OLFU

Introduction to Nematodes
2021 – 2022
CLINICAL PARASITOLOGY LEC 6 1st Semester
RMT 2023 Instructor: Prof. Sherlyn Joy P. Isip, RMT, MSMT
Date: November 12, 2021 TRANS 7 PARA311
LEC

OUTLINE

At the end of the session, the student must be able to learn:

I. Introduction to Nematodes
A. General Characteristics
B. Life Cycle
C. Classification of Nematodes
1. Presence of Absence of Chemoreceptors
2. Infective stages and Mode of Transmission
3. Habitat

I. INTRODUCTION TO NEMATODES C. Classification of Nematodes

 Phylum Nemathelminthes (Nematoda) a. Presence of Absence of Chemoreceptors

 Nematodes are the most worm-like of all the helminths because
they resemble the common earthworm appearance, which is
considered as the prototype of the worms.
A. General Characteristics
 Phasmid nematode- with caudal chemoreceptors
 Aphasmid nematode- without caudal chemoreceptors
 Ex. of aphasmid nematode: Trichuris trichiura, Trichinella
spiralis, Capillaria philippinensis

 The name nematode came from “nema” which means thread. They b. Infective stages and Mode of Transmission
are thread-like helminths/worms.
 Free-living forms found in soil and water
 Shape: elongated, cylindrical or filariform in shape, unsegmented  Ingestion of embryonated eggs- Ascaris, Trichuris, Enterobius
worms with tapering ends.  Ingestion of infective larva- Capillaria, Trichinella, Angiostrongylus
 Sensory organs (with exception): amphids (anterior) and  Ingestion of encysted larvae in muscle- Trichinella
phasmids (posterior)  Skin penetration of L3- Hookworms and Strongyloides
 Amphids- these are cuticular depressions present on the lips  Predominantly found if you are walking barefoot on the soil
surrounding the mouth of the nematode and it serves as  Vector-borne- Wuchereria and Brugia
chemoreceptors.  Autoinfection- Strongyloides and Enterobius
 Transmission through inhalation- Enterobius and Ascaris
 Phasmids- useful in grouping the nematodes and it is found at
posterior part or at the caudal portion of the parasite.
 Locomotion: move by contraction of the longitudinal muscles c. Habitat
 Body wall: covered with a tough outer cuticle (smooth, striated,
bossed, or spiny), middle layer is hypodermis and the inner layer is Table 1.0: Intestinal Human Nematodes and Somatic Human
the somatic muscular layer Nematodes
 Sexes: Diecious (separate sexes) Intestinal Human Nematodes Somatic Human Nematodes
 Some are parthenogenic (female worm is capable of fertilizing Small intestine Lymphatics
her own eggs without the benefit of the male)  Ascaris lumbricoides  Wuchereria bancrofti
 Male is generally smaller than female and its posterior end is  Ancylostoma duodenale  Brugia malayi
curved or coiled ventrally.
 Necator americanus  Brugia timori
 Female nematodes may be oviparous (producing eggs), viviparous
 Strongyloides stercoralis
(producing larvae) or ovoviviparous (producing eggs that will hatch
out to become larvae).  Trichinella spiralis
 Capillaria philippinensis
Large intestine Skin/subcutaneous tissue
 Trichuris trichiura  Loa loa
 Enterobius vermicularis  Onchocerca volvulus
 Dracunculus medinensis

Mesentery
 Mansonella ozzardi
 Mansonella perstans

Conjunctiva
 Loa loa
B. Life Cycle

 Consists typically of 4 larval stages and the adult form  Somatic Human Nematodes- extrainstestinal nematodes
 The cuticle is shed while passing from one stage to the other
 Man is the optimum host for all the nematodes. (humans are
the final host)
 They pass their life cycle in one host, except for the Filarial worms
and Dracunculus medinensis where two hosts are required.
 Nematodes localize in the intestinal tract and their eggs pass out
with the feces of the host.
 Most commonly encountered nematodes in the laboratory are
intestinal in nature.

Gurrea, A.N - TRANSCRIBER

[PARA311] 2.03 Introduction to Nematodes I Prof. Sherlyn Joy P. Isip, RMT, MSMT
References:

 Belizario, V. and De Leon, W. (2015). Philippine

Textbook of Medical Parasitology. Third Edition.
University of the Philippines Manila. Ermita, Manila.
 Zeibig, Elizabeth A. (2013). Clinical parasitology: a practical
approach. (2nd ed.). Singapore : Elsevier.
 Mikhail A. Valdescona, RMT, MPH. PAR313 Lecture. Our
Lady of Fatima University. Valenzuela CityMikhail A.
Valdescona, RMT, MPH. PAR313 Lecture. Our Lady of
Fatima University. Valenzuela City.
 http://www.cdc.gov
 Lecture Sidenotes of Prof. Sherlyn Joy Isip, RMT, MSMT –
OLFU VALENZUELA

Gurrea, A.N - TRANSCRIBER

 OLFU Coccidian Parasites
CLINICAL PARASITOLOGY LEC 5 2021 – 2022
1st Semester
RMT 2023 Instructor: Prof. Sherlyn Joy P. Isip, RMT, MSMT
TRANS 6 PARA311
Date: November 5, 2021 LEC

