filarial worms of humans
• Gnathostoma spinigerum can cause
• More common industrialized countries due to – Camallanina infections in humans
increase in bedding, drapery, etc. in the • Includes Dracunculus medinensis – Most common in Japan and Far East
home. – Usually from eating undercooked fish, chicken,
• Most are parasites of wild animals
• Because of low pathology, very little effort to ducks, or any other amphibian, reptile, or bird.
eradicate this species. – First discovered in stomach of a tiger
• Caucasians are much more susceptible than – Can cause cutaneous larval migrans (like A.
non-Caucasians. caninum)
18

19. • Large, stout worms Live on the surface of the eye
Spirurina: • Found in stomach or intestine Spirurina: Gongylonematidae Spirurina: •• Found in birds and mammals
in all classes of vertebrates
Physalopteridae• • Single genus Gongylonema Thelaziidae • Two species have been found
Physaloptera sp. is largest in humans
genus – About 25 species – Thelazia callipaeda parasite of
– 3 spp. in amphibians
• Live in the upper digestive tract dogs in Southeast Asia, China,
– 45 spp. in reptiles and Korea
– 24 spp. in birds • Birds and Mammals are definitive hosts – Thelazia californiensis parasite
– 90 spp. in mammals of deer and other mammals in
– P. praeputialis common in dogs • Only one, G. pulchrum, have been western U.S.
of U.S. found in humans
– P. rara most common one in • Use face flies as I.H.
North America (edemic) – Wrong host so it wanders extensively • T. skrajabini and T. gulosa
• Variety of mammals through upper G.I. tract and mouth occur in U.S. cattle
• Appears to use field crickets for
I.H. and snakes P.H. – Little pathology but very irritating • T. lacrymalis is found in U.S.
– P. caucasica only species found – Treat with albendozole or surgery horses
in humans
• Primates normal host
• Found in mammals only
Spirurina: Tetrameridae Spirurina: Spirurina: Filarial Worms
• Best known is Spirocerca lupi
• Extreme sexual dimorphism
Spirocercidae – Dogs are definitive host • Superfamily Filariodea
– Males typical nematode
– Female greatly swollen and – Uses dung beetle as I.H. • Live within the tissues of the body
red – Paratenic hosts include birds,
• More like a flatworm • Release live larvae
reptiles, and mammals
• Very commonly found in • Dogs usually get it from chickens – No egg stage
gizzard or proventriculus of – Infected dogs may develop – Larval stage called microfilaria
birds spondylosis • Very important causes of disease and
• Cause very little damage • Deformation of the vertebrae disfigurement in humans
• Use arthropods as – In dogs, it is the most frequent
intermediate hosts • Most are in the family Onchocercidae
cause of esophageal sarcoma
• Relatively small family – Includes many species that parasitize wildlife
– Much of the biology is still
– Geopetitia – 5 rare species unknown – Several are very important human parasites
– Tetrameres – 50 species • Wucheria, Brugia, Onchocerca, and Loa
– Microtetrameres – 40 species – Distribution patchy
19

20. • Definitive Host: Humans • Symptoms: Filariasis
– No known reservoir host
Wuchereria • Three phases
• Intermediate Host: Night- Asymptomatic Phase
Wuchereria bancrofti • – Large number of microfilaria in blood
feeding mosquitoes (wide
– Some have swelling of lymph nodes
bancrofti variety of genera and – May lead to other two phases
species) • But not always
• Geographic Range: • Inflammatory (Acute) Phase
Around the equator, from – Due to antigens of adult worms Elephantiasis – a
• No disease caused by microfilaria
central Africa, to Turkey, symptom of W.
– Dilate lymph channels
India, Southeast Asia, • Interferes with lymph flow
Philippines, Australia, and bancrofti infections
– Attacks are marked by sudden onset of
South America fever, chills, rigors, sweating, swollen,
warm skin over lymph nodes, painful
– Originally an Old World lymph node
species spread to New – May also show orchitis (swelling of
World by slave trade testes) and epididymitis.
Location: Lymph channels
Wuchereria• near major lymph glands
Obstructive Phase Social and Psychological Impact
Wuchereria • – Lymph channels become blocked by
Wuchereria • – Elephantiasis can result in chronic
bancrofti • Pathology: Depends on
immune and inflammatory bancrofti dead worms bancrofti disfigurement
response of host. – Lymph backs up and causes – May lead to sexual dysfunction
• People with first exposure in swelling of the area • 27 million men have elephantiasis of
adulthood quickly kill the worm scrotum
– Area is then filled in with scar tissue
and do not develop disease • 13 million people, mostly women, have
– Of 10,431 U.S. naval personnel
– Results in elephantiasis elephantiasis of breast
that contracted W. bancrofti • Extreme enlargement of body parts • Can result in marriages devoid of
during WWII, none developed • Particularly common in arm, legs, and physical and sexual intimacy
elephantiasis scrotum
• Where the parasite is endemic, – Elephantiasis of the scrotum can
– May be due to repeated re- also cause leaking of lymph through
fetus is exposed to parasite’s
infections of the worm. scrotal skin
antigens
– Body’s immune system “learns” – Not fatal • Makes it look like person wet his pants
that microfilaria are “normal” and • Can cause thoughts of suicide
doesn’t kill them.
20

