Paralec 1 To 12 With 5678 Lab

OLFU
Introduction to Parasitology
2021 – 2022
CLINICAL PARASITOLOGY LEC 1 1st Semester
RMT 2023 Instructor: Prof. Sherlyn Joy P. Isip, RMT, MSMT
Date: September 14, 2021 TRANS 1 PARA311
LEC
 Tropical Disease
At the end of the session, the student must be able to learn:  An illness, which is indigenous to or endemic in tropical area
I. Parasitology but may also occur in sporadic or epidemic portions in areas
A. Divisions of Parasitology that are not tropical.
II. Host Parasite Relationship  Parasite
A. Symbiosis  Lives on or in the host usually on a larger organism, which
B. Parasites according to the Mode of Living provides physical protection and nourishment.
C. Parasites according to Duration of Parasitism  Host
D. Parasites according to Pathologic Conditions  Harbours parasite and gives nourishment.
III. Types of Host
IV. Sources of Exposure to Infection II. HOST PARASITE RELATIONSHIP
A. Contaminated soil and water
B. Food containing immature infective stage of parasite  The organisms may develop unique relationship due to their
C. Arthropods, blood sucking insects and other wild or habitual and long associations with each other.
domesticated animals
D. Another Person A. Symbiosis
E. One’s self
V. Types of Vectors  Living together of unlike organisms, protection or other advantages
VI. Modes of Transmission to one or both partners.
VII. Portal of Entry  Mutualism
VIII. Portal of Exit  Relationship is beneficial to both organisms.
IX. Nomenclature  Termites
X. Types of Life Cycle  Commensalism
A. Life stage of a parasite  Parasite derives benefit without reciprocating and without
XI. Mode of Reproduction injury to the host or both.
XII. Epidemiologic Measures  Entamoeba coli can be found in intestinal lumen
XIII. Distribution of Diseases and is being supplied with nourishment without
XIV. Pathophysiology and Symptomology of Parasitic causing any damage to the tissue of the host.
Infections  Parasitism
XV. Factors that determine the Intensity of Parasitic  Relationship where one organism, the parasite, lives in or
Infection another, depending on the latter for its survival and usually at
XVI. Treatment the expense of the host.
XVII. Prevention and Control
 Entamoeba histolytica derives nutrition from
XVIII. Eradication and Elimination
human host at the same time it causes amoebic
dysentery.
I. PARASITOLOGY B. Parasites according to the Mode of Living
 An area of science, which deals with the study of organisms living  Ectoparasites
permanently or temporarily on or within another organism.  Living outside the body of the host.
 The branch of biology or medicine concerned with the study of  Infestation
parasitic organisms  Endoparasites
 It is the study of parasites, their hosts, and the relationship between  Living inside the body of the host.
them.  Infection
 Concerned with the phenomena of dependence of one living  Facultative parasites
organism on another.  Able to live outside or inside the host and lead both to a free
and parasitic existence.
A. Divisions of Parasitology  Obligate parasite
 Completely dependent to the host for its existence throughout
 Protozoology its life.
 Protozoans: small, unicellular organisms, which contain  Accidental/Incidental parasite
nucleus and functional organelles.  Establishes itself in the host in which it does not ordinarily live.
 Helminthology  Occasional/Periodic
 Worms: larger, multicellular organisms normally visible to the  Seeks its host intermittently to obtain nourishment.
naked eye in their adult form.  Saprophytes
 Medical Entomology  Live in organic substances in state of decomposition.
 Insects and arthropods  Erratic
 Those that live in an organ different from the one it usually
parasitize.
OTHER TERMINOLOGIES  Zoonotic
 Animal parasites, non-human parasites that may cause
 Medical Parasitology human infections.
 Concerned primarily with the parasite that affects humans and
their medical significance, as well as their importance in
human communities.
 Tropical Medicine
 Branch of medicine, which deals with tropical diseases and
other special medical problems of tropical regions.
Gurrea, A.N, Ortiz, M.J - TRANSCRIBER

[PARA311] 1.01 Introduction to Parasitology I Prof. Sherlyn Joy P. Isip, RMT, MSMT
C. Parasites according to Duration of Parasitism  Autoinfection
 Infected individual becomes his own direct source of infection.
 Temporary parasites  Enterobius vermicularis
 Free living during part of existence, larval stage has different  Superinfection or Hyperinfection
host from its adult stage.  already affected individual is further infected with the same
 Permanent parasites species leading to the massive infection with the parasite
 Remain on the body of the host in all stages of its life cycle.  Co-infection
 simultaneous infection of a host by two or more parasite
 Presence of Ascaris lumbricoides and Trichuris
D. Parasites according to Pathologic Conditions
trichiura in the stool sample.
 Spurious/Coprozoic parasite
 Passes digestive tract of humans without infecting them. A. Contaminated soil and water
 Coprophilic parasite
 Parasite multiply in fecal matter outside the human body.  lack of sanitary toilets and use of night soil
 Hematozoic parasite  Soil: Ascaris lumbricoides, Trichuris trichiura, Hookworm,
 Lives inside the red blood cells Strongyloides stercoralis
 Cytozoic parasite  Water: Amoeba, Flagellates, Blood flukes
 Lives inside the cells or tissues
 Coelozoic parasite
 Lives in the body cavities B. Food containing immature ineffective stage of parasite
 Enterozoic parasite
 Lives in the intestine  consumption of undercooked or raw freshwater fish, crab,
snail, beef and pork
III. TYPES OF HOST

C. Arthropods, blood sucking insects and other wild or
domesticated animals
 Definitive host
 final host, harbours the adult and sexually mature form
 If infected with Taenia saginata and Taenia solium,  Mosquitoes (Filaria and Malaria)
humas are considered as definitive host.  Triatoma bugs ( Trypanosoma cruzi)
 These helminths develop into adult form inside the  Sandflies (Leishmania)
human body.  Cats, dogs and house rats
 Intermediate host
 harbours the larvae or asexual stage of the parasite
D. Another Person
 In some Helminths, their first intermediate host can
be plants. While their second intermediate host can
be snail or fish.  Beddings and clothing
 Reservoir host  Immediate environment he has contaminated
 Animal that harbours the same parasite of man
 Pigs are reservoir of Balantidium coli E. One’s self
 Paratenic host
 harbours a stage of the parasite where in no further
development in parasite takes place.  Autoinfection: self is the source of infection
 Angiostrongylus cantonensis is in larva form when  Enterobius vermicularis, Hymenolepis nana, and
resided in the human body and will not develop into Strongyloides stercoralis
adult form. Their definitive host is the house rats
while humans are considered as their paratenic
host. V. TYPES OF VECTORS
 Vector is responsible for transmitting the parasite from one host to

IV. SOURCES OF EXPOSURE TO INFECTION another.
 Pathogens A. Biological vector

 can be animal parasites that are harmful and frequently cause
mechanical injury to their host  the parasite is seen inside the body of this organism and the
 Carrier parasite needs this organism for its development. Ex:
 harbours a particular pathogen without manifesting signs and mosquitoes, tsetse flies
symptoms
 Exposure
 process of inoculating an infective agent B. Mechanical vector
 Infection
 establishment of the infective agent in the host  Responsible only for transporting the parasite, the parasite is
 Incubation period only seen on the surface of this organism and there will be no
 period between infection and evidence of symptoms development on the parasite. Ex: cockroaches, house flies
 Pre-patent period
 Biological incubation period, period between infection and
acquisition of the parasite and evidence or demonstration of VI. MODES OF TRANSMISSION
infection.
 Soil transmitted
 Arthropod/ Vector transmitted

 Food-borne XI. MODE OF REPRODUCTION
 Water-borne
 Skin penetration A. Sexual
 Congenital transmission
 Direct contact
 Oviparous: "egg birth", give birth to eggs that must develop before
hatching
 Ovoviviparous: ones that produce eggs but retain them inside the
VII. PORTAL OF ENTRY
female body until hatching occurs, so that "live" offspring are born
 Larviparous/ Viviparous: being born alive without eggs
 By mouth: most common area of invasion, entrance for intestinal
protozoa
 Skin penetration B. Asexual
 Intranasal: inhalation of eggs
 Transplacental infection  Binary fission: division in half
 Transmammary  Parthenogenesis: unfertilized ovum develops directly into a new
 Sexual intercourse individual, natural form of asexual reproduction in which growth and
development of embryos occur without fertilization by male sex cell
VIII. PORTAL OF EXIT