OUTLINE C. Mode of Transmission

At the end of the session, the student must be able to learn:  ingestion of food and water contaminated with sporulated oocyst
I. Coccidian Parasites
II. Cystoisospora belli D. Life Cycle of Cystoisospora belli
A. Morphology
B. Infective Stage
 When a sporulated oocyst is swallowed, 8 sporozoites were
C. Mode of Transmission
released from the 2 sporocyst in the small intestine and will
D. Life Cycle of Cystoisospora belli
E. Pathology invade the intestinal epithelial cells.
F. Diagnosis  In the epithelium, the sporozoites will transform to become
G. Treatment trophozoites, which will multiply asexually by schizogony.
H. Prevention and Control  In the process of schizogony, a number of merozoites will be
III. Cryptosporidium hominis produced.
IV. Cyclospora cayetanensis  The merozoites will invade the adjacent epithelial cells to repeat
V. Toxoplasma gondii the sexual cycle.
VI. Sarcocystis hominis & Sarcocystis suihominis  Some of the trophozoites will undergo sexual cycle or
gametogony in the cytoplasm of enterocytes. Eventually, they will
transform to become microgamete and macrogamete (capable of
fertilization).
I. COCCIDIAN PARASITES
 After fertilization a zygote is formed which secretes a cyst wall
 Unicellular protozoans and develop into an immature oocyst.
 Live intracellularly. At some stage in their life cycle, they possess a  The immature oocysts will be excreted and will mature outside.
structure called apical complex (important for attachment and  Diagnostic Stage: immature oocyst (in the feces)
penetration in cells).
 Some do not have intermediate host
 Under class Sporozoa (Phylum Apicomplexa)
 In class Sporozoa, the life cycle is characterized by an alternations
of generation:
 Sexual : Sporogony (Oocyst as the products)
 Asexual : Schizogony (Merozoites > gametocytes are
produced)
 Cystoisospora belli (Isospora belli)
 Cryptosporidium hominis
 Cyclospora cayetanensis
 Toxoplasma gondii
 Sarcocystis hominis and Sarcocystis suihominis

II. CYSTOISOSPORA BELLI

 The name belli came from the word bellum “war”. Several cases
of the infection with this parasite were seen among troops stationed
in the Middle East during the First World War. E. Pathology

A. Morphology
 Oocysts of Cystoisospora belli are elongated ovoid and measure
25 um x 15 um.
 Each oocyst is surrounded by a thin smooth 2 layered cyst wall.
 Immature oocyst seen in the feces of patients contain two
sporoblasts.
 The oocysts mature outside the body. On maturation, the
sporoblast convert into sporocysts. Each sporocyst contain 4
crescent shaped sporozoites.
 There is a need of environmental contamination for the cyst to
develop and become mature.
 Infection is usually asymptomatic among the immunocompetent.
May present a self-limiting gastroenteritis.
 Symptomatic: diarrhea, fever, malaise, abdominal pain and
flatulence
 Disease is common to children and male homosexuals with AIDS
 In AIDS patients, reports on dissemination of parasite to other
organs are present. (Opportunistic pathogens)
 The stool may contain fatty acid crystals and charcot-leyden
cystals. There is a flattened mucosa and damaged villi causing
high fecal fat content in the stool (steatorrhea). These findings are
not specific.

F. Diagnosis

 Direct microscopy
 Concentration techniques (FECT, ZnS04 and sugar floatation)
 Staining techniques (Iodine, Kinyoun, Auramine-Rhodamine, Ziehl
Neelsen)
 Coccidians are acid fast organisms
 Enterotest and duodenal aspirate
B. Infective Stage
 Molecular testing

 Sporulated oocyst containing 8 sporozoites of the parasite.

Gurrea, A.N - TRANSCRIBER
[PARA311] 2.02 Coccidians I Prof. Sherlyn Joy P. Isip, RMT, MSMT
G. Treatment

 Asymptomatic: bland diet (foods that are soft, not spicy and low in
fiber) and bed rest
 Symptomatic: Trimethoprim-sulfamethoxazole

H. Prevention and Control

 Good sanitary practices

 Thorough washing and cooking of food
 Provision for safe drinking water

III. CRYPTOSPORIDIUM HOMINIS

A. Morphology

 The oocyst is spherical or oval and measures about 5 um in

diameter
 Oocysts does not stain with iodine and is acid fast.
 Thin walled oocysts are responsible for autoinfection
 Thick walled oocyst (passed out with feces).
 Both thin walled and thick walled oocyst contain 4 crescent-
shaped sporozoites

D. Pathology

 Immunocompetent: self-limiting diarrhea within 2-3 weeks

B. Infective Stage
 Oocyst
C. Life Cycle of Cryptosporidium hominis
 Thick-walled oocyst is infectious when ingested. Sporozoites will
attach to the surface of epithelial cells of the GIT.
 Sporozoites will develop to become small trophozoites, and the
trophozoites will divide (schizogony) producing merozoites.
Gametocytes are produced
 Gametocytes > zygote > oocyst (both sporulated)
 Thin walled oocyst will infect other enterocytes > autoinfection
 Immunocompromised: severe diarrhea, bile duct and gallbladder
maybe heavily infected, blunted intestinal villi, varying degrees of
malabsorption and excessive fluid loss
 AIDS patient: severe form of diarrhea, progressively worse
and life-threatening
E. Sources of Infection
 Faulty water purification system
 Swimming in contaminated recreation water
 One person to another: infected food handlers
 Nosocomial infection
F. Diagnosis
 Sheather's sugar floatation, Zinc sulfate floatation technique and
Formalin ether/ethyl acetate concentration technique.
 Kinyoun's modified acid-fast stain (method of choice in
diagnosing. Oocyst appear as red-pink doughnut-shaped circular
organisms): cheapest and simplest method of diagnosis
 IFA
 DNA probe