21. • Diagnosis: Microfilaria in
peripheral blood sample at night Adults in Females Microfiliaria Microfilaria • Definitive Host: Humans
Wuchereria – Blood should be taken between 10 lymph release are swept in peripheral
Onchocerca – Up to 90% of people are
p.m. and 2 a.m. channels microfiliara into blood blood at
bancrofti • Microfilaria spend day in deep volvulus infected in some areas
tissues night
• Move to peripheral blood during
• Intermediate Host: Black
night to be picked up by mosquitoes Flies
• Treatment: Hetrazan or DEC
(Diethylcarbamazine) used to kill Molt and Mosquitoes • Distribution: Africa,
adults. migrate to
Life Cycle of pick up Arabia, Guatemala,
– Nasty side effects lymph vessels microfilaria in
– Repeated treatment needed W. bancrofti Mexico, Venezuela, and
blood meal
• Ivermectin prevents infection. Columbia
– Cheaper and fewer side effects – Reached the New World
• Best is combination of the two. with slave trade
• DEC impregnated table salt is Injected with Move to J3 J2 J1
available as well. – Most common along rivers
blood meal proboscis
• Surgery for elephantiasis • Preferred habitat of I.H.
Wuchereria • Avoid mosquito bites at night
Onchocerca • Transmission: Larvae
• Annual or semiannual doses of move into tissues through
bancrofti - DEC (Diethylcarbamazine) and
Brugia malayi
volvulus wound made by bite
Prevention Ivermectin • Very similar biology to W. bancrofti
• Location in D.H.: Just
– One of the diseases the Gates • Limited to Far East and Philippines
foundation is fighting
under the skin in nodules
– Not found in Africa or the New World – most below waist in Africa
• Education
• Pathology and symptoms similar to W. – Most above waist,
– In endemic areas, <50% knew particularly head, in New
what caused filariasis bancrofti World
– Only 6% knew you could catch it – Elephantiasis generally restricted to distal – Due to biting preferences
from mosquitoes of the flies
portions of arms and legs
• 25% had microfilaria in their blood,
• 5% of the women had elephantiasis
• 30% of men had enlargement of
testes
21

22. O. volvulus – • Most pathology due to immune • Definitive Host: Humans
and inflammatory response of Onchocerca volvulus
body. • Diagnosis: Microfilaria in bloodless skin snip. • Intermediate Host: Deer fly
Pathology and Microfilaria can also be seen in eye during
Loa loa
• Adults live in skin nodules • Distribution: Rain forests
Symptoms – Called onchocercomas exam. of west Africa and equatorial
• Little pathology from live larvae • Treatment: Ivermectin kills microfilaria and
and adults
Sudan.
eventually kills adults – Existed for short time in West
• Dead worms cause
– Also a preventative Indies but disappeared
inflammatory response
– Causes severe dermatitis over the – Fewer side effects than DEC (former treatment)
• Transmission: Enters
area – Gates Foundation is actively fighting this parasite
– May result in thickening, wound from fly bite
– Merck & Co. donated large quantities of the drug
depigmentation of skin
• Reduced the incidence of River Blindness significantly • Location: Just under skin
• Often mistaken for leprosy
– Causes “hanging groin” in Africa – May be eliminated soon and in eye.
and Venezuela • Prevention: reduction of Black Fly populations
– Elephantiasis is rare
• Causes River Blindness Black fly
O. volvulus – Adults Females Microfiliaria • Pathology and Symptoms:
– Onchocerciasis Loa loa
under release under the picks up
Pathology and • Microfilaria migrate through the Infection called Loiasis.
skin microfiliara skin microfilaria
eyes in tissue • Causes very little pathology.
Symptoms – Some times they die there
fluids • Wander just under skin, causing
• Inflammatory response causes allergic reactions
the cornea to harden and become
– Called Calabar swelling or fugitive
opaque swelling
Molt Life Cycle of Goes to
– Causes blindness
thoracic • Frequently wanders through eye
• In many areas of Africa and O. volvulus muslces – Can cause emotional distress!
Central America, everyone over
the age of 40 is blind • Most frequent symptoms are
– Little children guide blind adults to Enters itching, joint pain and fatigue.
work in the fields wound
Move to • Rarely, wanders deeper and can
– Blindness is more common in J3 J2 J1
Central America than Africa
made by fly cause fatal encephalitis
proboscis
• Flies prefer to bite on the head
22

