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HELMINTHS

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b.

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Neglected Tropical Diseases: diseases that rather cause high mortality, cause high morbidity (global burden). Symptoms often associated
with social stigma (river blindness, guinea worm, lymphatic filariasis
Impacts primarily school-age children (5-15 years old) which consequently causes impaired growth and development. This leads to lasting
impact throughout adulthood.
Schistosomiasis (11.7k deaths and 3.3M DALYs/yr) and Hookworm (no deaths 3.2M DALYs/yr) cause the most disease burden
Classification of Parasites Eukaryotes!
Worms (helminths): multicellular, large
Types: nematodes, cestaodes, trematodes (flukes)
WHO Resolution (54.19) de-worming/MDA (mass drug administration; especially to children) goes out to population and administers
Benzimidazoles everywhere once a year. However, reinfection can still happen; May help with breaking transmission cycles (especially for the
mosquito-borne ones); also aims to improve sanitation and access to safe drinking water
Protozoa: unicellular, small (refer to other set of notes)

Intestinal Nematodes (Roundworms)


- Unholy Trinity: ascariasis, trichariasis, hookworm
- Long-lived: often survive for years in host and are generally soil transmitted
- Host can be infected with multiple species
Organism

Epidemiology
Very common.

Ascaris
lumbricoides
(Roundworm)

Trichuris trichiuria
(Whipworm)

-Necator
americanus (80%)
-Ancylostoma
duodenale
(Hookworm)

Africa, South America,


Asia
Most at risk: children
and child-bearing aged
women

-Leads to eosinophilia: during tissue migration phases of helminths


-Crude diagnosis via feces samples and looking for eggs (size and morphology).
- Morbidity related to worm burden
- Do not reproduce within human host (except Strongyloides and Echinococcus)
Pathogenesis
Clinical Manifestations
Diagnosis, Tx, other
Life Cycle: ingest eggs enter
Ascariasis. Usually asymptomatic.
D: eggs in feces (eggs are
heat resistant)
intestine and penetrate through the
Pulmonary phase: eosinophilic
blood stream travels to lungs,
pneumonitis, asthma-like
Tx: single dose of
Intestinal phase: migration into biliary
reaching the throat when
anthelmintic drug
(obstruction) and oral (expulsion) with high
swallowed, become adults and
loads,
remain in the SI; Feces can have
Chronic infection: malnutrition, growth
fertilized eggs, which are hardy and
retardation
last for years new infection
Life Cycle: ingest eggs, but remain in
Dysentery syndrome, Colitis, Rectal
D: eggs in feces (bipolar
large intestine and develop there.
prolapse (usually only in heavy
plugs)
infections); light infections generally
Thin end embeds into colon, while
asymptomatic
thick end waves in lumen and
Tx: albendazole
releases eggs.
Cutting plates/hooks bite into intestine and Iron deficiency: Worm releases Fe into
D: eggs in feces cant tell
cause disease feed on blood (Hb
difference between the two
lumen causing loss.
allows them to survive). Vampires of the
species
Hookworm infection
gut!
= Blood Loss
Tx: single dose of
Life Cycle: Larvae in soil enter skin of feet. Children and child-age
antihelminic drug
bearing women at most
Burrow and enter blood stream. Go
through lungs and develops after Pt
risk because of low Fe
Chronic infections (years)
swallows into SI where it grows and
stores
spreads/gets excreted into soil

Organism
Ancylostoma
caninum/brazilien
se
(dog/cat hookworm)

Epidemiology
Florida, Gulf Coast,
Caribbean

Tropical & subtropical


regions of Africa, Asian,
Latin America; In US
Appalachians

Strongyloides
stercoralis
(threadworm)

Enterobius
(pinworm)