Gurrea, A.N - TRANSCRIBER

[PARA311] 2.02 Coccidians I Prof. Sherlyn Joy P. Isip, RMT, MSMT
G. Treatment

 No acceptable treatment yet

 Supportive therapy with fluid, electrolytes, and nutrient
replacement
 Nitazoxanide is said to be effective in preliminary studies
 Bovine colostrum (milky fluid that comes from the breast of
cows), paromomycin and clarithromycin: treatment of severe
diarrhea

H. Prevention and Control

 Chlorination is NOT effective (infective stage has thick wall)

 Use of multiple disinfectant and combined water treatment
 Proper disposal of human and animal excreta

IV. CYCLOSPORA CAYETANENSIS

A. Morphology

 The oocyst is a non-refractile sphere, measuring 8-10um in

diameter.
 It contains 2 sporocysts
 Each sporocyst contains 2 sporozoites. Hence, each sporulated
oocyst contains 4 sporozoites.

D. Mode of Transmission

 Ingestion
 Disease is usually self-limiting

B. Infective Stage E. Pathology

 Oocyst  Chronic and intermittent watery diarrhea occurs in early infection

and may alternate with constipation.
C. Life Cycle of Cyclospora cayetanensis  Fatigue, anorexia, weight loss, nausea, abdominal pain,
flatulence, bloating and dyspnea may develop. Infections are
 The oocyst is shed in the feces and it sporulates outside the host. usually self-limiting.
(requires environmental contamination before it develops)  No death is associated.
 The sporulated oocyst are infectious to humans.
F. Diagnosis

 DFS
 Concentration techniques
 Kinyoun stain
 Fluorescent microscopy
 Safranin staining
 PCR

Gurrea, A.N - TRANSCRIBER

[PARA311] 2.02 Coccidians I Prof. Sherlyn Joy P. Isip, RMT, MSMT
G. Treatment D. Life Cycle of Toxoplasma gondii

 No treatment needed  Enteric Cycle

 If pharmacologic treatment is warranted, cotrimoxazole is given.  Asexual and sexual reproduction occurs in the mucosal
 If diarrheal symptoms are prominent, either metronidazole or epithelial cells of the small intestine of cats. (gametogony,
iodoquinol can be used. schizogony)
 Cats acquire the infection by ingestion of the tissue cyst from
H. Prevention and Control the meat of the rats or by ingestion of the oocyst.
 Exoenteric Cycle
 Good sanitary practices  Humans acquire the infection by eating undercooked or
 Access to safe and clean drinking water uncooked infected meat particularly lamb or pork containing
 Proper food preparation tissue cyst.
 May be passed from mother to fetus (congenital
V. TOXOPLASMA GONDII toxoplasmosis during pregnancy), blood transfusion or organ
transplantation.
A. Morphology  The sporozoites from the oocyst and bradyzoites will enter
into the intestinal mucosa > multiply asexually > tachyzoites
 Crescentic tachyzoites- extracellular and intracellular form within are formed.
a macrophage. Tachy means fast (fast multiplying).  Tachyzoites will continue to multiply and spread locally
 Tissue cyst- bradyzoite (slow multiplying) through the blood or lymphatic system. (some spread in
distant extra intestinal organs like brain, eyes, liver, spleen,
lungs and skeletal system then it will form a tissue cyst)
 The slow multiplying forms (bradyzoites) may remain viable
for years. Dormant and may reactivate (in immune
suppression) causing renewed infection in the host.
 Human infection is a dead end for the parasite.

E. Pathology

 Toxoplasmosis commonly asymptomatic, if immune system is

good.
 Active progression of infection is more likely in
immunocompromised individuals.
 Encephalitis is the most common manifestation
 Clinical manifestation is apparent if immune system is
B. Infective Stages suppressed.

 Trophozoite (tachyzoite), tissue cyst (bradyzoite) and the 1. Congenital Toxoplasmosis

oocyst
 Only the asexual forms (trophozoites and tissue cyst) are present  Results when T. gondii is transmitted transplacentally from mother
in other animals including humans and birds. to fetus.
 Most infected newborns are asymptomatic at birth and may
C. Host remain so throughout. Some develop clinical manifestations of
toxoplasmosis weeks, months, and even years after birth.
 Definitive Host: Cats (complete life cycle occurs in cats)  Manifestations:chorioretinitis, cerebral calcifications, convulsions,
 Intermediate Host: Humans strabismus, deafness, blindness, mental retardation,
microcephaly, and hydrocephalus.

