Nematodes / Soil-

Transmitted Helminths
(STH)

A. Intestinal Nematodes
B. Blood & Tissue Nematodes
 Intestinal Nematodes

1. Ascaris lumbricoides
2. Trichuris trichiura
3. Hookworms
4. Strongyloides stercoralis
5. Enterobius vermicularis
6. Capillaria philippinensis
 Ascaris lumbricoides

Causes Ascariasis or Roundworm infection.

Lives in the SI of the human host.
A.k.a. large intestinal roundworm.
Has a diameter as big as a pencil or about as thick as
the small finger.
Adult worm may measure 8-18 inches long which is
separated into male & female.
Female is usually bigger than the male because of
the important function of reproduction.
Adult Ascaris male & female worms:
Bulk infection of Ascaris
 How big a problem is Ascariasis?

In local setting, it is present in 50-70% of Filipinos.

Mostly found in the younger age group: preschoolers
& schoolchildren.
Prevalence of infection is usually higher in poor rural
communities & in urban slum areas where it is found
90% of the population. This may probably explain
why most laymen wrongly believe that it is normal to
have ascaris in the GIT.
Life Cycle of Ascaris
 What did you learn from the
diagram?
Embryonated eggs are the infective
stage which are passed out with the
feces of an infected individual & which
have stayed in the soil for 1-2 weeks.
Eggs enter the host thru swallowing of
food or water containing them.
 Pathogenesis & Clinical
Manifestations:
1. Irritation of the intestine
10-20 worms may not show symptoms.
2. Lung migration lung infiltration,
asthmatic attacks & edema of the lips.
 Consequences of the disease:

The parasite competes with the host for

food taken in.
May cause malnutrition & definitely
aggravates an existing malnourished
state.
The more worms are, the more severe
is the loss of food nutrients to the host.
The heavier the worm burden, the more
are the negative effects on the growth &
development of children & productivity
of the adult patients.
 Prevention and Control
1. Stopping the passing out of eggs by the infective
human host by giving antihelminthics which kill the
adult parasite in the intestine thus removing the
source of eggs.
2. Use of proper excreta disposal & sanitary toilets.
3. Avoiding the use of night soil as fertilizer.
4. Control the mechanical vectors: flies &
cockroaches.
5. Sanitary food preparation.
6. Good personal hygiene.
7. Health education.
 Laboratory Diagnosis:

1. Direct Fecal Smear (DFS)

2 mg feces + 1 drop NSS mixed in a
glass slide, coverslip is placed &
viewed under LPO to check for the
presence of eggs.
Fertile/Decorticated Eggs
Unfertilized/Infertile Eggs:
Embyronated Eggs:
2. Kato-technique/Cellophane thick smear
method = qualitative method.
3. Kato-Katz technique = quantitative
method.
 Treatment:

1. Broad spectrum antihelminthics

a. Albendazole
b. Mebendazole
c. Pyrantel pamoate
 Trichuris trichiura

Causes Trichuriasis or Whipworm infection.

Inhabits the LI of humans.
Called whipworm because of the shape of its body.
The posterior 1/3 of its body is fleshy while the
anterior 2/3 is slender & shaped like a whip.
A lot smaller than the Ascaris & measures from 3.5 to
5 cm. long.
The whiplike anterior end is embedded into
the intestinal mucosa of the LI.
This mode of attachment & means of
getting nourishment makes it difficult for
the host to expel it.
Extent of the Problem with Trichuris:
Like ascariasis, it is an important public health
problem & is highly prevalent among Filipinos.
Prevalence parallels that of ascariasis & in some
areas may even be higher than that of ascariasis.
Found nationwide in both rural & urban areas.
Prevalence rates may be 70-80% for the whole
country.
Children are the most affected age groups but may
infect any age group.
Life Cycle
 Similar to the life cycle of Ascaris except
that it is simpler & more straightforward.
What makes it simpler is that the larva
does not have to pass thru the heart &
lungs before maturation in the LI.
Infective stage is the embryonated egg.
Portal of entry is thru the mouth or mode of
infection is thru ingestion of embryonated
eggs.
Longer life span of 3 years compared to
Ascaris which is 1 year.
 Consequences of Trichuriasis:

The worms competition for the hosts

nutrients.
May cause irritation & inflammation of
intestinal mucosa leading to dysentery.
Aside from diarrhea, patients with heavy
worm load may actually develop
wasting & anemia.
Sometimes children with heavy trichuris
may even develop rectal prolapse.
 Prevention & Control:

Essentially the same measures

necessary for the control of ascariasis
will also be applicable to trichuriasis
since both these parasites are soil-
transmitted with exactly the same portal
of entry.
 Laboratory Diagnosis:

1. DFS
Unembryonated Embryonated
 Egg is lemon-shaped with bipolar plugs.
Have yellowish outer & transparent inner shell.
More susceptible to dessication compared to Ascaris eggs.
2. Kato cellophane thick smear
Highly recommended & useful both for
diagnosis of clinic patients & mass stool
examinations in community surveys.
3. Kato-Katz technique
Quantitative method for egg counting used
to assess the success or failure rate of a
control program.
3. Acid-ether technique
4. Formalin- ether technique
 Rectal Prolapse = rectum
descends to lie outside the anus.
 Treatment:

Albendazole = 400mg single dose

Mebendazole = 500mg single dose
The following should be determined pre- & post-
treatment to help evaluate the success or failure of
control measures using chemotherapy.
1. Egg reduction rate
2. Cure rate
3. Reinfection rate
4. Egg count
 Hookworms
Cause hookworm infection.
Roundworms that live in the SI of man.
Called such because they are curved & shaped like
hooks.
Smaller than Trichuris with an average body length
of 1 cm.
Have 2 species that parasitize man:
a. Necator americanus = New World Hookworm
b. Ancylostoma doudenale = Old World Hookworm
Adult Hookworms
 Extent of the Problem with
Hookworms:
Prevalence rates range from 5-60%.
The wide range depends on the
geographic location & type of rainfall.
Hookworm prefers sandy loam soil &
plenty of humidity.
There are also animal hookworms (dog
& cat species) which may accidentally
cause minor pathological conditions in
humans.
Necator americanus is the more
predominant species in the Philippines.
Life Cycle:
 Infective stage is the filariform larva
hatched in the soil which penetrates the
skin of the definitive host, reach the
circulation & are carried thru the heart &
lungs, reach the SI where they mature &
from where the adult females lay eggs.
These eggs are passed with the feces &
reach the soil for embryonation.
Rhabditiform larva Filariform larva
 Hookworms are also called geohelminths.
Cannot be passed on from 1 infected
person to another.
Must also pass thru the soil before they
are transmitted to other hosts.
The site of entry is the skin of whatever
body part which has been exposed to the
larvae-laden soil.
 Consequences of the disease:

Initial pathology is dermatitis at the site

of entry of the larvae.
Development of cutaneous larva
migrans or creeping eruptions.
 When worms attach themselves in the
intestinal mucosa, they suck blood from
the host.
N. americanus causes blood loss of 0.03
mL blood per worm per day.
A. duodenale sucks 0.15 mL blood per
worm per day because of its larger size.
As the worm burden increases, the blood
loss also proportionately becomes more
severe.
As the disease becomes more chronic, the
anemia becomes more pronounced.
 Prevention & Control:

The same preventive & control measures used for

ascariasis & trichuriasis can be applied.
Wearing of proper footwear to protect feet from the
infective larvae coming from the soil.
Wearing gloves when handling soil to prevent entry of
the larvae thru the skin of the hands.
Control of stray animals may also limit the spread of
the animal hookworms.
 Does it mean that if you have hookworms
in your intestines, you will automatically
develop anemia?
No, because as long as you have
adequate intake on dietary iron & your
iron stores are not depleted, you will not
develop anemia even if you have
hookworms.
 Laboratory Diagnosis:

1. DFS = does not detect the parasite in light

infections.
Eggs cannot be distinguished from 1 another which
have bluntly rounded ends & a single thin
transparent hyaline shell.
2. Zinc-sulfate & Formalin-ether
concentration techniques
Recommended for determining whether
the stool is positive or negative for eggs of
hookworms.
3. Harada-Mori culture method
Allows hatching of larvae from eggs on
strips of filter paper with 1 end immersed in
water.
Recommended for determining the actual
species of hookworm.
 Treatment:

Mebendazole = not recommended for

children <2 years old.
Albendazole = not recommended for
pregnant women.
Adverse effects:
1. Epigastric pain
2. Diarrhea
3. Headache
4. Dizziness
 Triumvirate Nematode Infection:

Caused by 3 different species of STH:

Ascaris, Trichuris & Hookworms which
may occur in the patient at the same
time.
 Strongyloides stercoralis
Causes strongyloidiasis.
The only species of nematodes naturally
pathogenic to humans.
Has 3 stages:
1. Free-living larvae
2. Rhabditiform larvae
3. Filariform larvae
Has the same life cycle & infective stage as
hookworms.
But unlike hookworms, larvae & not eggs are
passed out with the hosts feces.
Adult female 3 stages of larvae
& male worms
Life Cycle:
 Free-living forms are found in the soil, the female lays embyronated
eggs which develop into rhabditiform after a few hours.
Rhabditiform develop into filariform & ready to infect human host.
Filariform infect humans thru the skin, enter the circulation, pass the
lungs, migrate to the larynx where they are subsequently swallowed,
develop into adults in a months time while in the duodenum.
Since there are no parasitic males at this time, females reproduce
by parthenogenesis where they invade the intestinal mucosa &
deposit their eggs.
Eggs hatch into rhabditiform, migrate into the lumen & pass out in
the feces.
Autoinfection occurs when rhabditiform pass down the LI & develop
into filariform which may invade the mucosa & enter circulation to
start a new parasitic cycle without leaving the body of the host.
 Consequences of the disease:
Involves 3 phases of infection:
1. Invasion of skin by filariform larvae = erythema & pruritic
elevated hemorrhagic papules.
2. Larvae migration thru the body = lobar pneumonia with
hemorrhage.
3. Penetration of the intestinal mucosa by adult female worms
Pathology is more diarrhea rather than anemia.
Instead of blood loss, Stronglyloides adult worms cause
sloughing off of mucosal patches leading to malabsorption &
diarrhea.
Massive strongyloidiasis is a common complication in
immunocompromised patients (AIDS).
 Laboratory Diagnosis:

Culture = (Harada-Mori & Baermann Funnel culture

methods) practical & economical.
Beales string test
Duodenal aspiration
Small bowel biopsy
Sputum & Urine examination = which may contain
the larvae in disseminated strongyloidiasis.
Serologic methods
Adult female worm & embryonated eggs.
 Prevention & Control:

Measures are similar to those for

hookworm infection.
Infected individuals should be treated to
prevent morbidity & mortality.
People with cancer, pulmonary TB,
malnutrition & those about to undergo
organ transplantation should be cleared
of strongyloidiasis.
 Treatment:

Albendazole
Thiabendazole
Comparison of Hookworm &
Strongyloides:
 Enterobius vermicularis

Causes enterobiasis or oxyuriasis or

pinworm infection.
Characterized by perianal itching or
pruritus ani.
Inhabits the cecum & the adjacent
portion of the SI & LI.
Although not usually fatal, migrating
worms could go beyond the perianal
region & cause pathology elsewhere.
 Adult female measures 8-13mm long with a
pointed tail; the uterus is distended with
eggs.
Adult male measures 2-5mm with a curved
tail; rarely seen.
 Extent of the problem with
Enterobius:
Pinworm infection is fairly common in the Philippines
& is not common in temperate countries where
sanitation measures are relatively more rigorous.
Considered a group infection because it is more
common in infected families or in asylums than in the
general population at large.
More common in children than in adults & is more
common in women than men.
Prevalence rate in the Phils varies from 10% in rural
areas to 75% in crowded urban areas.
Brought about by ingestion or inhalation of infective
eggs which eventually hatch to become adults in the
intestines.
Life Cycle:
 Adult worms inhabit the cecum & adjacent portions of SI & LI.
The fully gravid female worm moves down the intestinal tract to pass
out of the anus & deposits eggs on the perianal skin.
Eggs are fully embryonated & infective within a few hours from the
time of deposition.
Reinfection of the host by contamination of the hands is quite
common & difficult to control.
Development of the adult worms takes about 6 weeks.
Infection thru contaminated clothing, beddings & other objects may
be the cause of familial outbreaks.
Eggs survive in dry dust for some days, & airborne eggs may infect
persons.
Autoinfection is responsible for chronic infection.
 Consequences of the disease:
Migration of the female worms from the anus
produces pruritus which at times may be severe.
In small children, the worms may invade the vagina
where they produce a local irritation (vaginitis).
The local itching is caused by migration of adults
from the anus which may interfere with the sleep of
infected children.
Because of the relatively easy mode of transmission,
it is not surprising to have familial or household
infections as well as epidemics in institutions &
asylums.
 Prevention & Control:

Early diagnosis & treatment of infected

individuals.
Personal hygiene
General cleanliness in the household.
All members of families & residents of
institutions may have to be treated to
prevent epidemics.
 Laboratory Diagnosis:
1. Cellophane tape swab or Grahams scotch tape
adhesive tape swab
Considered as the diagnostic method.
Done by swabbing the perianal area early in the
morning to recover the characteristic Enterobius eggs
which appear as D-shaped or inverted D under the
microscope.
2. DFS
Finding of adult worms or eggs on microscopic
examination.
Eggs are D-shaped or inverted D when
seen under the microscope.
3. Examination of the perianal region
Finding of adult worms.
 Treatment:

Albendazole
Mebendazole
Pyrantel
Cure is considered only after 7 negative
perianal smears using scotch tape
method.
Trichinella spiralis
 Trichinella spiralis

Causes Trichinosis or Trichinellosis.

Morphology: Encysted larvae and Adults
Infection is initiated after consuming
undercooked contaminated meat,
primarily striated muscle.
Meat ingested by human host releases
the larvae which mature into adult worms
rapidly.
Femaled gravid adults lay live larvae in
the intestinal mucosa, larvae enters
 Characteristics of the Encysted
larvae:
1mm in full length.
Settle by coiling up in muscle fibers and
becoming encysted.
Biopsies often reveal inflammatory
infiltrates and a striated muscle cell
known as nurse cell surrounds the
coiled larva.
 Characteristics of Adults:

Males: thin anterior end with mouth,

digestive tract and curved posterior end
with rounded appendages.
Females: blunt rounded posterior end with
single ovary and vulva located in the
anterior fifth of the body.
 Epidemiology:

Found worldwide particularly in meat-

eating populations.
Transmitted by pigs, deer, bear, walrus,
and rat.
 Clinical Symptoms:

Known as a great imitator.

Mild infections: diarrhea and flu-like
symptoms.
Heavy infections: vomiting, nausea,
abdominal pain, diarrhea, headache, and
fever.
Larvae migration: eosinophilia, pain in
pleural area, fever, blurred vision, edema,
and cough. Death is possible in this stage.
 Laboratory diagnosis:

1. Examination of affected skeletal

muscle = method of choice for
encysted larva.
2. Eosinophilia and Leukocytosis
3. Elevated enzymes = LDH, Aldolase,
Creatinine phosphokinase.
 Treatment:

No medication for non-life-threatening

strains.
Plenty of rest
Fluid supplements
Antipyretics
Pain relievers
Prednisone = severe infections
Thiabendazole
Prevention and Control:

Thorough cooking of meat

 Dracunculus medinensis

A.k.a. Guinea worm causing Dracunculosis,

Dracunculiasis, or Guinea worm infection.
Larval stages:
1. First stage or Rhabditiform larva = diagnostic stage
2. Third stage larva = resides in the Intermediate Host
Adults = largest adult nematode.
1. Female adult = larger than male with prominent
blunt rounded anterior end.
2. Male adult = anterior end coils on itself.
 Life cycle:
Ingestion of drinking water contaminated with infected copepods
(freshwater fleas) containing the infective third stage larva.
Larva matures in the intestine into adults, penetrate intestinal wall
and proceed to connective tissues or body cavities.
Gravid female migrates into subcutaneous tissue, especially skin in
the extremities where the first stage larva is deposited.
An infected ulcer results & ruptures when comes into contact with
cool freshwater releasing the larva.
Copepods in the water consume the first stage larva serving as the
IH.
Larva matures into third stage larva.
Ingestion of infected copepods begins the cycle again.
 Epidemiology:

Found in Africa, India, Asia, Pakistan and

Middle East.
Step wells used for drinking and bathing
are the sources of infection.
First stage larva escapes from the
infected person coming into contact with
water.
Ponds, human-made water holes, and
standing water also serve as sources of
infections.
 Clinical symptoms:

Allergic reactions due to migration of

organisms.
Secondary bacterial infections.
 Laboratory diagnosis:
Examining infected ulcers for worms.
Induced rupture of infected ulcers by immersing in cool water
reveals the first stage larva.