Toxocariasis

Anisakiasis

Reservoir hosts: Dogs


and non-human primates

Pathogenesis
Penetrate skin only

Clinical Manifestations
Larva Migrans: Creeping eruption itchy
and irritation

Life Cycle: Developed larvae in soil


penetrate skin enter circulatory
system Go through lungs, trachea
swallowed adult female worms
live in intestine where they deposit
eggs which can re-infect host (autoinfection) or be excreted

Immunocompetent: asymptomatic usually


Mild GI symptoms, perianal rash due to
larva currens (migration through skin,
pulmonary migration causing
dyspnea/cough; migratory infiltrates on
CXR; high peripheral eosinophilia

female worms present in intestine can


produce eggs without male/fertilization
(parthenogenesis; causing
hyperinfection)
Auto-infection cycle: can last decades
Hyperinfection: immunosuppressed at
higher risk larvae dissemination
Most common in children Life Cycle: Ingest eggs hatch in SI
mature in colon females lay eggs on
perianal region scratch crack, get
under nails, suck thumb, reinfect
Dog and Cat Condition Eggs from canine feces deposited into
humans infected
sandboxes and playgrounds.
incidentally
Accidental ingestion (hopefully)
Larvae hatch in SI and penetrate wall
Puerto Rico
Larvae emerge and invade viscera
(liver, lungs, brain, and eye); Do not
develop into adult worms.
Can get from eating raw
fish.

Life Cycles: L3 larvae are developed in


fish ingested by human Matures
and burrows into stomach wall (dead
end host)

Hyperinfection: Acute enteritis (severe


diarrhea, ulcers in SI and LI; ileus,
hemorrhage; severe pulmonary
manifestation)
Dissemination: Aberrant larvae migration
often carrying intestinal bacteria; high
mortality unless treated early
-Perianal pruritits
-Restless sleep
-Aberrant vaginal infection
-Appendicle inflammation
Visceral larva migrans (VLM)- in toddlers
-pneumonitis, hepatitis, cerebritis
(seizures), eosinopihilia

Diagnosis, Tx
Dx: Clinical
Tx: single dose of
antihelminic drug
D:
-Peripheral eosinophilia
-Fecal Examination:
Microscopy w/ larvae in
fresh stool or agar plate
with bacterial colonies
along track of migrating
larvae
-Serology
Prevention: Screen
immunosuppressed,
improve sanitation,
minimize contact with
contaminated soil
D: scotch tape test
T: Anthelmintic drug; treat all
family members

Ocular larva migrans (OLM) - >5 y/o


-unilateral visual impairment which can
cause permanent blindness
- differential: retinoblastoma or TB
By law, sushi must be flash
frozen to kill this worm.
Tx: Wait until it dies or
remove endoscopically.

Tissue Nematodes (Roundworms)


Human Filariases: Lymphatic filariasis, Onchoceriasis, loa loa, dracunculiasus
- Females produce larvae that migrate throughout blood, allowing for mosquito to feed on and inject into someone else
Organism
Epidemiology
Pathogenesis
Clinical Manifestations
-Zoonosis
Life Cycle: Ingest meat with cyst
Biphasic
-Outbreaks in
-Intestinal phase: GI symptoms
penetrates intestinal wall, develops,
Trichinella
raw/undercooked meat
-Systemic: fever, myalgia, facial edema,
and disseminates through lymph then
containing cysts
eosinophilia
blood Enters skeletal muscle

Diagnosis, Tx
D: muscle biopsy, serology
Tx: steroids (bc
inflammation) & anthelmintic

(pork, bear, walrus and seal)

Endemic in: Africa, SE


Asia/India, Western
South America

Lymphatic
filariasis
Wuchereria
bancrofti (90%)

Onchoceriasis

Transmitted by
mosquito bite
Wuchereria bancrofti
worm causes 90% of
LF, but Brugia malayi,
timori in SE Asia
Children often infected
young and carry for life
Africa
Transmitted by blackfly.
-Massively reduced
prevalence due to MDA
Rainforest area of
West/Central Africa

Loa loa

Dracunculus
medinensis
(Guinea worm)

Larvae enter through bite wound of


mosquito to LN and develop there
obstruction and chronic lymphedema;
the worms enter the blood stream at
night where they can spread to a
mosquito

Not reversible.