XII. EPIDEMIOLOGIC MEASURES
 Stool
 Urine  Epidemiology
 Sputum  science concern with the propagation of the disease,
 Blood study of patterns, distribution and occurrence of
 Tissue aspirates and biopsy disease
 Orifice swab
 Discharge  Incidence
 number of new cases of infection appearing in a
population in a given period of time
IX. NOMENCLATURE  Absolute number
 Prevalence
 Classified according to the International Code of Zoological
 usually expressed in percentage, number of
Nomenclature individuals in a population estimated to be infected
 Scientific name are Latinized with a particular parasite at a certain time
 Names of genera and species are italicized or underlined when
written.  Cumulative prevalence
 Generic names consist of a single word written in initial  percentage of individuals in the population infected with
capital letter, the specific name always begins with a at least one parasite
small letter.
Kingdom: Animalia  Intensity of infection
 number of worm per infected person (worm burden)
Phylum: Nematoda  Direct: counting expelled worms during treatment
Class: Secernentea  Indirect: counting helminth egg excreted in feces,
expressed in egg per gram
Order: Ascaridida
Family: Ascarididae
XIII. DISTRIBUTION OF DISEASES
Genus: Ascaris
 Sporadic
Species: Ascaris lumbricoides  appears only occasionally in one or at most a few members of
the community
 eg. Tetanus and rabies
X. TYPES OF LIFE CYCLE  Endemic
 there is a steady moderate level of disease in human
 Simple or complicated population
 Most parasitic organisms attain sexual maturity at the  eg. Malaria in Palawan
definitive host.  Epidemic
 Larval stage of parasite may pass through different  there is a sudden outbreak or rise of incidence in human
stages in an intermediate host. population
 As life cycle becomes complicated, the lesser chances
 SARS-CoV and MERS-CoV
are for the individual parasite to survive.
 Pandemic
 when the disease have been disseminated in extensive area
A. Life Stage of a Parasite of the world
 COVID-19, AIDS and HIV
1. Ova
2. Egg
3. Larva
XIV. PATHOPHYSIOLOGY AND SYMPTHOMOLOGY OF
4. Trophozoite
PARASITIC INFECTIONS
5. Cyst
6. Adult
 Traumatic or physical damage
 when parasites invade the skin and other tissues causing
destruction

 Deprivation of the host’s essential nutrients and substances

 the parasite competes with its host for the available supple of
vitamin.
 Diphyllobothrium latum competes on vitamin b12
Creeping eruption, a skin infection caused by hookworms
 Lytic necrosis
 secretory and excretory products elaborated by many
parasites allow them to metabolize nutrients obtained from the Hookworms
host and store these for energy production.
 Entamoeba histolytica secretes enzyme cysteine proteinase
to digest cellular materials and degrade epithelial basement XV. FACTORS THAT DETERMINE THE INTENSITY OF
membrane facilitating tissue invasion. PARASITIC INFECTION
 Topography of locality
 Social condition
 Age
 Hygienic measure
 Sewage disposal
 Water supply
XVI. TREATMENT
Entamoeba histolytica in rectal biopsy  There are several options for treating parasitic infections. Many of
these drugs are toxic to the host and care should be exercised
 Tissue reactions when selecting the proper course of treatment.
 Cellular proliferation, white cell infiltration at the side of the  Antiparasitic medications
parasite  Change in diet
 Vitamin supplements
 Fluid replacement
 Blood transfusion bed rest
 Deworming
 Use of anti-helminthic drugs in an individual or public health
program.
 Cure rate: usually expressed in percentage,
number of previously positive subjects found to be
egg-negative in examination of a stool or urine
Filarial larvae of Strongyloides stercoralis sample using a standard procedure at a set time
after deworming.
 Toxic allergic phenomena  Egg reduction rate: percentage fall in egg counts
 When proteins or other metabolites of the parasites are after deworming based on examination of a stool or
introduced into the body, there is sensation to the foreign urine sample using a standard procedure at a set
substance, which may produce hypersensitization to time after deworming
anaphylactic shock.
 Selective Treatment
 Individual-level deworming with selection of treatment based
on a diagnosis of an infection or based on presumptive
grounds
 Targeted Treatment
 Group-level deworming where the risk group to be treated
(with or without prior diagnosis) may be defined by age,
gender or other social characteristics irrespective of infection
status.
 Universal treatment
Punctuate keratitis
 Population-level deworming in which the community is
treated irrespective of age, gender, infection status or other
social characteristics.
 Coverage
 Proportion of target population reached by an intervention.

 Drug resistance
 Genetically transmitted loss of susceptibility to a drug in a
worm population that was previously sensitive to the
appropriate therapeutic dose.
 Efficacy
 Effect of a drug against an infective agent in deal experimental
conditions and isolated form of any context.
 Performance of intervention under ideal or control
circumstances mostly used in research or in trial.
 Is the drug working or not?
 Effectiveness
 Measure of the effect of a drug against infective agent in a
particular host, living in a particular environment with specific
ecological, immunological, and epidemiological determinants.
 Is the drug working or not? Is it effective or safe?
XVII. PREVENTION AND CONTROL
 Morbidity Control
 Avoidance of illness caused by infections, may be achieved
by periodically deworming individuals or groups, known to be
at risk of morbidity.
 Targeted treatment may be given
 Information-education-communication (IEC)
 health education strategy that aims to encourage people to
adapt and maintain healthy life practices
 Environmental management
 planning, organization, performance and monitoring of
activities for the modification and/or manipulation of
environmental factors or their interaction with human beings
 preventing or minimizing vector and intermediate
host propagation
 reducing contact between humans and the infective
agent
 Environmental sanitation
 intervention to reduce environmental health risk
 safe disposal and hygienic management of human
and animal excreta, refuse and waste water
 control of vectors, intermediate host and reservoir
of diseases
 provision of safe drinking water and food safety
 housing that is adequate in terms of location,
quality of shelter and indoor living conditions
 facilities for personal and domestic hygiene
 safe and healthy working conditions
 Sanitation
 provision to access to adequate facilities for safe disposal of
human excreta, usually combined with access to safe
drinking water
XVIII. ERADICATION AND ELIMINATION
 Disease eradication
 Permanent reduction to zero of the worldwide incidence of
infection caused by a specific agent, as a result of deliberate
effort. Once this is achieved, continued measures are no
longer needed.
 Small pox
 Disease elimination
 Disease elimination: reduction to zero of the incidence of a
specified disease in a defined geographical area as a result
of deliberate effort. Continued intervention and surveillance
are still required.

OLFU
Intestinal and Extraintestinal Amoebae
2021 – 2022
Date: October 01, 2021 TRANS 2 PARA311
LEC
OUTLINE B. Classification of Protozoan Parasites
At the end of the session, the student must be able to learn:

I. Protozoa
A. Composition
B. Classification of Protozoan Parasite
C. General Rule for Amebae
II. Entamoeba histolytica
A. Life Cycle of E. histolytica
B. Morphologic comparison between E. histolytica and
E. coli
C. Pathogenesis
D. Pathology
E. Pathogenic Determinants/Virulence Factor
F. Laboratory Diagnosis
G. Treatment
H. Prevention and Control
III. Non-Pathogenic species
A. Entamoeba coli
B. Entamoeba dispar
C. Entamoeba hartmanni
D. Entamoeba polecki
E. Entamoeba gingivalis
F. Entamoeba moshkovskii
G. Endolimax nana
H. Iodamoeba butschlii
IV. Free Living Pathogenic Amoeba
A. Acanthamoeba spp. (Acathamoeba castellani)
B. Naegleria fowleri
V. Phylum ciliophora cilates
A. Balantidium coli
I. PROTOZOA
 Proto ( first), Zoa (animals) Encystation

 Unicellular organism that performs all the functions: reproduction,
digestion, respiration, excretion, etc.  Stage forming a cyst or becoming enclosed to a capsule, this
event takes place in the rectum of the host as feces are dehydrated
A. Composition or soon after the feces have been excreted
1. Nucleus
 usually single but may be double or multiple; contains one or Excystation
more nucleoli or a central karyosome; DNA containing body
2. Cytoplasm  Escape from cyst or envelope, produces a trophozoite from the
 Endoplasm: inner (often granulated), dense part. cyst stage, and it takes place in the large intestine of the host after
 Granulated because it shows number of structures such the cyst has been ingested.
as golgi bodies. endoplasmic reticulum, food vacuoles,
and contractile vacuoles
 Contractile vacuoles regulate osmotic pressure between
the parasite and its environment
 Ectoplasm: outer (non-granulated), typically watery
 Homogenous and serves as an organ for motility and
engulfment of food by producing pseudopodia
 Helps in respiration, discharging waste material and
providing protective covering
3. Structures for locomotion
 Psuedopodia: fingerlike
 Flagella: Tail-like
 Cilla: Hair-like
 Undulating membrane
4. Plasma membrane
 controls secretions and excretions
5. Cytosome
 cell mouth
6. Chromatoidal bodies
 storage for glycogen protein
GURREA, A.N - TRANSCRIBER

[PARA311] 1.02 Intestinal and Extraintestinal Amoebae I Prof. Sherlyn Joy P. Isip, RMT, MSMT
C. General Rules for Amebae A. Life Cycle of E. histolytica
 All Entamoeba are commensal except for Entamoeba histolytica.