Gurrea, A.N - TRANSCRIBER

[PARA311] 2.02 Coccidians I Prof. Sherlyn Joy P. Isip, RMT, MSMT
2. Acquired Toxoplasmosis
 Infection acquired postnatally is mostly asymptomatic (if
immunocompetent).
 The most common manifestation of acute acquired toxoplasmosis
is lymphadenopathy. The cervical lymph nodes being most
frequently affected.
3. Ocular Toxoplasmosis
 It may present as uveitis (eye inflammation affects the middle
layer of the tissue in the eyewall called uvea), choroiditis, or
choriorentinitis.
4. Toxoplasmosis in Immunocompromised Patients
 Most serious and often fatal in immunocompromised patients,
particularly in AIDS, whether it may be due to reactivation of latent
infection or new acquisition of infections.
F. Diagnosis
1. Microscopy
 Tachyzoites and tissue cysts can be detected in various
specimens like blood, sputum, bone marrow aspirate,
cerebrospinal fluid (CSF), amniotic fluid, and biopsy material from
lymph node, spleen, and brain.
 Smear made from above specimens is stained by Giemsa, PAS,
or Gomori methenamine silver (GMS) stain. Tachyzoites appear
as crescent shaped structures with blue cytoplasm and dark
nucleus.
 Gomori methenamine silver (GMS) stain- special stain used in
histopathology particularly in CNS.
2. Antibody Detection
 Acute infection with T. gondii can be made by detection of the
simultaneous presence of lgM and lgG antibodies.
 Tests for detecting lgG antibody include: Enzyme linked
immunosorbent assay (ELISA), Indirect fluorescent antibody test
(IFAT), Latex agglutination test and Sabin Feldman dye test.
 Sabin Feldman dye test- special test incorporated to diagnose T.
gondii. (usually used to confirm Toxoplasmosis infection)
 Serodiagnosis. (Serology is the mainstay for the diagnosis of
toxoplasmosis)
3. Antigen Detection
 Detection of antigen by ELISA indicates recent Toxoplasma
infection
 Useful in AIDS and other immunocompromised patients
 Detection in amniotic fluid is helpful to diagnose congenital
toxoplasmosis.
4. Skin test of Frenkel
 Diluted toxoplasmin is injected intradermally and delayed positive
reaction appears after 48 hours. This test is not very reliable for
diagnosis of toxoplasma.
 Wheal-and-flare reaction indicates a positive test
5. Molecular Methods
 DNA hybridization techniques and polymerase chain reaction
(PCR) are increasingly used to detect Toxoplasma from different
tissues and body fluids
6. Imaging
 Magnetic resonance imaging (MRI) and computed tomography
(CT) scan are used to diagnose toxoplasmosis with central
nervous system involvement.
 Ultrasonography (USG) of the fetus in utero at 20—24 weeks of
pregnancy is useful for diagnosis of congenital toxoplasmosis
G. Treatment
 Congenital toxoplasmosis: pyrimethamine and sulfadiazine
 Ocular toxoplasmosis: pyrimethamine plus either sulfadiazine or
clindamycin.
 Immunocompromised patients: Trimethoprim sulfamethoxazole
is the drug of choice, dapsone-pyrimethamine is the
recommended alternative drug of choice.
 Adverse effect of pyrimethamine- lowers the blood count. It
should be taken together with leucovorin or folic acid.
Gurrea, A.N - TRANSCRIBER
[PARA311] 2.02 Coccidians I Prof. Sherlyn Joy P. Isip, RMT, MSMT
H. Prevention and Control
 Good sanitation and hygiene
 Proper food preparation
 Pregnant women should avoid contact with cats
VI. SARCOCYSTIS HOMINIS & SARCOCYSTIS SUIHOMINIS
 Sarcocystis species produce cyst in the muscle of the
intermediate hosts. These cysts are called Sarcocysts, contain
numerous bradyzoites
 Sarcocystis hominis from cattle
 Sarcocystis suihominis from pigs
 Definitive host: Humans
A. Life Cycle of Sarcocystis spp.
B. Mode of Transmission
 acquired by eating raw or undercooked beef/pork
C. Pathology
 Sarcosporidiosis and sarcocystosis
 Gastroenteritis, diarrhea, myalgia, weakness, fever
 For intermediate host, brain, muscle and kidney tissues may be
damaged.
 May cause abortion to cows
D. Diagnosis
 Fecal floatation methods: sporocysts will be seen
 Fecal floatation wet mount using Bright Field Microscopy
 Floatation methods- based on high-density solutions
incorporating sodium chloride, cesium chloride, zinc sulfate,
sucrose, percoll, Ficoll-Hypaque and other density gradient
media.
 Demonstration of sarcocysts in the skeletal muscle and cardiac
muscle by biopsy or during autopsy
 Western blot
 Serologic tests (IFA, ELISA)
 PCR
E. Treatment
 No specific treatment is available for sarcocystosis
 Corticosteroids were found to be useful in muscular
inflammation
 Trimethoprim-sulfamethoxazole is seen as potentially effective
in treating intestinal infections
F. Prevention and Control
 Uncooked animal carcass should not be fed to other animals
 Avoiding eating raw or undercooked beef or pork
 Thoroughly cooking and freezing meat to kill bradyzoites
(Freeze: -5C for several days)
References:
 Belizario, V. and De Leon, W. (2015). Philippine
Textbook of Medical Parasitology. Third Edition.
University of the Philippines Manila. Ermita, Manila.
 Zeibig, Elizabeth A. (2013). Clinical parasitology: a practical
approach. (2nd ed.). Singapore : Elsevier.
 Mikhail A. Valdescona, RMT, MPH. PAR313 Lecture. Our
Lady of Fatima University. Valenzuela CityMikhail A.
Valdescona, RMT, MPH. PAR313 Lecture. Our Lady of
Fatima University. Valenzuela City.
 Lecture Sidenotes of Prof. Sherlyn Joy Isip, RMT, MST –
OLFU VALENZUELA
Gurrea, A.N - TRANSCRIBER
 OLFU
Filarial Worms
2021 – 2022
CLINICAL PARASITOLOGY LEC 6 1st Semester
RMT 2023 Instructor: Prof. Sherlyn Joy P. Isip, RMT, MSMT
Date: November 12, 2021 TRANS 8 PARA311
LEC