Treatment:
Total worm removal

Prevention and Control:

Use of properly treated water
Boiling water
Education
 Capillaria philippinensis or
Pudoc worm
Causes capillariasis.
The very 1st case involved a male Filipino school teacher from
Bacarra, Ilocos Norte in 1963.
Then from 1965-1967, there was an epidemic outbreak of
intractable diarrhea in the border towns of La Union & Ilocos
Sur.
The first victim came from Barrio Pudoc, so people started
calling it Pudoc disease.
The causative agent was unidentified then, so it was also called
mystery disease.
Most of the victims were males & they were dying.
DOH helped in the investigation & found out that the cause of
the epidemic was the C. philippinensis.
Inhabit the intestinal mucosa of the SI mainly the jejunum.
 Transmission is by ingestion of the infective larvae in
the fish intermediate host.
Adult male & female worms are slender & delicate.
Members of the Trichurid family & like the other
members of this family, Capillaria has stichosomes at
the anterior end.
The stichosome is made up of stichocytes lining the
esophagus.
1. Adult male
Has a retractile, chitinized copulatory spicule at the
posterior end which is provided with a long protective
sheath that can extend beyond the length of the
worm.
 Prevention & Control:

Sanitary waste disposal

Eating thoroughly cooked fish
Health education

Treatment:
1. Mebendazole = drug of choice.
2. Replacement of lost electrolytes thru IV fluids.
3. High protein diet
Adult male Capillaria
 Adult female Capillaria

Are of 2 types: Typical & Atypical

Can be differentiated by examining the
eggs in the uterus.
Typical females have only 1 row of eggs
which are peanut-shaped, pale yellow,
moderately thick, striated & with
flattened bipolar plugs & passed out in
the stool.
 Atypical females have 2-3 rows of eggs &
are larviparous.
Eggs are thin-shelled, embryonated &
without bipolar plugs & hatch while still in-
utero.
Larvae are passed out with the stools but
most remain in the intestines where they
develop into new Capillaria adults.
This unusual characteristic is termed as
internal multiplication & sometimes called
autoinfection.
Adult female Capillaria
Life Cycle:
 Eggs passed out with the feces embryonate in water
within 5-10 days & are taken up by small fresh or
brackish water fish where they develop into
infective larvae in the fish intestines.
The fish are small & they could be eaten whole.
If these fish are eaten raw or improperly cooked,
man ingest the infective larvae which in turn
develops into adult Capillaria.
By ingesting the infective stage, one develops
capillariasis.
 Consequences of the disease:
Patients may be asymptomatic or midly
symptomatic but most infected individuals suffer
from the characteristic enteropathy.
First signs & symptoms include:
1. Borborygmi = gurgling of the stomach
2. Diarrhea = 4-10 x per day or prolonged.
3. Anorexia
4. Nausea & vomiting
5. Hypotension
These will result to massive protein & electrolyte
loss leading to weight loss & extreme emaciation.
If untreated, patient may die in 2-3 weeks time.
 On autopsy, parasites occur in enormous numbers in
the intestinal mucosa primarily the jejunum.
On histopathologic studies, the following marked
changes in the intestines are observed:
1. Blunted, flattened or completely destroyed villi.
2. Crypts of Lieberkuhn are deep.
3. Submucosa is inflamed.
4. Mucosa becomes thin.
> These changes are suggestive of malabsorption
syndrome.
 Diagnosis can be established thru:

1. Clinical picture of the condition

2. History of eating raw food mainly fish
3. Laboratory examination of stools =
where eggs, larvae & even adult
worms can be seen.
 Laboratory Diagnosis:

1. DFS
2. Concentration methods
3. Duodenal aspiration
Capillaria eggs are very similar to Trichuris eggs,
since both have bipolar plugs.
 How to differentiate Capillaria ova
from Trichuris ova?
Trichuris ova Capillaria
ova
1. Shape barrel-shaped peanut-
shaped
2. Bipolar protruded flat
plugs
3. Egg not striated striated
shell
 Blood & Tissue Nematodes:

1. Wuchereria bancrofti
2. Brugia malayi
3. Onchocerca volvulus
4. Loa loa
5. Mansonella perstans
6. Mansonella ozzardi
 1. Wuchereria bancrofti

Causes Bancroftian filariasis,

Wuchereriasis, Elephantiasis.
Man is the only DH.
Transmission is thru bite of mosquito.
Adult worms are located in the
lymphatics wherein both sexes lie tightly
coiled in the lymph vessels & sinuses of
the lymph nodes.
Microfilariae are found in the blood.
 2. Brugia malayi

Causes Malayan filariasis.

Man is the DH but may also infect
monkeys & felines.
The fine, white, threadlike adult worms
closely resemble W. bancrofti.
 W. bancrofti & B. malayi

Are both tissue nematodes that cause

Lymphatic filariasis which require a
mosquito IH for transmission.
The juvenile & adult parasites are
roundworms or nematodes that live in
the lymph vessels & lymph nodes.
The microfilariae are found in the blood.
Adults are threadlike worms.
Sexes are separate.
 Bancroftian filariasis:
Is endemic in the ff. provinces: Mountain Province,
Quezon, Mindoro, Marinduque, Romblon, Camarines
Norte, Camarines Sur, Albay, Sorsogon,
Catanduanes, Samar, Leyte, Bohol, Palawan,
Provinces in Mindanao.
Prevalence rates vary from 4%-15%.
Most prevalent in areas where abaca & banana trees
are abundant in which the vector, Aedes poecilius,
happens to breed on the axils of these plants.
Another mosquito, Anopheles flavirostris, a clear
mountain stream breeder, has also been implicated
with this form of filariasis.
 Malayan filariasis:

Is endemic in Palawan, Agusan,

Eastern Samar, Sulu.
Prevalence rate is less than 3%.
Disease is endemic in areas where
freshwater swamps & ricefields exist.
Mosquito vectors implicated include
Mansonia bonnae & Mansonia uniformis.
The cat is an important reservoir host
for B. malayi & may transmit the
infection to man by means of a cat-
mosquito-man cycle.
Life cycle of Filariasis:
Lymph life cycle of Filariasis:
 Parasite is transmitted by the mosquito as the IH in
which the microfilariae develop into the infective
stage.
Microfilariae transform into first (L1), second (L2), &
third (L3) larvae which then migrate from the
thoracic muscles toward the head & proboscis.
It usually takes 10-14 days for W. bancrofti to reach
the infective stage, & 7-10 days for B. malayi.
When the now infected mosquito takes a blood
meal, some or all the infective larvae escape from
the proboscis, actively enter the human host thru
the wound made by the mosquito & eventually
reach the lymph vessels & lymph nodes.
 L3 larvae develop into 4th stage (L4)
larvae in the lymphatics, to the young
adult stage, & finally to the mature adult
worms, males or females.
After fertilization, female worms produce
microfilariae which find their way from
the lymphatic system to the blood
stream.
Life span of the microfilariae is about a
year at the most.
 Consequences of the disease:

The clinical course of lymphatic filariasis can be

divided into Asymptomatic, Acute, & Chronic stages.
1. Asymptomatic stage
Characterized by the presence of microfilariae in the
peripheral blood, although there are no clinical
manifestations of filariasis.
Some individuals may remain asymptomatic for
years, while others progress rapidly to acute &
chronic stages.
2. Acute/Inflammatory stage
Marked by recurrent attacks of fever
associated with inflammation of the
lymph nodes (lymphadenitis) & lymph
vessels (lymphagitis).
In bancrofitan filariasis, the lymphatic
system of the male genitalia is
frequently affected in addition to the
lymph nodes in the inguinal, axillary, &
epitrochlear regions.
This may lead to funiculitis, epididymitis,
or orchitis or to a combination of these.
An attack of adenolymphagitis may be
3. Chronic/Obstructive stage
Microfilariae are usually absent from the blood.
In bancrofitan filariasis, the common manifestations
are hydrocele & swelling of the testicles, followed by
elephantiasis of the entire lower limb, the scrotum,
the entire arm, the vulva, & the breast in a
descending order of frequency.
In brugian filariasis, the leg below the knee is
characeristically affected, & sometimes the arm
below the elbow.
Genital involvement has not been reported, except
in areas where brugian filariasis exists together with
bancroftian filariasis.
Images of bancroftian filariasis:
Images of brugian filariasis:
 Persons with chronic clinical manifestations may be
characterized as having no physical pain & suffering
when there is no associated adenolymphagitis.
However, patients with elephantiasis or hydrocele
may have social & marital problems.
They have lesser chances of getting married, or when
the disease manifests during married life, it may lead
to separation or other marital problems.
In addition, persons with extremely large legs or
hydrocele may not be able to work or take care of
themselves. Hence, they may be a burden to the
family & community.
 Laboratory diagnosis:

1. Blood obtained at night

1 drop blood on a slide examined
under LPO for actively moving
microfilariae.
W. bancrofti B. malayi
 2. Thick blood smears

To determine the species of

microfilariae.
Blood smear is stained with Wrights or
Giemsa stain which will bring out the
diagnostic characteristics.
 3. Serologic test

To detect antibodies to filarial antigen

when microfilariae cannot be found in
the blood.

Treatment:

1. Diethylcarbamazine DEC, Hetrazan

is the standard drug.
 Prevention & Control:

1. Reducing the amount of transmission by any or

combination of the following methods:
A. Decreasing the microfilaria rate
B. Decreasing vector density
C. Decreasing contact between vector & human host
2. Parasite control thru chemotherapy.
3. Vector control thru insecticides, biological control,
environmental modification, & general community
measures.
4. Health education.
 3. Onchocerca volvulus

Causes Onchocerciasis, Onchocercosis,

River blindness.
Man is the DH.
IH are the blackflies of the genus
Simulium.
Adult worms are found in the
subcutaneous tissues, usually
encapsulated in fibrous tumors within
which the worms are intricately coiled.
Tumors contain adults and microfilariae
Life cycle:
 Metamorphosis to an infective larva in
the blackfly requires 6-10 or more days
in the thoracic muscles, from which the
mature larvae migrate to the proboscis
of the fly.
When the infected blackfly bites, larvae
escape to the skin of the new host &
penetrate the bite wound.
The worm becomes adult in less than a
year & lives for at least 5 years.
 Consequences of the disease:

1. Hanging groin folds in the thick,

wrinkled skin of the inguinal area.
2. Onchocercal dermatitis
A. Lizard skin dry & scaly changes.
B. Leopard skin blotchy depigmentation.
 3. Ocular involvement most
serious clinical manifestations.
 Laboratory diagnosis:

1. Skin snips
2. Eye examination
3. ELISA
4. Mazzotti test done only when skin
snips are negative.
 Treatment:

1. Ivermectin
2. Analgesics
3. Antihistamines
Prevention & Control:
1. Vector control
2. Reduction or elimination of infected
reservoir
3. Health education
 4. Loa loa

Causes Loiasis, Eye worm, Fugitive

swellings, Calabar swellings.
Humans & monkeys are the DH.
IH are the insects Chrysops.
The adult, threadlike, cylindrical worms
inhabit the subcutaneous tissues.
Microfilariae have diurnal periodicity in
blood.
May live iin humans for 4-17 years.
Life cycle:
Ingested microfilariae passes thru a
cyclic development in the fly in 10-12
days.
Person bitten by the fly is infected by the
escape of the infective larvae from the
skin membrane near the bite wound.
Within an hour, larvae penetrate the
subcutaneous & muscular tissues where
they become adult worms in about 12
months.
Loa loa in the eyes:
 Laboratory diagnosis:
1. Blood smear
2. Serologic testing = presence of antifilarial
antibodies.

Treatment:
1. Diethylcarbamazine (DEC)
= drug of choice
1. Ivermectin
2. Albendazole

Prevention & Control:

1. Use of insect repellants
2. Use of light-colored clothing
Jeremiah 29:11 KJV
[11] For I know the thoughts that I think
toward you, saith the Lord , thoughts of
peace, and not of evil, to give you an
expected end.
 Godbless, Future RMTs!!!!!!
Matthew 6:33 KJV
[33] But seek ye first the kingdom of God,
and his righteousness; and all these things
shall be added unto you.