 With pseudopodium (false feet): finger-like structures for
movement formed by sudden jerky movements of the ectoplasm
in one direction.
 Undergoes ENCYSTATION except for E. gingivalis and
Dientamoeba fragilis.
 E. gingivalis and Dientamoeba fragilis do not have a
cyst form and stays in trophozoite form.
 Inhabits the large intestine except for E. gingivalis (gums)
 Amebiasis— presence of amoeba in any part of the body
(exclusively applied to E. histolytica)
 Asexually multiplies through binary fission.
II. Entamoeba histolytica
Morphologic forms
1. Tropozoite: divides through "binary fission", capable of encystation

(overpopulation, pH change, food supply, availability of oxygen)
 Trophozoite undergo encystation in intestinal lumen or
rectum
2. Precyst: contains large glycogen vacuole and two chromatid bars
and then secretes a highly retractile cyst wall around it and
becomes cyst.
3. Cyst: with protective thick cell wall (hyaline), capable of excystation
 Cyst found on contaminated food and water could
withstand the acidic pH of our stomach because of its
thick cell wall made up of hyaline.
4. Metacyst: liberated quadrinucleate amoeba during excystation
 No morphologic difference among other Entamoeba
spp. such as E. moshkovskii and E. dispar. However,
they can be differentiated through isoenzyme analysis,
PCR, and monoclonal antibody typing.
Infective Stage
 mature quadrinucleate cyst passed in feces
Mode of Transmission
 Ingestion of contaminated food and/or water with E. histolytica

cyst.
 Primary route is fecal-oral
 Venereal transmission
 Direct colonic inoculation through contaminated enema
equipment.
TROPHOZOITE CYST
Vegetative and motile stage Non-motile, feeding stage
(feeding stage)
Found in fresh watery, soft or Found in soft to formed stool
semi-formed stool B. Morphologic comparison between E. histolytica and E. coli
Fragile Resistant to acidic pH
A. Trophozoite
Point of E. histolytica E. coli
Differentiation
Movement Unidirectional, Sluggish, non-
progressive progressive and non-
directional
Shape of Finger-like Blunted
pseudopodia
Manner of One at a time/explosive Several at a time
release of
pseudopodia
Nucleus Uninucleated Uninucleated
(central karyosome) (eccentric karyosome)
Inclusion RBC Bacteria, yeast, debris
Cytoplasm Clean looking Dirty looking
Size Bigger Smaller

B. Cyst C. Pathogenesis
Point of E. histolytica E. coli
Differentiation  Symptoms
No. of nuclei Quadrinucleated More than 4  Gradual onset of abdominal pain
 Diarrhea (with or without blood)
Chromatoidal bar Sausage, rod, cigar- Broomstick,  In children: bloody diarrhea, fever and abdominal pain
shaped splinter-like  Abscess formation > Amoebic liver abscess
Manner of Thin Thick
release of  Pathology (Intestinal amebiasis)
pseudopodia  Amoebic dysentery vs. Bacillary Dysentery
 Presence of Charcot-Leyden crystals, product from
metabolism of eosinophils, found microscopically in the stool
in cases of amoebic dysentery
Amoebic dysentery Bacillary dysentery
Onset Gradual Acute
Signs/
No significant fever or Fever and usually
Symptoms
vomiting vomiting
Odor of feces
Offensive, Fishy odor Odorless
Blood and Often watery and
(+)
mucus
bloody
pH
Acidic Alkaline
Pus cell/ PMN/
Neutrophils Few Numerous
Cellular
exudates Scant Massive
Pyknotic
residues Numerous Few
Charcot Leyden
crystals Present Absent
Pathogenic
amoeba Present Absent
Bacteria
Few Numerous
Macrophages
Absent Present
D. Pathology
 Common associated disease: Intestinal amebiasis, amebic

colitis, amebic dysentery, extraintestinal amebiasis
 Amebic colitis- gradual onset of abdominal pain and diarrhea
with or without blood and mucus on the stool
 Ameboma – mass-like lesions with abdominal pain and
history of dysentery. It may be mistaken for carcinoma or
malignant tumor.

 Can cause ulceration "flask-shaped ulcer" in the intestines (cecum,
ascending colon and sigmoid) F. Laboratory Diagnosis
 Microscopic detection of cyst and trophozoite is the standard

method of parasitological diagnosis.
 Minimum of 3 stools specimen on different days should be
examined (one stool sample for each day)
 For the detection of trophozoite, fresh stool specimen should be
examined 30 mins after defecation.
 Detection of E. histolytica trophozoite with ingested RBC under
saline solution is diagnostic of amebiasis.
E. Pathogenic Determinants/Virulence Factor
1. Direct Fecal Smear
 saline solution: trophozoite motility
1. Galactose-inhibitable adherence lectin (Gal Lectin): receptor
mediated adherence of amoeba to target cells  saline + methylene blue: Entamoeba spp. stain blue
2. Amoeba ionophore: cell lysis and tissue invasion (differentiate Entamoeba spp. from WBC)
 Ionophore can attract calcium (anion), the calcium helps the  saline + iodine: nucleus of E. histolytica can be
Gal lectin so the parasite can adhere on the target cells observed (differentiate E. histolytica from
3. Cystein proteinase: most important, tissue invading factor nonpathogenic amoeba)
2. Concentration Techniques
Extraintestinal amoebiasis  In case of light infection, cyst and trophozoite may not
be detected in direct fecal smear.
 Through the portal vein (liver), trophozoite reach other parts of the  Formalin Ether/ Ethyl Acetate Concentration
body (liver, brain, lungs and kidneys). Technique (FECT) Merthiolate Iodine Formalin
 Metastatic amoebiasis- involvement of distant organs by Concentration (MIFC) – Sedimentation technique
hematogenous spread or through lymphatic resulting to abscesses
in the kidney, brain, spleen, and adrenals 3. Culture
 Amoebic hepatitis – repeated invasion in the  More sensitive than stool microscopy but not routinely
liver can cause inflammation available (Ex: Robinson's and Inoki medium, Boeck
 Amoebic liver abscess – most common and Drbohlav media, NIH polygenic media, Craig's
extraintestinal form of amoebiasis; fever, upper medium and Nelson's medium
right quadrant pain; thick chocolate brown pus
(liquefied necrotic liver tissue) 4. Serologic Testing
 Amoebic appendicitis and peritonitis  ELISA (Enzyme-linked Immunosorbent Assay), CIE
 Pulmonary amoebiasis (Counter Immunoelectrophoresis), AGD (Agar Gel
 Cerebral amoebiasis Diffusion), IHAT (Indirect Hemeagglutination Test)
 Splenic abscess and IF-AT (Indirect Fluorescent Antibody Test)
 Cutaneous amoebiasis  IHAT and IFAT considered as gold standard in
 Genitourinary amoebiasis –destructive detecting E. histolytica infection
ulcerative lesions may resemble carcinoma
5. Molecular Testing : PCR
 Asymptomatic carriers: cysts becomes unnoticed, ameba  In case of extraintestinal amoeba, CT-scan and MRI
reproduce but infected individual shows no clinical symptoms. may be used to detect amebic liver abscess.
 Diagnostic Stage: identification of the cyst or trophozoite
 Sample for ID: stool (examined within 30 minutes from collection)
G. Treatment
 To cure invasive disease at both intestinal and extraintestinal site

and to eliminate passage of cyst from intestinal lumen
 Metronidazole: drug of choice for invasive amebiasis
(Tinidazole and secnidazole are also effective)
 Diloxanide furoate: drug of choice for asymptomatic cyst
passers
 Percutaneous drainage of the liver abscess: Patients who
do not respond to metronidazole and need prompt relief of
severe pain
 Proper hygiene
 Provision for sanitary disposal of human feces
 Improve access to clean and safe drinking water
 Good food preparation practices
 Avoid using "night soil"
 Food handler should be examined for cyst carriage
 Health education and promotion

III. Non-Pathogenic species 4. Entamoeba polecki
1. Entamoeba coli  Parasite of the pigs and monkeys (rarely infect humans)
 Humans are accidental/incidental host
 Harmless inhabitant of the colon  Entamoeba chattoni: found in apes and monkeys, identical to E.
 Cysts: Size (10 — 35 microns) polecki, identification via isoenzyme analysis
 Larger than E. histolytica
 Consists of 8 nuclei with very diffuse karyosomes
 May become hypernucleated with 16-32 nuclei
 May also contain needle-like chromatoidal bodies with
irregular fragmented/sharp/splintered ends
 Trophozoites: Size (15-50 microns)
 Smaller than E. histolytica
 Has one nucleus containing large, diffuse karyosomes
 Peripheral chromatin is usually dense and irregular
 Cytoplasm is usually rough and contain few to many
ingested debris
Entamoeba polecki
5. Entamoeba gingivalis
 Not capable of encystation. Trophozoite form only