OUTLINE
d. Covering and Habitat
At the end of the session, the student must be able to learn:
 Sheathed microfilaria (retain their egg membrane)
I. Filarial worms
 Unsheathed microfilaria (during fertilization, their egg membrane
II. Lymphatic filarial parasites
ruptures > unsheathed)
A. Life Cycle of Wuchereria bancrofti
B. Life Cycle of Brugia malayi
Table 1.0 Covering of filarial worms
C. Pathology
D. Staging System for Chronic Lymphedema Sheathed microfilaria Unsheathed microfilaria
E. Diagnosis  Wuchereria bancrofti  Onchocerca volvulus
III. Loa loa  Brugia malayi  Mansonella perstans
A. Pathology  Loa loa  Mansonella ozzardi
B. Life Cycle of Loa loa
IV. Unsheathed Microfilaria Table 1.1 Habitat of filarial worms
A. Onchocerca volvulus Lymphatic Subcutaneous Serous cavity
B. Mansonella perstans filariasis filariasis filariasis
C. Mansonella ozzardi  Wuchereria  Loa loa  Mansonella
V. Dracunculus medinensis bancrofti  Onchocerca perstans
 Brugia malayi volvulus  Mansonella
 Brugia timori  Mansonella ozzardi
I. FILARIAL WORMS streptocerca
 Considered as somatic nematodes
 Came from the Latin word filum (thread)
II. LYMPHATIC FILARIAL PARASITES
a. General Characteristics
 Wuchereria bancrofti and Brugia malayi
 Slender thread-like worms  One of the "most debilitating disease" in tropical countries
 Female worms are viviparous and give birth to larvae known as  Filariasis- parasitic infection caused by microscopic threadlike
microfilariae. worms acquired through a mosquito bite (vector borne)
 Microfilariae- infective stage  If the threadlike worms (microfilaria) are acquired, it will
develop to become adult worms, with the adult worms being
lodge in the lymphatic system, these worms will cause lymph
edema, lymphangitis and elephantiasis in chronic cases.
 Has its social and economic impact
 Habitat: Lymphatic vessels (lymph nodes)

a. Mode of Transmission

 Skin penetration through a vector

b. Vector
b. Mode of Transmission
 Aedes spp., Culex spp. and Anopheles spp. (W. bancrofti)
 Mansonia spp. eg. M. bonnae and M. uniformis (B. malayi)
 By the bite of blood-sucking insects (vectors are mosquitoes)
c. Infective stages
c. Periodicity
 L3 larva or filariform larva (man)
 Rhythmical appearance of the microfilaria in the peripheral blood  Microfilariae (mosquito)
circulation.
 Nocturnal periodicity: when the largest number of
d. Diagnostic Stage
microfilariae occur in blood at night.
 Wuchereria bancrofti
 Diurnal periodicity: when the largest number of microfilariae  Microfilariae in the peripheral blood
occur in blood during day.
 Loa loa e. Definitive Host
 Nonperiodic: when the microfilariae circulate at constant
levels during the day and night.  Man
 Onchocerca volvulus
 Subperiodic or nocturnally subperiodic: when the Table 2.0: Differentiation of Wuchereria bancrofti and Brugia malayi
microfilariae can be detected in the blood throughout the day Parameter Wuchereria bancrofti Brugia malayi
but are detected in higher numbers during the late afternoon Malayan filarial
or at night. Common name Bancroft's filarial worm
worm
 Brugia malayi Culex spp.
 The microfilariae are found in the capillaries and blood vessels Vector Anopheles spp. Mansonia spp.
of the lungs during the period when they are not present in the Aedes spp.
peripheral blood. Area affected Lower lymphatics Upper lymphatics
Nocturnal
Periodicity Subperiodic
(8PM-2AM)

Gurrea, A.N - TRANSCRIBER

[PARA311] 2.04 Filarial Worms I Prof. Sherlyn Joy P. Isip, RMT, MSMT

f. Bancroftian filariasis

 Vector Biology:
 Anopheles flavirostris
 Aedes poecillus
 Aquatic habitat: axils of abaca and banana plant (watery)
 Adult biting: day and night biting, indoor and outdoor
 Adult resting: base of abaca plants (cool, shady area)

C. Pathology

a. Classical Filariasis

 Due to blockage of lymph vessels and lymph nodes by the adult

worms.
A. Life Cycle of Wuchereria bancrofti  Prefers lymph because it is less aggressive than blood. No
platelets, complement system, incomplete coagulation system, no
 Definitive host is man. No animal host or reservoir host is known granulocytes and the flow is less violent than in blood.
for Wuchereria bancrofti  The blockage could be due to mechanical factors or allergic
 Intermediate host is female mosquitoes. Different species acts as inflammatory reaction to worm antigens and secretions.
vectors in different geographic area.
 The major vector in India and most other parts of Asia is
Culex.
 The adult worms are usually localized in the lymph vessels of lower
extremities, inguinal lymph nodes, epididymis of male and the labia
of female.