23. Other filarial worms of humans Dirofilaria • Location: Right side of
Loa loa heart and pulmonary artery
• Mansonella ozzardi
• Diagnosis: Microfilaria in the peripheral blood – Live in the mesenteries and peritoneum
immitis • Transmission: Injected
during the day – Found in New World only during blood meal.
– Microfilaria move to lungs at night – Uses mosquitoes and black flies as I.H. • Pathology: Large number
• Treatment: DEC (Diethylcarbamazine) is usual • Mansonella perstans of worms block the valves of
treatment but is worse than the worm. – Tropical Africa and South America heart
Ivermectin does not kill adults but prevents – Uses primates as reservoir host – Results in inefficient pumping
reinfection. Adults just under the skin or in eye – Live in coelom of blood
can be removed surgically. – Use mosquitoes as I.H.
• Respiratory complications
• Prevention: Avoid deer fly bites and reduction • Mansonella streptocerca can occur
of deer fly populations. – Lives just under skin of humans in rainforest of
Africa
Adults Females Microfiliaria Deer fly • Heartworm
under release to picks up Dirofilaria • Definitive Host: Dogs, cats,
Dirofilaria immitis
skin microfiliara bloodstream microfilaria • Symptoms: Vomiting, Respiratory insufficiency,
ferrets, sea lions, and other
in tissue immitis chronic cough, exercise intolerance. Death
fluids mammals including humans. usually comes from cardiopulmonary failure
• Intermediate Host: – Human cases are rare but can result in chest pain,
Mosquitoes cough, coughing up blood, fever, malaise
Molt Life Cycle of Goes to • Distribution: Cosmopolitan • Diagnosis: ELISA test. Microfilaria not
Loa loa fat body diagnostic
– In U.S., most common along
Mississippi River, Atlantic and • Treatment: Difficult. Early cases can be cured.
Gulf Coast states Dead adult worms may cause more damage
Enters
• Incidence 45% in dogs than live ones. Can be prevented by giving
wound
Move to – Rare in the western U.S. Ivermectin (Heartguard) during mosquito season
made by fly J3 J2 J1
proboscis • Incidence can be as high as 5% or year round.
in California and Oregon dogs
23

24. Adults in Females Microfilaria • Definitive Host: Humans
Dracunculus medinensis -
heart or release in peripheral Dracunculus – Rhesus monkeys have been Symptoms
pulmonary microfilaria blood infected in the lab
artery
medinensis • Intermediate host: Cyclopoid • Dracunculiasis
copepods • Caused by three factors
• Distribution: Africa, India, – Emerging worms cause severe allergic reaction to
Mosquitoes Middle East worm waste
Molt
Life Cycle of pick up – Reports from North America are • Rash, nausea, diarrhea, dizziness, localized swelling
D. immitis microfilaria in probably different species, D. • Symptoms stop after female emerges
blood meal insignis
– Bacterial infections are common at site of
• Transmission: Ingestion of emergence.
copepods in drinking water.
– Nonemergent “dead” worms can cause
Injected with Move to • Location: just under the skin inflammatory response.
J3 J2 J1
blood meal proboscis • Symptoms can include arthritis and paralysis
Dracunculus • Female becomes swollen Diagnosis: Larvae can be
Suborder Camallanina with larvae and body wall Dracunculus • found in fluid of blister. Large
medinensis - white worm protruding from
• Three families breaks
Pathology medinensis wound also diagnostic.
– Family Camallanidae – Releasing juveniles just under
• Treatment: Adult female is
• Inhabit intestines of fish, amphibians, and reptiles
skin. removed by slowly winding her
• Use cyclopoid copepod as I.H. – Causes inflammation which on a stick.
• No tissue migration results in a blister – Cold water is washed over the
worm
– Family Philometridae – Blister breaks and part of worm
– She expels juveniles and can be
• Tissue parasites of fishes sticks out pulled out about 5 cm
– Family Dracunculidae – Area of blister is very hot – Takes about 3 weeks to remove
entire worm
• Tissue parasites of reptiles, birds, and mammals • Relief comes from putting area in
cold water • Breaking the worm can result
• Dracunculus medinensis and D. insignis have been found in
• Stimulate uterine contractions in massive allergic reaction
humans
– D. insignis is zoonosis from muskrats, opossums, and raccoons. • Female releases up to half a • Surgery can be used to
million larvae in water remove calcified worms
24

25. Dracunculus medinensis Female moves Creates Female releases
to just under blister which J1 into water
• Eradication: WHO predicted it would be the skin ruptures the when D.H. puts
eradicated by 1995. Missed the deadline but skin blister in water
incidence continues to decline.
• Involves Mates and
– Supplying safe drinking water males die Life Cycle of D.
– Education about transmission in unclean water J1 eaten
– Early case containment and keeping infected body Mature medinenesis by
parts out of drinking water copepod
– Vector control – using chemical that kills copepods
but had very little effect on other animals Copepod Penetrate
J3 J2
• Incidence increases during droughts ingested hemocoel
by human
– Larvae and I.H. host concentrated and more likely
to be ingested.
Dracunculus • Long history with humans
– “Fiery serpent” of Bible
medinensis – Found in the writings of ancient
Greeks and Romans
– Caduceus carried by God of
Medicine probably depicts worm
on stick
– Treatment officially described in
1674
• But I.H. wasn’t discovered until
1869
• Males are rarely observed,
reach 40 mm
• Females frequently grow up to
800 mm
25