 Can be found in the mouth (gum and teeth surfaces)
 Abundant in cases of oral diseases
 No cyst stage, does not inhabit the intestines
 Transmission through kissing, droplet spray, sharing utensils
2. Entamoeba dispar  May ingest RBC (rarely), associated on lesions inside the mouth
 Morphologically similar to E. histolytica, but with different DNA and

RNA.
3. Entamoeba hartmanni
 Similar to E. histolytica except much smaller and no RBC inclusions

 "small-race E. histolytica”
Entamoeba gingivalis
6. Entamoeba moshkovskii
 Morphologically indistinguishable from those of the disease

causing species E. histolytica and the non-pathogenic E. dispar,
but differs from them biochemically and genetically. Although
sporadic cases of human infection with E. moshkovskii have been
reported, the organism is considered primarily a free-living
amoeba.
 physiologically unique: osmotolerant, able to grow at room
temperature and able to survive at 0-41 o c
7. Endolimax nana
 "Smallest amoeba"
 "Cross eyed cyst" — 4 eccentric nuclei
Entamoeba hartmanni
 Blot-like karyosome

 Aspiration or nasal inhalation: use of contaminated swimming
pools, deep well, etc.
 Direct invasion of the eye: contaminated saline
Endolimax nana
8. Iodamoeba butschlii
 "iodine-cyst" because of its affinity to iodine Acanthamoeba spp.

 Large glycogen vacuole/ body which stains deeply with iodine
 Uninucleated — resembling a "basket of flowers" shape
Specimen
 Discharges, exudates and tissue secretions
Pathogenesis
 Granulomatous Amoebic Encephalitis (GAE)
 destructive encephalopathy and associated meningeal
irritation
 Disease of immunocompromised (AIDS)
 Laboratory diagnosis: made by demonstration of
trophozoites and cysts in brain biopsy (post-mortem in most
cases), culture, and immunofluorescence microscopy-using
monoclonal antibodies.
 CSF shows lymphocytic pleocytosis (abnormal
increase in the number of lymphocyte in the CSF),
slightly elevated protein levels, and normal or
slightly decreased glucose levels.
 CT scan of brain provides inconclusive findings.
Iodamoeba butschlii Acanthamoeba spp. cycst
 Amoebic keratitis (contact lens users)

IV. FREE LIVING PATHOGENIC AMOEBA  perforation of the cornea and results to subsequent loss of
vision
1. Acanthamoeba spp. (Acathamoeba castellani)  Laboratory diagnosis: made by demonstration of the cyst in
corneal scrapings by wet mount, histology, culture (growth
can be obtained from corneal scrapings inoculated on nutrient
 Ubiquitous, free-living ameba
agar, overlaid with live or dead Escherichia coli and incubated
 With an active trophozoite stage with characteristic prominent at 300 C), demonstration of cyst and trophozoites in stool and
"thorn-like" appendages (acanthopodia) and resilient cyst stage PCR.
 Aquatic organism, can survive in contact lens cleaning solutions
 Most common ameba of freshwater and soil
 No flagellate state

2. Naegleria fowleri
Laboratory diagnosis
 Free-living protozoan with two vegetative forms: an ameba  CSF examination
(trophozoite form) and a flagellate (swimming form)  cloudy to purulent
 "brain-eating amoeba"  neutrophilic leukocytosis
 Thermophilic organism that thrive best in hot springs and other  elevated protein and low glucose
warm aquatic environment  resembling pyogenic meningitis
 True pathogen  Wet film examination of CSF: (+) trophozoites
 Incubation period varies from 2 days to 2 weeks.  Autopsy: (+) trophozoites in immunofluorescent staining
 Disease almost ends fatally within a week  Culture: can be grown in several kinds of liquid axenic media or
non-nutrient agar plates coated with Escherichia coli, (+) both
trophozoites and cysts.
 Molecular Diagnosis: Polymerase chain reaction (PCR)
Prevention
 Frequent cleaning
 Chlorination
 Salination
V. PHYLUM CILIOPHORA
CILATES
1. Balantidium coli
 Causative agent of "balantidiasis or balantidial dysentery", similar

to amoebic dysentery
Naegleria fowlei  Largest protozoan parasite
 Only parasitic ciliate
 Primarily associated with pigs
Pathogenesis
 Fatal Primary amoebic encephalitis (PAM)
 patients initially complain of fever, headache, sore throat,
nausea and vomiting
 Hemorrhagic necrosis in post mortem examination of infected
brain
Balantidium coli
Morphology
 "Kernig's sign"
 Has trophozoite and cyst stage
 diagnostic sign for meningitis where the patient is unable to
 Parts:
fully straighten his or her leg when the hip is flexed at 90
 Cytosome: entry of food
degrees because of hamstring stiffness  Cytophyge: excretes waste
 Two dissimilar nucleus: Large kidney-shaped macronucleus
and micronucleu
 One or two contractile vacuoles
 Oral and intranasal routes while swimming in contaminated pools,
rivers and lakes
Balantidium coli

Pathogenic determinant
 Hyaluronidase: causes the ulceration, secreted by trophozoite
 Ulceration is described as flask-shaped ulcer but with rounded
base and wider neck.
 Unlike like Entamoeba histolytica, Balantidium coli does not invade
the liver or other extraintestinal site.
Laboratory diagnosis
 Stool examination: microscopic demonstration of cyst and
trophozoite in direct
 Biopsy: specimens and scrapings from intestinal ulcers can be
examined for presence of trophozoites and cysts.
 Culture: can also be cultured in vitro in Locke's egg albumin
medium or NIH polyxenic medium like Entamoeba histolytica, but
it is rarely necessary.
 ingestion of food/water contaminated with B. coli cyst
Infective stage
 Cyst
Treatment
 Tetracycline is the drug of choice. Alternatively Doxycycline can be
given.
 Metronidazole and nitroimidazote have also been
reported to be useful in some cases.
Prevention
 Avoidance of contamination of food and water with
human or animal feces.
 Prevention of human-pig contact.
 Treatment of infected pigs.
 Treatment of individuals shedding B. coli cysts.

OLFU
Intestinal and Reproductive Organ Flagellates
2021 – 2022
LEC
OUTLINE  Microscopy and direct fecal smear

 Purged stool- provides more suitable material for examination than
At the end of the session, the student must be able to learn: the average formed stool. We use laxatives in purged stool.
I. Other Intestinal Protozoan Suitable specimen for detecting Dientamoeba fragilis.
A. Dientamoeba fragilis
II. Basic Structure of flagellates 5. Treatment
III. Pathogenic flagellates
A. Giardia lamblia  Iodoquinol (Tetracycline and Metronidazole are also effective)
B. Trichomonas vaginalis
IV. Non-pathogenic atrial flagellates 6. Prevention and Control
A. Chilomastix mesnili
B. Trichomonas hominis  Proper sanitation
C. Trichomonas tenax  Proper disposal of human waste
D. Enteromonas hominis
E. Retortamonas intestinalis II. BASIC STRUCTURE OF FLAGELLATES
V. Summary
 Flagellum/Flagella- locomotor apparatus
 Kinetoplast- provides energy
I. OTHER INTESTINAL PROTOZOAN  blepharoplast
 parabasal body
A. Dientamoeba fragilis  Cytostome- cell mouth
 Undulating membrane- a membrane laterally projecting from the
 Despite of its name, it is not an amoeba but an intestinal flagellate. body of certain flagellates, participate in active motility of the
 No cyst stage identified, only the trophozoite stage is known. flagella.
 Originally described as an amoeba (based on EM and immunologic  Axostyle or axial rod- for support in locomotion
and molecular phylogenic findings it is actually a flagellate)  Costa- rib-like structure within the cytostome for support
 Resembles Trichomonas
1. Morphology of the trophozoite
 Rosette shaped nuclei (1 to 2)