1. Acute Filarial Disease

 Adenolymphagitis (ADL) or
Dermatolymphangioadenitis (DLA)
 Characterized by sudden onset high-grade fever with rigors and
last for 2 or 3 days, lymphatic inflammation (lymphangitis and
lymphadenitis), and transient local edema.
 Lymphangitis- inflamed lymph vessels seen as red streaks
underneath the skin.
 Acute lymphangitis- usually caused by allergic or
inflammatory reaction to filarial infection. May be often
associated with Streptococcal infection as well.
B. Life Cycle of Brugia malayi  Lymphadenitis- inflammation of lymph nodes.
 Most commonly affected lymph nodes: inguinal nodes followed by
axillary nodes.
 Same life cycle with Wuchereria bancrofti but it prefers the upper
 Lymphatics of the testes and spermatic cord are frequently
lymphatic.
involved, with epididymo-orchitis and funiculitis
 Intermediate host of Brugia- genera of Mansonia

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[PARA311] 2.04 Filarial Worms I Prof. Sherlyn Joy P. Isip, RMT, MSMT

5. Lymphorrhagia

 Chylocele, milky appearance caused by the presence of lymph,

2. Chronic Filarial Disease rupture of lymph varices leading to release of lymph or chyle and
resulting in chyluria (kidney damage: “milky urine”), chylous
 more commonly encountered than its acute form diarrhea, chylous ascites, and chycothorax, depending on the
 Lymphedema involved site.
 Follows successive attacks of lymphangitis and usually starts
as swelling around the ankle, spreading to the back of the foot
and leg.
 It may also affect the arms, breast, scrotum, vulva, or any
other parts of body. The edema is pitting in nature but in the
course of time, it becomes hard and non-pitting.
 Edema forms because there is fibrosis and cellular
hyperplasia in and around the lymphatic walls, postulated to
render the lymphatic endothelial cells less effective in
transporting the interstitial fluid and forming abnormal
accumulation of the lymph and the tissues causing swelling.
 The lymphangitis and the lymphadenitis can involve the upper
and lower extremities in both Bancroftian and Bruigian
filariasis
 The involvement of genital lymphatics occurs exclusively with
6. Expatriate Syndrome
Wuchereria bancrofti.
 Genital involvement can be in the form of funiculitis,
epididymitis and hydrocoele formation  Occurs to migrants who were infected from endemic regions. It is
 Lymphoangiovarix characterized by clinical and immunologic hyperresponsiveness to
 Dilatation of lymph vessels commonly occurs in the inguinal, maturing worms. Exhibits acute manifestations and allergic
scrotal, testicular, and abdominal sites. reactions (hives, rashes and blood eosinophilia).

3. Elephantiasis

 Disabling and disfiguring of lymph edema of the limbs, breast and

genitals accompanied by a mark thickening of the skin.
 Delayed sequel to repeated lymphangitis, obstruction and
lymphedema.
 There is non-pitting brawny edema with growth of the new
adventitious tissue and thickened skin, cracks, and fissures with
secondary bacterial and fungal infections.
 Lower limbs are commonly affected but upper limb and male
genitalia may be involved. Breast and genitalia of females may be
affected but relatively uncommon.
4. Hydrocoele
b. Occult Filariasis
 Synonyms: Weingartner's syndrome, Meyer's-Kouwenaar
syndrome, Pseudotuberculosis of the lung, Eosinophilic pseudo-
leukemia, Tropical eosinophilic asthma and Frimödt-Möller and
Barton syndrome.
 Hypersensitivity reaction to microfilarial antigens, not directly due
to lymphatic involvement.
 Microfilariae are not found in blood, as they are destroyed by the
tissues.
 Clinical manifestations: massive eosinophilia (30-80%),
hepatosplenomegaly, pulmonary symptoms (dry nocturnal cough,
dyspnea, and asthmatic wheezing)
 Has also been reported to cause arthritis, glomerulonephritis,
thrombophlebitis, tenosynovitis, etc.

 Accumulation of fluid occurs due to obstruction of lymph vessel of
the spermatic cord and also by exudation from the inflamed test
and epididymis.
 The fluid is usually clear and straw colored but may sometimes be
cloudy, milky, or hemorrhagic.
c. Tropical pulmonary eosinophilia
 Manifestation: low-grade fever, loss of weight, and pulmonary
symptoms
 Children and young adults are more commonly affected in areas of
endemic filariasis including the Indian subcontinent.
 There is a marked increase in eosinophil count (>3000 um which
may go up to 50,000 or more)
 Chest X-ray shows mottled shadows similar to miliary tuberculosis.

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[PARA311] 2.04 Filarial Worms I Prof. Sherlyn Joy P. Isip, RMT, MSMT
 It is associated with a high level of serum lgE and filarial
antibodies.
 Serological tests with filarial antigen are usually strongly positive.
 The condition responds to treatment with diethylcarbamazine
(DEC).