Tropical Pulmonary Eosinophilia: young


men

D: microfilariae in blood smear


(at night); Ag detection;
serology; ultrasound of LN
(worms moving (Filaria Dance
Sign); Clinical suspicion

-Chronic: lymphedema in extremities,


breasts, and genitalia; hydrocele and
scrotal elephantiasis
Do not treat with microfilaricide (DEC) if
they have overlapping infection of
onchocerciasis or loiasis

Enter skin through blackfly bite


migrate to subcutaneous tissues
forming nodules (including eye)fly
eats again and cycle restarts; no blood
involvement in this condition
Entry into skin and live in
subcutaneously affecting conjunctivae
and causing calabar swelling

Transmitted by Chrysops
fly.

Mali, Chad, South


Sudan, Ethiopia
- 99.999% reduction in
disease since GW
eradication program
began (3.2mil50!!)

-Early: lymphangitis, lymphadenitis

After ingestion, larvae penetrates


intestine Slowly travels to
subcutaneous lower extremities and
grows
Transmitted by water containing
copepods that have worm larvae.

River Blindness
Chronic infection of the subcutaneous
tissues, skin, and eyes due to parasites
dying and releasing their Agpruritus,LAD,
dermatitis, ocular lesions (blindness)
Calabar swellings: angioedema, worm
moving around skin (visually detectable);
May cause inflammation.
Even across the eye!

-Pain and secondary infections at site of


worm leaving skin.
-Super, super, super long worms.

Tx: Cant kill adult worms


easily so use prolonged and
repeat; Microfilaricide; DEC
Manage: interrupting
transmission via MDA of
diethylcarbamazine (DEC) and
morbidity control

D: skin snips for


microfilariae; palpable
onchoceromas
Tx: ivermectin q6-12 months
D: LAB:microfilaria in blood
smear (during the day);
eosinophilia;
Clinical: visual inspection
T: DEC or ivermectin;
surgery to remove worms
Relatively eliminated via
filtering water education and
preventing infected people
from entering water.
Dx: clinical

Platyhelminths- Flukes (Trematodes)


-water-borne infections with the snail as the obligate intermediate host
-Most are food borne (exception: schistosomiasis)
Organism

Epidemiology
Africa, South America,
Asia
Children especially (1015 peak).

S. mansoni
S. japonicum
S. hematobium
(Schistosoma)

-Clonorchis
-Opisthorchis

Fasciola hepatica

Paragonimus
westermni
Paragonimiasis

Transmitted with skin


contacting
contaminated fresh
water.

Pathogenesis
BLOOD FLUKE
Larvae known as cercariae leaves
snail, swims in water, and enters skin
penetrate into blood vessels
Deposit in SI and liver (a) OR in
bladder (b) where they mature and lay
eggs which are shed in bowel
excretion
(a) S. mansoni, S. japonicum
(b) S. hematobium

China and SE Asia

ORIENTAL LIVER FLUKE

Transmitted via
uncooked freshwater
fish.

Encyst worm obtained from fish releases


and travels up bile duct/matures Lives in
bile duct of liver causing fibrosis excreted
through feces

Bolivia, Peru, Ecuador,


Iran, Egypt
Transmitted via
watercress (water
plant)

WESTERN LIVER FLUKE

China, Philippines

LUNG FLUKE

Transmitted via crab or


crayfish.