 Cytoplasm may contain vacuoles with ingested debris
 Shows progressive motility
 Broad hyaline pseudopodia that possess characteristic "serrated
margin”
2. Mode of Transmission
 fecal-oral route via transmission of helminth eggs (eg., Enterobius

vermicularis)
 It has been observed that some of Dientamoeba flagilis are found
in the lumen of the Enterobius vermicularis adult.
3. Pathogenesis
 Infections are asymptomatic because it does not invade the

tissues compare to E. histolytica. The presence of this parasite in
GIT only produces irritation of the mucosa with secretion of excess III. PATHOGENIC FLAGELLATES
mucus and hypermotility of the bowel.
 In chronic infections, it may only mimic the irritable bowel A. Giardia lamblia
syndromes but primarily the infection is asymptomatic because the
parasite is not invading the tissues.  Causes diarrhea
 Possible co-infection with E. vermicularis and A. lumbricoides  Cercomonas intestinalis : Initial name (Dr. F. Lambl)
 Giardia lamblia : (by Stiles > Dr. Giard and Dr. Lambl)
 Chronic infections may mimic Irritable Bowel Syndrome (IBS)
 Giardia intestinalis: synonymous to Giardia duodenalis
 Other name: Lamblia duodenalis or L. intestinalis
4. Diagnosis and Specimen  Habitat: duodenum, jejunum and upper ileum of humans
 Observation of binucleate trophozoites in multiple fixed and stained

fresh stool
Gurrea, A.N - TRANSCRIBER

[PARA311] 1.03 Intestinal and Reproductive Organ Flagellates I Prof. Sherlyn Joy P. Isip, RMT, MSMT
1. Life Cycle of Giardia lamblia 4. Mode of Transmission
 Ingested mature cyst will pass safely through the stomach; it will  Ingestion of contaminated food and water with G. lamblia mature
undergo excystation in the duodenum for about 30 mins, cyst
developing into trophozoites that rapidly multiply (binary fission)
and attach to intestinal villi causing pathologic changes.
 As the feces dehydrates, the parasite will undergo encystation.
 The mature cyst will pass through the feces (infectious)
 Trophozoites may be isolated on the fecal sample. Diagnostic
stage are cyst and trophozoites.
2. Morphology
 Trophozoite: "Old-man with eyeglasses", "Monkey Face"

 pear/tear drop shaped, pyriform, shape of a tennis racket
 Bilaterally symmetrical with large ventral sucking disc-
pathogenic determinant.
 ventral sucking disc- attachment to intestinal villi 5. Pathogenicity
 4 pairs of flagella, 2 ventral sucking disc
 2 ovoidal nuclei with distinct karyosome (symmetrically  Parasite attach to intestinal walls via adhesive sucking disc located
bilateral) on the ventral side, it causes mechanical irritation in the affected
 "falling leaf motility"- movement tissue.
 Covered with variant-specific surface proteins (VSPs) -  It produces lectin for attachments.
function is not fully elucidated but it is used as resistance for  The parasite is able to avoid peristalsis by trapping itself between
intestinal proteases attributing to the survival of the parasite. the villi or within the intestinal mucosa.
 Cyst  Villous flattening and crypt hypertrophy- may lead to decrease
glucose, electrolytes, fluid absorption, and deficiency in
 Ovoidal in shape
disaccharide (malabsorption and maldigestion).
 Thick shell (double wall), surrounded by a hyaline cyst wall
 Nuclei: 2 (young), 4 (mature)
 Presence of axostyle
3. Infective Stage
 Mature cysts (resistant to routine chlorination)

 Ovoidal, composed of double wall thick shell surrounded by
hyaline cyst wall.
 Can be mature (4 nuclei) or immature (2 nuclei)
 Presence of axostyle on cyst

6. Pathology 1. Morphology of the trophozoite
 The onset is between 1-4weeks on an average of 9 days. Half of  Pyriform shape

patients are asymptomatic.  4 free anterior flagella and one posterior flagellum beside
 causative agent of Giardiasis or Lambliasis undulating membrane
 "Traveler’s diarrhea" - St. Petersburg, Russia (first recorded  Prominent axostyle and single nucleus
water outbreak and involved a group of visiting travelers) Gay  Presence of undulating membrane
bowel syndrome, Failure to thrive syndrome  "rapid jerky tumbling" or "twitching"
 Acute infections : "rotten eggs" odor (hydrogen sulfide)
 Chronic infections: steatorrhea (malabsorption of fats) > passage
of greasy, frothy stools that may float on toilet water
7. Diagnosis
 Specimen: Stool and Duodenal contents

 Diagnostic Stage: Trophozoite and Cyst
 Lab Test:
 Direct Fecal Smear
 Entero test/Enterotube test/string test/ Beale
 String's test (non-invasive)
 Aspirate and Biopsy (invasive)
 Concentration techniques in low level of light infections
 Antigen detection test and immunofluorescence commercial
test kit- Cyst wall protein 1 (Giardia antigen found in the
stool)
 Direct fluorescent antibody testing- Gold standard
because it provides high sensitivity and high specificity.
Trichomonas vaginalis
2. Infective and Diagnostic stage
 Trophozoite
8. Treatment
3. Pathology
 Metronidazole: (3x a day of 1 week): drug of choice
 Tinidazole, Albendazole, Furazolidone, Quinacrine and  Correlates strongly with the number of sexual partners
Paromomycin as alternative.  Trichomoniasis (persistent urethritis, persistent vaginitis, infant
infections)
9. Prevention and Control  Most prevalent non-viral sexually transmitted infection
 Coinfection with Candidiasis, Gonorrhea, Syphilis, and
 Proper disposal of human excreta HIV
 Improve access to clean and safe drinking water - (Proper water
treatment that includes combination of chemical therapy and 4. Symptoms
filtration)
 Good food preparation practices
 Males
 Avoid using "night soil”
 asymptomatic
 Health education and promotion
 (less persistent, self-limiting)
 Females:
 Greenish-yellow discharge
B. Trichomonas vaginalis
 Edema, itching, burning sensation
 "Strawberry cervix"
 The only pathogenic Trichomonas
 No cyst stage.  Infects squamous epithelium
 Habitat: Urogenital tract  Secretes cysteine proteases, lactic acid, acetic acid
 Female: Vulva (vagina) and may ascend to renal pelvis which disrupts the glycogen level and lowers the pH of
(pH 5.2-6.4) vaginal fluid
 Male: prostate gland, urethra, prostatic tissue  Low pH may cause infertility. High pH is prone to fungal
or bacterial infection.

Symmetry Symmetrical Asymmetrical
Motility Falling-leaf Rapid Jerky Tumbling
Pathogenicity Pathogenic Pathogenic
B. Cyst
Point of
Giardia lamblia Trichomonas vaginalis
Comparison
Shape Ovoid
Thick shell, axostyle
Characteristic No cyst stage
present
Nuclei 2 to 4
IV. NON-PATHOGENIC ATRIAL FLAGELLATES
 Sexual intercourse
 Can be passed through newborns through the birth canal A. Chilomastix mesnili
 Contaminated underwear or towels, or sitting at contaminated toilet
bowl  Largest flagellates in man
6. Specimen 1. Trophozoite
 Male: urine sample, prostatic fluid or seminal fluid  Asymmetrical

 Female: urine sample, vaginal discharge, cervical scrapings  Pear-shaped
 Spiral groove on midportion
7. Laboratory Test  3 anterior flagella
 1 flagellum within the cytostome > Cystostomal fibril (shepherds
 Microscopy- wet smear or wet mount. Sensitivity of Microscopy is crook, safety pin appearance)
between 60-70%  “Boring/spiral movement or Cork-screw movement”
 Saline preparation- quickest and most inexpensive way but may be
subjective.
 Fixed and stained wet drop: Giemsa, Papanicolaou,
Romanowsky and Acridine Orange
 Culture
 Gold standard
 Culture between 2-5 days
 Feinberg-Whittington medium
 Diamond Modified medium
 Trypticase Luver Serum medium 2. Cyst
 lnPouch TV Test- novel transport and culture system (sealed
pouch with culture media)  Pear or lemon shaped
 Conical anterior with knob-like or "nipple-shaped" protuberance
8. Treatment
 Oral Metronidazole (Tinidazole)

 Acidic Douche (10% vinegar) – Dilute with distilled water
9. Prevention and Control
 Both the male and female must be treated

 4 Cs (Counselling, Compliance, Contact Tracing, Correct and
Consistent use of Condom)
 Case Finding
 Choice and number of sexual partner
 ABSTINENCE
C. Morphologic Comparison of the Cyst and Trophozoite
A. Trophozoite
Point of
Giardia lamblia Trichomonas vaginalis
Comparison
Shape Pear, tear-drop, pyriform Pyriform
Round anterior, pointed
Prominent axostyle,
Characteristic posterior, with large
undulating membrane
sucking disc
4 pairs (anterior, mid,
Flagella sucking disc, extreme 4 anterior
posterior)
Nuclei 2 nuclei Uninucleated

B. Trichomonas hominis
 Usually found in cecal area of large intestine

 Commensal, occurs only in trophozoite
 Pyriform shape
 5 anterior flagella and a posterior flagellum
 Relatively smaller than T. vaginalis
V. SUMMARY
C. Trichomonas tenax
 Usually found in the mouth living in tartar around teeth and cavities
of carious teeth, occurs only in trophozoite
 Pyriform shape
 smaller and slender than T. vaginalis
 4 free equal flagella and a 5th one on the margin of the undulating
membrane
D. Enteromonas hominis
 Demonstrates "jerky motility"