Table 2.1 Difference between Classical and Occult Filariasis

Classical Filariasis Occult Filariasis
Cause Due to adult and Hypersensitivity to
developing worms microfilaria antigen
Basic lesion lymphangitis, Eosinophilic
lymphadenitis granuloma formation
Organs involved lymphatic vessels lymphatic system,
and lymph node lung, liver, spleen,
joints
Microfilaria Present in blood Present in tissues
but not in blood
Serological test Complement fixation Complement fixation
test test
not so sensitive highly sensitive
Therapeutic No response Prompt response to
response DEC

 diethylcarbamazine (DEC)- drug of choice for lymphatic filarial

diseases

D. Staging System for Chronic Lymphedema (Dreyer et. al 2002)

 Stage 1: swelling increases during day but reversible once the

patient lies flat in bed
 Stage 2: irreversible swelling
 Stage 3: presence of shallow skinfolds
 Stage 4: knobs, lumps and protrusions
 Stage 5: deep skin folds
 Stage 6: mossy lesions with leaking of translucent fluid b. Knott's concentration technique
 Stage 7: foul-smelling infected area, patient is unable to
adequately or independently perform activities of daily living.  Anticoagulated blood (1 ml) is placed in 9 ml of 2% formalin and
centrifuged 500 x g for 1 minute. The sediment is spread on a slide
to dry thoroughly. The slide is stained with Wright or Giemsa stain
and examined microscopically for microfilariae.

c. Nucleopore filtration

 In the filtration methods used at present, larger volumes of blood,

up to 5 ml, can be filtered through millipore or nucleopore
membranes (3 um diameter). The membranes may be examined
E. Diagnosis as such or after staining, for microfilariae.

a. Microscopy d. DEC provocation test

 A small dose of diethylcarbamazine (2 mg per kg body weight)

 “wet smears”- demonstrate motile microfilariae
induces microfilariae to appear in peripheral blood even during
 "thick blood smears" daytime.
 Giemsa stain
 demonstration of the microfilaria e. Other specimens
 most practical diagnostic procedure
 Microfilaria may be demonstrated in centrifuged deposits of lymph,
Table 2.2: Differences in Microfilariae hydrocele fluid, chylous urine or other appropriate specimens.
Parameter Wuchereria bancrofti Brugia malayi
Mean length (um) 290 222 f. Ultrasonography
Cephalic space/ 1:1 2:1
breadth  High frequency ultrasonography (USG) of scrotum and female
Sheath affinity to Unstained Pink breast coupled with Doppler imaging may result in identification of
Giemsa motile adult worm (filaria dance sign) within the dilated lymphatics
Body nuclei regularly spaced irregular and
overlapping g. Radiology
Terminal nuclei none 2 nuclei
Appearance in smoothly or gracely kinky  Dead and calcified worms can be detected occasionally by X-ray.
blood film curved In tropical pulmonary eosinophilia (TPE), chest X-ray shows
mottled appearance resembling miliary tuberculosis

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[PARA311] 2.04 Filarial Worms I Prof. Sherlyn Joy P. Isip, RMT, MSMT
h. Demonstration of Antibody

 Complement fixation, indirect hemagglutination (IHA), indirect

fluorescent anti- body (IFA), immunodiffusion, and immunoenzyme
tests have been described.

i. Demonstration of Circulating Antigen

 Highly sensitive and specific test for detection of specific circulating

filarial antigen (CFA) have been developed for detection of recent
bancroftian filariasis.

j. Molecular Diagnostic Technique

 Polymerase chain reaction (PCR) can detect filarial DNA from

patient's blood, only when circulating microfilaria are present in
peripheral blood but not in chronic carrier state.

III. LOA LOA

Table 3.0: Characteristics of Loa loa

Parameter Loa loa
Common name African eye worm
Chrysops spp.
Vector (deerflies, mango flies or IV. UNSHEATHED MICROFILARIA
mangrove flies)
Area affected Subcutaneous tissue A. Onchocerca volvulus
Periodicity Diurnal
 “Convoluted filaria", "Blinding filaria", "Gale filarienne", "Craw craw"
A. Pathology  Onchocerciasis, River blindness (destroys optic nerve), Roble's
disease
 Loaisis, Fugitive swellings or Calabar swellings (causes localized  Subcutaneous nodule or onchocercoma: a circumscribed, firm,
subcutaneous edema as the microfilaria die in the capillaries non-tender tumor, formed as a result of fibroblastic reaction around
around the eye) the worms.
 Onchodermatitis (Sowdah): lesions in the skin and eyes the
affected skin darkens as a result of intense inflammation, which
occurs as result of clearing of microfilariae from blood

B. Mansonella perstans

 Old name: Acathocheilonema perstans

 Culicoides species are the vectors
 Infection may cause dermatitis with pruritus and hypopigmented
macules
 rare parasite of man

C. Mansonella ozzardi

 rare parasite of man, infections does not cause any illness

Table 4.0 Differentiation of O. volvulus, M. perstans and M. ozzardi

Parameter O. volvulus M. perstans M. ozzardi
Black flies
B. Life Cycle of Loa loa Small flies (gnats) Small flies (gnats)
Vector Simulium
Culicoides austeni Culicoides furens
damnosum
 The infective L3 larvae enters the subcutaneous tissue and will Subcutaneous
develop into adult worm over 6-12 months. Habitat Body cavities Body cavities
tissue
 The female worms’ produces sheathed, which have diurnal Onchocerciasis,
periodicity. Pathology Non-pathogenic Non-pathogenic
River blindness
 The microfilariae ingested by the Chrysops (during its blood meal - -
Specimen Skin snips
to an infected host) will cast off their sheaths, penetrate the
stomach wall of fly and will reach the thoracic muscles wherein they
develop into infective larvae (L3 larvae).