Encyst worm obtained from watercress


releases and travels up bile duct/matures
Lives in bile duct of liver causing
fibrosis excreted through feces

Clinical Manifestations
ACUTE:
Swimmers itch:
-12-24hrs after infection; intensely pruritic
urticarial rash which lasts a few days
Katayama fever
-4-8wks after infection; egg deposition by adult
worms begins which can cause hypotension,
shock, and eosinophilia; treat with praziquantel
+/- steroids
CHRONIC: Years post infection
-High worm burden with egg deposition over yrs
-Granulomas form in GI tract, liver, bladder
-S. mansoni/japonicum: periportal fibrosis;
portal hypertension, abdominal pain, GI
blood loss,
-S. haematobium: obstructive uropathy
(fibrosis), bladder carcinoma; genital tract
involvement increases HIV risk in females and
can lead to infertility
-Rarely involves CNS

Acute: fever, abdominal pain,


hepatomegaly, eosinophilia
Chronic: recurrent ascending cholangitis
and pancreatitis, cholangiocarcinoma ,
biliary fibrosis
Acute: abdominal pain (RUQ),
eosinophilia

Diagnosis, Tx
D:
CBC: eosinophilia,
Urine/Stool sample for eggs;
serology
(S. hematobium has
terminal spine while S.
mansoni has lateral spine)

Tx: Praziquantel for >4y/o;


used in MDA programs
Tx: Praziquantel

Dx: Ultrasound/CT/serology
Tx: Anthelmintic

Chronic: destruction of liver


parenchyma
Chest pain, hemoptysis, cough; presence
of pulmonary infiltrates on CXR

D: eggs in sputum
Tx: Praziquantel

Platyhelminths - Cestodes (Tapeworms)


-Food-borne infections
-Adult tapeworms have low pathogenicity, but the larval tapeworm infections cause much more problems (such as seizures). -Every continent except for Antarctica.
Organism

Epidemiology
Undercooked beef
(saginata) or pork
(solium).

Taenia
-T. saginata
-T. solium

Diphyllobothrium
latum
(Diphyllobothraisis)

Humans are the sole


definitive host, but pigs
(solium), cows
(saginata) can be
intermediate hosts
Intermediate host:
Copepod and freshwater
fish
Alaska, Canada, Great
Lakes, Scandinavia
Worldwide distribution
Dog is definitive host,
sheep and humans are
intermediate hosts

Echinococcus
granulosus
(Hydatid disease)

Pathogenesis
Adult: Cyst containing larvae in meat
muscle Ingestion causing release
into SI and develops until adult form
Head (scolex) imbeds in gut and
formed eggs are excreted.
Cysticerosis (alternative T. solium
route): Human ingests egg that has
been released from feces. Larvae
released and penetrates throughout
body and creates cysts.
Disseminates throughout all
tissues/organs and causes
holes/inflammation.

Clinical Manifestations
Cysticeri (solium larvae) present
extraneurally in skeletal muscles and
subcutaneous tissue or in brain
(neurocysticercosis; seizures/convulsions);
cycticercus = lesion which causes
inflammatory response on death that
causes seizure
Note: solium get up to 6m long and live 25
years!

Diagnosis, Tx
Neurocysticercosis Dx:
CT/MRI, serology
Neurocysticercosis Tx: none
if lesion calcified; if viable
praziqantel or albendazole
for months; steroids and
surgery may be necessary
Prevent via pig vaccination,
personal hygiene, meat
inspections, thoroughly
cooking meat, proper
sanitation

Vague abdominal pain

Ingest egg; possibly being liked by dog


in mouth Releases larvae and
disseminates to the liver, lungs, other
sites causing cysts

Megaloblastic anemia and pernicious


anemia (worm uses B12 causing anemia in
host).
Cystic lesions (hyatid cysts) in liver, lungs, D: CT/MRI, ultrasound,
and other sites which can cause
serology
obstruction and possible allergic reaction
when they rupture; Beware if surgery!
Tx:
Albendazole for months or
Hydatid Disease: slow growing cystic
surgery to remove large
tumor in liver, lung, brain
cysts (Puncture cyst,
Aspirate cyst, Inject
chemicals, Re-aspiration)
Prevention: De-worm dogs;
avoid feeding infected
sheep to dogs

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