 Very small like Endolimax nana
E. Retortamonas intestinalis
 Demonstrates "jerky motility", 2 anterior flagella

 Stained stool preparation is the best sample to examine its
presence

OLFU
Blood and Tissue Flagellates
2021 – 2022
LEC
OUTLINE

I. General Characteristics
A. Morphologic forms
II. Trypanosoma spp.
A. Life Cycle of Trypanosoma spp.
B. Pathology 2. PromastigoteI. SUMMARY
C. Infective stage
D. Specimen  lanceolate
E. Laboratory Test  Elongated flagellum
F. Treatment
G. Prevention and Control
III. Trypanosoma brucei complex
A. Life Cycle of Trypanosoma brucei complex
B. Pathogenesis
C. Specimen
D. Laboratory test
E. Treatment
3. Epimastigote
F. Prevention and Control
IV. Leishmania spp.
A. Life Cycle of Leishmania spp.  Elongated
B. Pathology  Undulating membrane
C. Infective stage
D. Specimen
E. Diagnostic test
F. Treatment
G. Prevention and Control
I. GENERAL CHARACTERISTICS
 Unique morphology 4. Trypomastigote

 They live in the blood and tissues of man and other vertebrate hosts
and in the gut of the insect vectors.  Elongated, spindle shape
 To transmit these parasites, you need an insect vector. Those  Long slender or short stumpy
vectors are biological vectors because they are included in the  C, U, S-shaped
lifecycle of the parasite.
 Habitat: humans - blood and tissues. Vectors- gut of vectors
 Members of this family have a single nucleus, a kinetoplast, and a
single flagellum
 Nucleus is round or oval and is situated in the central part of the
body
 Kinetoplast consists of a deeply staining parabasal body and
adjacent dotlike blepharoplasty
 Flagellum is a thin, hairlike structure, which originates from the
blepharoplast.
A. Morphologic forms
1. AmastigoteIII. SUMMARY
 round, ovoid
 usually found in small groups of cyst-like collection in tissues

[PARA311] 1.04 Blood and Tissue Flagellates I Prof. Sherlyn Joy P. Isip, RMT, MSMT
II. Trypanosoma spp. B. Pathology
Etiologic Disease Vector Stages  "Chagas' disease" or American trypanosomiasis

Agent exhibited  usually serious and fatal in young children
T. cruzi Chaga's Disease Assassin bug,  "Chagoma"
or Kissing bug,  furuncle-like lesions, inflammation at the site of inoculation
American Cone nose bug,  small, painful, reddish nodule
Trypanosomiasis Triatomine bug,
(Reduviid bug) ALL
Triatoma,
Rhodnius,
Panstrongylus
T. brucei Gambian or West Tsetse fly,

gambiense African Sleeping Glossina spp. Epimastigote
Sickness and
T. brucei Rhodesian or East Trypomastigote
rhodesiense African Sleeping only
Sickness
1. Acute trypanosomiasis
A. Trypanosoma cruzi  generalized lymphadenopathy

 focal or diffuse inflammation mainly affecting the myocardium
 Belongs to the group Stercoraria (multiplies within the mammalian  "Romaña's sign"- edema of the eyelid if the parasite penetrates
host in a continuous manner) through the conjunctiva. May involve lacrimal gland or surrounding
 Stercoraria- the trypanosome to be transmitted is found in the tissues
feces of the vector. The reduviid (vector) will take a blood meal
on a host; the bite wound will be contaminated with feces. The 2. Chronic trypanosomiasis
feces of reduviid bug contains the infective stage of parasite.
 The metacyclic trypanosomes being transmitted are found on the
 no characteristic symptom and may last for 20 years or more
feces of vector.
 cardiomyopathy, megaesophagus and megacolon (chronic
 Infected cells (intracellular parasite):
constipation)
 Skin
 Cardiomegaly, congestive heart failure, thromboembolism, and
 Gonads
arrhythmia
 Intestinal mucosa  Primary organ affected: heart
 Placenta  these advanced conditions can lead to death
 Myocytes (particularly myocardial tissues)  Achalasia- lower part of esophageal sphincter fails to open up
 Reticuloendothelial system cells during swallowing > leads to back up of food. Associated with
 The myocytes and reticuloendothelial system cells are the megaesophagus
heavily infected cells
A. Life Cycle of Trypanosoma cruzi C. Infective stage
 to vector : trypomastigote
 to man : metacyclic trypomastigote
D. Specimen
 blood, CSF, fixed lymph node tissues and lymph juices
E. Laboratory Test
 Complete patient history is the primary tool for diagnosing Chaga’s

disease. Signs and symptoms of Chaga’s disease are nonspecific.
 Establish possible exposure to the parasite base on complete
patient history.
 Stained smear -Giemsa staining (stain in diagnosing blood
parasite: demonstration of trypomastigote)
 Concentration methods (Micro hematocrit- capillete with
acridine orange stain)
 Blood Cultures - NNN medium (Novy-MacNeal-Nicolle)
 Xenodiagnosis - use of laboratory animal to isolate parasite
(negative bugs > feed on suspective patients > examine for
the presence of Trypanosoma cruzi metacyclic
trypomastigote)

 Serologic test - IFAT, CFT (Machado Guerreiro test), IHAT, A. Life Cycle of Trypanosoma brucei complex
ELISA
 Dot-immunobinding: small amounts of sample is
used
 Molecular— testing (PCR) amplify DNA from kinetoplast
 The WHO recommends using at least two
techniques with concurrent positive results before
diagnosis of Chaga’s disease is made.
F. Treatment
 Nifurtimox and Benznidazole B. Pathogenesis
G. Prevention and Control  Chancre- earliest sign of African trypanosomiasis, hard, painful
lesion at the site of inoculation.
 vector control (insecticide spraying)  Both human African Trypanosomiasis has 2 stages
 screening and sterilization of transfusion blood  Early/Hemolymphatic phase- parasite proliferate in lymphatic
 health education and blood stream.
 Late phase/chronic phase- meningoencephalitic phase
(involvement of CNS)
III. Trypanosoma brucei complex
 Belong to the trypanosome family Salivaria. 1. Gambian trypanosomiasis

 Saliva of the vector
 Collectively the three subspecies represent the Trypanosoma
brucei complex:  Acute: fever, headache, joint and muscle pain, tachychardia,
 Trypanosoma brucei gambiense – cause of West African dizziness and rashes
sleeping sickness  “Winterbottom's sign"- enlargement of the posterior
 Trypanosoma brucei rhodesiense – causative agent of East cervical lymph node and have a ripe plum consistency.
African sleeping sickness  Chronic : with CNS invasion
 Trypanosoma brucei brucei  Severe headache, alternately morose and excitable, and
lack interest in work.
Characteristics West African East African  Tremors and "Kerandel's sign" or hyperesthesia and
Organism T. brucei gambiense T. brucei rhodesiense inversion of sleep cycle can be observed
Distribution West and Central
East and Central Africa
Africa
Vector Tsetse fly (Glossina Tsetse fly (Glossina
palpalis group) morsilans group)
Reservoir Wild and domestic
Mainly humans
animals
Virulence Less More
Course of disease Chronic (late central Acute (early central
nervous system nervous system
invasions); months to invasion); less than 9
years months
Parasitemia Low High and appears early
Lymphadenopathy Early, prominent Less common
Isolastion in rodents No Yes  Antigenic variation- Trypanosomes are able to invade the
immune system of the host, the ability of Trypanosomes to
Mortality Low High
continuously change its surface coat. Compose of variant
surface glycoproteins. > Host’s immune system cannot
recognize the parasite

2. Rhodesian trypanosomiasis IV. Leishmania spp.
 more rapid and fatal than Gambian trypanosomiasis Etiologic

 CNS involvement appear early Agent
Disease Vector Stages exhibited
 Neurologic deterioration is rapid Leishmania Cutaneous Sandfly
 More virulent and fatal tropica leishmaniasis vectors F. host:
(Phlebotomus Amastigote
C. Specimen American or
Leishmania spp.) (reticuloendothelial
Mucocutaneous
braziliensis system)
Leishmaniasis
 Blood, CSF, and lymph juices l. host:
Visceral Promastigote
D. Laboratory Test Leishmania Leishmaniasis/ (midgut and
donovani Kala-azar/ proboscis)
 Wet smear : presence of live parasite Dumdum fever
 Stained smear- Giemsa staining: demonstration of trypomastigote
 Buffy coat concentration method: low level of parasitemia Etiologic Agent Other name
 CSF examination- mandatory in patients suspected with Human Leishmania tropica Old world leishmaniasis, Oriental
African Trypanosomiasis (increase cell counts, opening pressure, leishmaniasis, Cutaneous
concentration of IgM, and protein levels) leishmaniasis, Jericho boil, Baghdad
 Serologic test boil
 IFAT Leishmania braziliensis New world leishmaniasis
 ELISA Leishmania donovani Kala-azar/ Dumdum fever
 Mini-anion centrifugation technique
 IHAT
 Test kit- Card agglutination test for Trypanosomiasis (CAT)
to detect circulating antigens. High sensitivity and high
specificity.
A. Life Cycle of Leishmania spp.
E. Treatment
 effective on earlier stages