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[PARA311] 2.04 Filarial Worms I Prof. Sherlyn Joy P. Isip, RMT, MSMT
a. Treatment c. Mode of transmission

 Diethylcarbamazine citrate (DEC) is the drug of choice. Following  drinking unfiltered water containing infected cyclops
treatment with DEC severe allergic reaction (Mazzotti reaction)
may occur due to death of microfilariae. d. Incubation period
 Administration:
 Mass therapy: In this approach, DEC is given to almost
everyone in community irrespective of whether they have  about 1 year
microfilaremia disease manifestation or no signs of infection
except those under 2 years of age, pregnant women, and A. Life Cycle of Dracunculus medinensis
seriously-ill patients.
 Selective treatment: DEC is given only to those who are
microfilaria-positive.
 DEC medicated salts: Common salt medicated with 1-4 g of
DEC per kg has been used for filariasis control in
Lakshadweep Island, after an initial reduction in prevalence
had been achieved by mass or selective treatment of
microfilaria carriers.
 Ivermectin: In doses of 200 ug/kg can kill the
microfilariae but has no effect on adults.
 Tetracyclines: Also have an effect in the treatment of
filariasis by inhibiting endosymbiotic bacteria
(Wohlbachia species) that are essential for the fertility
of the worm
 Supportive therapy: elevation of the affected limb, use of
elastic bandage, and local foot care reduce some of the
symptoms of elephantiasis. Medical management of
chyluria includes bed rest, high protein diet with exclusion
of fat, drug therapy with DEC, and use of abdominal
binders. Surgery is required for hydrocele.

b. Prevention and Control

 Detection and treatment of carriers.

 Eradication of Vector Mosquito
 Antilarval measures: The ideal method of vector control would
be elimination of breeding places by providing adequate
sanitation and underground waste water disposal system
 Chemical control: Using antilarval chemicals (Mosquito
larvicidal oil, Pyrosene oil-E, Organophosphorous larvicides
like temephos and enthion)
 Removal of Pistia plant: mainly restricted to control of Mansonia
mosquitoes leading to brugian filariasis.
 Personal prophylaxis: using mosquito nets and mosquito repellants
is the best method.
 It has been suggested that the Rod of Asclepius (which represents
V. DRACUNCULUS MEDINENSIS the medical practice since ancient times) once represented a worm
wrapped around a rod; parasitic forms such as Dracunculus
 "Guinea worm", "Worm of Medina", "Dragon worm" or "Fiery medinensis were common in ancient times, and were extracted
serpent" from beneath the skin by winding it slowly around the stick.
 Longest nematode to man (1 meter)  According to this theory, physicians might have advertised this
 Causes "Dracunculiasis" or "Guinea worm disease" (GWD) common service by posting a sign depicting a worm on a rod.
 Mature female worms migrate along the subcutaneous tissue to  The technique of extracting the worm by twisting it on the stick,
reach the skin below the knee, forming a painful ulcerating blister still practiced by patients in endemic areas, is devised by Moses.
 Can also emerge to the head, torso, upper extremities, buttocks  The picture of “serpent worm” on a stick may have given rise to
and genitalia the physician’s symbol, the Caduceus.
 Common symptoms: rashes, fever, nausea, vomiting, diarrhea,
dizziness B. Treatment and Management
 Until there is formation of blister and causes a burning sensation
 Complications: cellulitis, abscess, sepsis, lock jaw (tetanus)  Immersion of affected body part to water
 Wound is cleaned
a. Host  Worm extraction
 Topical antibiotics are given to prevent infection
 Aspirin and Ibuprofen are given to ease the pain
 Definitive Host: man
 Antihistamines and steroids are of help in the initial stage of allergic
 Intermediate host: Cyclops
reaction
 Metronidazole, niridazole, and thiabendazole are useful in
b. Infective form treatment.

 third-stage larva present in the hemocele of infected cyclops

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[PARA311] 2.04 Filarial Worms I Prof. Sherlyn Joy P. Isip, RMT, MSMT
C. Prevention and Control

 Surveillance and case containment

 Provision of protected piped water supply is the best method of
prevention or else boiling of filtering water through a cloth and then
consuming water.
 Destroying cyclops in water by chemical treatment with Abate
(temephos).
 Not allowing infected persons to bathe or wade in sources of
drinking water.

References:

 Belizario, V. and De Leon, W. (2015). Philippine

Textbook of Medical Parasitology. Third Edition.
University of the Philippines Manila. Ermita, Manila.
 Zeibig, Elizabeth A. (2013). Clinical parasitology: a practical
approach. (2nd ed.). Singapore : Elsevier.
 Mikhail A. Valdescona, RMT, MPH. PAR313 Lecture. Our
Lady of Fatima University. Valenzuela CityMikhail A.
Valdescona, RMT, MPH. PAR313 Lecture. Our Lady of
Fatima University. Valenzuela City.
 http://www.cdc.gov
 Lecture Sidenotes of Prof. Sherlyn Joy Isip, RMT, MSMT –
OLFU VALENZUELA

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