 Suramin sodium and Pentamidine – cannot cross blood-brain
barrier, not used with CNS involvement
 Melarsoprol- drug of choice for CNS involvement
 Melarsoprol and Tryparsamide (w/ CNS involvement), febrile
episode, Jarisch-Herxheimer reaction, due to trypanosome
lysis following melarsoprol treatment
 DL-alpha-difluoromethylornithine (DFMO, Eflornithine) for T.
brucei gambiense only
 Nitrofurazone (second-line drug) in cases of Melasorprol B. Pathology
treatment failure
1. Cutaneous Leishmaniasis (Leishmania tropica)
 most common form, skin ulcer (leaving an ugly scar on healing) -
 control of tsetse flies (traps, screens, insecticides) oriental button at inoculation site
 reduction of pool of human infection  painless lesions
(Diagnose as many individuals as possible)  Diffuse Cutaneous Leishmaniasis resembles "leprematous
 trimming of bushes leprosy"
 lesions do not heal spontaneously and tend to relapse after
treatment

 Serologic Test
 Complement Fixation Test
 Montenegro's intradermal test: (+) CL and MCL and (-)
for DCL and VL
 IFAT
 Counter current electrophoresis techniques
 Antigen testing: ELISA or RK39 antigen dipstick test
F. Treatment
 Pentavalent antimonials: sodium stibogluconate and n-

methylglucamine antimonite (meglumine)
 Second line drugs
 Amphotericin B: intravenous
 AmBisome: lipid-based drug for CL, and VL
 Pentamidine: for Kala-azar, limited use because of drug
resistance
2. American or Mucocutaneous Leishmaniasis (Leishmania  Miltefosine: current oral drug for VL
braziliensis)  Topical paromomycin (for CL) – combination therapy
 Combination therapy (sodium stibogluconate plus
 “Espundia”- metastatic spread of lesion to oronasal and paromomycin, and liposomal amphotericin B plus either
pharyngeal mucosa. miltefosine, or sodium stibogluconate)
 "Tapir nose" -disfiguring leprosy-like tissue destruction and
swelling G. Prevention and Control
 "Chiclero ulcer"- erosion of the pinna of the ear
 "forest yaws", "pian bois" "uta"
 Skin lesions must be protected from insect bites
 Health education
3. Visceral Leishmaniasis (Leishmania donovani)
 Kala-azar or Dumdum fever

 twice-daily elevation of fever: prominent finding
 splenomegaly and cachexia
 Parasites are numerous in reticuloendothelial cells of the
spleen, liver, lymph nodes, bone marrow and other organs.
 FATAL
C. Infective Stage
 to man : promastigote
 to vector : amastigote
D. Specimen
 Blood and Tissue sample
E. Diagnostic tests
 Microscopic determination from tissue scrapings, lesions and

biopsy
 Cutaneous : skin
 Visceral: spleen or bone marrow
 Stain: Giemsa and Hematoxylin-Eosin stain,
demonstration of amastigotes
 Culture: unreliable due to difficulty in isolating parasites especially
old lesions
 Ex: Novy, Mcneal and Nicolle medium (NNN) and
Schneider's medium – a bit unreliable due to difficulty in
isolating parasites from old lesions.

OLFU
Sporozoa (Plasmodium spp. and Babesia spp.)
2021 – 2022
LEC
1. Vector
OUTLINE
At the end of the session, the student must be able to learn:  female Anopheles mosquito
I. Sporozoa  female mosquitoes – bite/suck blood while male mosquitoes –
A. Plasmodium spp. acquire nutrients from fruits and flowers
B. Babesia spp.  Vector of Malaria: Anopheles minimus var. flavirostris
II. Malaria  Other spp. under Anopheles family:
A. Life Cycle of Malaria Parasite  Anopheles litoralis
1. Sporogony  Anopheles maculates
2. Schizogony (Pre-erythrocytic Cycle)  Anopheles mangyamus
3. Schizogony (Erythrocytic Cycle)  Mostly, the children and pregnant women are affected with
B. Gametogony malaria.
C. Components of the Malaria Life Cycle  Children- chronic malaria may lead to anemia, impaired
D. Clinical Feature physical and mental growth and development.
E. Recrudescence and Relapse  Pregnant women- anemia is the leading contributor of
F. Pathological Process of the RBC maternal morbidity and mortality.
G. Morphology  Vector Biology: Anopheles flavirostris
H. Immunity  Aquatic Habitat: slow flowing streams; shaded streams
I. Diagnosis
 Adult biting: Night biting (indoor and outdoor)
J. Treatment
K. Prevention  Adult resting: inside walls
L. Control
III. Plasmodium knowlesi
IV. Babesia spp.
A. Life Cycle of Babesia spp.
B. Pathology
C. Diagnosis
D. Treatment
E. Prevention and Control
2. Host
I. SPOROZOA  Final Host: female Anopheles mosquito

 The sexual stage/sexual cycle occurs in Anopheles mosquito
 The protozoan parasite characterized by the production of the
(invertebrate and definitive host)
spore-like oocyst containing the sporozoites is known as the
 Intermediate Host: Man
Sporozoa.
 They live intracellularly  The asexual stage occurs in humans (vertebrate and
 At some stage in their life cycle, they possess a structure called intermediate host)
apical complex (important for attachment and penetration in cells).
3. Infective stages
a. Plasmodium spp.
 Sporozoites (man)
 Plasmodium falciparum  Gametocytes (mosquito)
 Plasmodium vivax
 Plasmodium malariae 4. Source of Exposure to infection
 Plasmodium ovale
 Plasmodium knowlesi  Vector borne (Arthropod borne) – also known as introduced
malaria
b. Babesia spp.
5. Other Modes of Transmission
 Babesia microti
 Babesia divergens
 Imported malaria – acquired by visitors or residents of country
 Babesia bovis
with endemic disease.
II. MALARIA  Transfusion malaria – associated with blood transfusion from
infected donors.
 The name Malaria was given in the 18th Century in Italy.  Mainline malaria – sharing of needles and syringes among drug
 Malaria from Italian word "mal'aria" which means "bad air" users.
 Believed to be caused by emanation from the marshy soil.  Congenital malaria – natural form of merozoites induced malaria
 Considered to be the most important parasitic disease affecting where the parasite is transmitted transplacentally from the mother
man (Belizario, 2015) to the fetus.
 Leading parasitic disease that causes mortality worldwide
 Identified by WHO as one of the major infectious disease threats
along with HIV, AIDS and tuberculosis
 Peak transmission of Malaria – beginning and end of rainy season.
 Primarily, Malaria is vector borne or arthropod borne.

[PARA311] 2.01 Sporozoa (Plasmodium spp. and Babesia spp.) I Prof. Sherlyn Joy P. Isip, RMT, MSMT
 The female gametocyte does not divide but undergoes a process
A. Life Cycle of Malaria Parasite of maturation to become the female gamete or macrogamete. It is
fertilized by one of the microgametes to produce the zygote.
 Ookinete: the zygote, which is initially a motionless, round body,
gradually elongates becomes a vermicular motile (traveling
vermicule) form with an apical complex anteriorly.
 Oocyst: rounded into a sphere with an elastic membrane within
which numerous sporozoites are formed.
 Sporozoites: when the oocysts ruptures, the sporozoites enter into
the hemocele or body cavity, from where some find their way to the
mosquito's salivary glands.
 The mosquito is now infective and when it feeds on humans, the
sporozoites are injected into skin capillaries to initiate human
infection.
b. Schizogony (Pre-erythrocytic Cycle)
 Inside the human body

 Asexual phase
 In this stage, the malaria parasite multiplies by division or splitting
process – Schizogony
 Schizo (split) gony (generation)
 Occurs in humans (so it is vertebrate, intrinsic and endogenous
phase) making humans as the intermediate host.
 In humans, Schizogony occurs in two locations: RBC (erythrocytic
schizogony) and in the liver (exo-erythrocytic schizogony or tissue
phase).
 Schizogony in liver is essential step before the parasite can
invade the erythrocyte it is called as Pre-erythrocytic Schizogony.
a.. Sporogony  Products are merozoites
 Sporozoite infect liver parenchymal cells (since the
 Sporogonic Cycle detoxifying organ is the liver, the sporozoites infect it)
 The sexual phase takes place in the female Anopheles  >Schizont
mosquito even though the sexual forms of the parasite or the  Rupture liver cells > merozoites
gametocytes are originating in the human red blood cells.
 It is the sexual cycle in the mosquito which leads to the formation
of sporozoites
 Sporozoites- infective stage to humans
 Union between the microgamete and macrogamete (sex
cells of Plasmodium spp. developed in the RBC of humans).
 Zygote > ookinete > oocyst
 Ruptured Oocyst > release Sporozoites
 The maturation and fertilization takes place in mosquito giving rise
to a large number of sporozoites (sporos = seed)
 Hence, this phase of sexual multiplication is called as sporogony
 Also called as invertebrate, extrinsic and exogenous phase
(because it occurs outside the human body)
Pre-erythrocytic (Tissue) Stage or Exoerythrocytic
 The hepatocyte is distended by the enlarging schizont and the

liver cell nucleus is pushed to the periphery.
 These normally rupture in 6-15 days and release thousands of
merozoites into the blood stream.
 In the latent stage of Plasmodium vivax and Plasmodium ovale
two kinds of sporozoites are seen.
 Some multiply inside the hepatic cell to form schizonts while
others persist and remain dormant/resting stage
 Hypnozoites (hypnos: sleep): resting forms in Plasmodium
vivax and Plasmodium ovale
The Mosquito Cycle (Sporogony)
 Dormant, exo-erthyrocytic forms and may remain for
quiet years.
 Exflagellating male gametocytes: the nuclear material and  Merozoites can go back into liver and rest and these
cytoplasm of the male gametocytes divides to produce 8 are the dormant/resting forms.
microgametes with long, actively motile, whip-like filaments.
 Some are activated to become schizonts and release
merozoites, which will infect RBC producing clinical
relapse.
 Clinical relapse is associated with resting/dormant
forms of parasite called Hypnozoites.
 In the case of P. falciparum and P. malariae, initial tissue
phase disappear completely and no hypnozoites are found.
c. Schizogony (Erythrocytic Cycle)
 The merozoites will invade the RBCs while some merozoites of

Plasmodium vivax and Plasmodium ovale reinvades the liver cells
forming the hypnozoites.
 Inside the RBCs they will develop to become young
trophozoites (ring formations)
 Mature trophozoites > Schizonts >Ruptured schizonts >
merozoites  The appearance of malaria pigments varies in different species
 Some proceed to the development as gametocyte. as follows:
 P vivax: numerous fine golden-brown dust-like particle
 P. falciparum: few 1-3 solid blocks of black pigment
 P. malariae: numerous coarse dark brown particles
 P ovale: numerous blackish brown particles.
 Amoeboid form or late trophozoite form: as the ring form
develops, it enlarges in size becoming irregular in shape and
shows amoeboid motility.
 When the amoeboid form reaches a certain stage of
development, its nucleus starts dividing by mitosis followed by a
division of cytoplasm to become mature schizonts or meronts.
 The merozoites invade fresh erythrocytes within which they go
through the same process of development.
 The rupture of the mature schizont releases large quantities of
pyrogens. This is responsible for the febrile paroxysms
characterizing malaria. (Erythrocytic Stage)
 Febrile paroxysms- one of the distinguishing features of
malaria. (on and off fever)
Erythrocytic Stage
 The merozoites released by pre-erythrocytic schizonts invade the

red blood cell:
 The receptor for merozoites is glycophorin, which is a
major glycoprotein on the red cells.
 Merozoites are pear-shaped bodies, about 1.5 um in
length, possessing an apical complex (rhoptery).
They attach to the erythrocytes by their apex.
 Ring forms or young trophozoites: the merozoite
loses its internal organelles and appears as a rounded
body having a vacuole in the center with the cytoplasm
pushed to the periphery and the nucleus at one pole.
 Malaria pigment or haemozoin pigment: parasite feeds on
the hemoglobin of the erythrocyte but it does not metabolize
hemoglobin completely and therefore, leaves behind a
hematinglobin pigment as residue.

C. Components of the Malaria Life Cycle
B. Gametogony
 Sexually differentiated form  The pre-patent and incubation period depends on the parasite
 Development of gametocytes generally takes place within the strain, dose of sporozites inoculated, immune status and
internal organs and only the mature forms appear in circulation. chemoprophylaxis therapy.
 The mature gametocytes are round in shape, except in P.
falciparum, in which they are crescent-shaped. a. Intervals and Periodicity/Febrile Cycle
 In all species, the female gametocyte is larger (macrogametocyte)
than the male gametocyte (microgametocyte).
 The gametocytes do not cause any clinical illness in the host, but Table 1.0 Intervals of Plasmodium spp.
are essential for transmission of the infection. Species Prepatent period Incubation period
 Gametocyte- Infective stage to mosquito P. falciparum 11-14 days 8-15 days
 A gametocyte concentration of 12 or more per cumm of blood in P. vivax 11-15 days 12-20 days
the human host is necessary for mosquitoes to become infected. P. malariae 3-4 weeks 18-40 days
P. ovale 14-26 days 11-16 days
Table 1.1 Periodicity/Febrile Cycle of Plasmodium spp.

Age of
Interval
Species Febrile cycle Infected
(hours)
Erythrocytes
* Malignant
P. falciparum 36-48 RBC of all stages
tertian
P. vivax Benign tertian 48 Young RBC
P. malariae Quartan 72 Aging RBC
P. ovale Ovale tertian 48 Young RBC
 The interval between the attacks is determined by the length of

erythrocytic cycle.
 P. falciparum, P. vivax, P. ovale – paroxysm occurs in alternate
days or every second day. (tertian)

 Quartan malaria- paroxysm occurs on day 1 and day 4 or every  Algid Malaria
third day.  Peripheral circulatory failure, rapid thready pulse with low
*Aestivoautumnal malaria - associated to P. falciparum (it occurs blood pressure, and cold clammy skin. There may be severe
commonly in late summer and autumn) abdominal pain, vomiting, diarrhea, and profound shock.
 Septicemic malaria
D. Clinical Feature  High continuous fever with dissemination of the parasite to
various organs, leading to multiorgan failure. Death occurs in
 No absolute clinical feature of malaria except for regular paroxysms 80% of the cases.
(sudden attack or violent expression of fever with asympyomatic
interval) c. Merozoite-induced Malaria
a. Benign Malaria  Injection of merozoites can lead to direct infection of red cells and
erythrocytic schizogony with clinical illness. Such merozoite-
 The typical picture of malaria consists of periodic bouts of fever induced malaria may occur in transfusion malaria, congenital
with rigor, followed by anemia and splenomegaly. Severe malaria, renal transplantation and mainline malaria.
headache, nausea, and vomiting are common.
d. Tropical Splenomegaly Syndrome
Classical Malaria Paroxysms
 Also known as hyper-reactive malarial splenomegaly (HMS) is a
1. Cold stage chronic benign condition seen in some adults in endemic areas,
 sudden coldness and apprehension mainly tropical Africa, New Guinea, and and Vietnam.
 mild shivering turns to teeth chattering and shaking of the
 Abnormal immunological response to malaria causing
whole body
splenomegaly, high titers of circulating anti-malaria antibodies and
 may last for 15 to 60 minutes
2. Hot stage/ flush phase : best stage to collect blood sample absence of malaria parasites in peripheral blood smears,
 High temperature (40-41 C), headache, palpitations, hypergammaglobulinemia (lgM), cryoglobulinemia reduced C3,
epigastric discomfort, thirst, nausea and vomiting. May lead to and presence of rheumatoid factor without arthritis
convulsion  Body produces immune analytes causing splenomegaly to the
 patient is confused and delirious infected host
 may last for 2 to 6 hours
3. Sweating stage (Defervescence or Diaphoresis) E. Recrudescence and Relapse
 profuse sweating, temperature lowers and symptoms
diminishes a. Recrudescence
 may last for 2 to 4 hours
 New malarial attacks that appear after a period of latency usually
b. Malignant Tertian Malaria within 8 weeks after the primary attack and resulting from
persistence of the erythrocytic cycle of the parasites.
 The most serious and fatal type of malaria is malignant tertian  Renewed outbreak of the disease. The disease is reduced to the
malaria caused by P. falciparum. point that it is undetectable but still persist in the body and will
 Pernicious malaria reoccur after some days or weeks.
 Has been applied to a complex of life-threatening  May persist inside the body but they are not active to cause signs
complications that sometimes supervene in acute falciparum and symptoms.
malaria.  Reduced/light infectivity – undetectable in blood smear.
 Cerebral Malaria  Stopping of the treatment early.
 Is the most common cause of death in malignant malaria,
capillary plugging of cerebral microvasculature, which b. Relapse
results in anoxia, ischemia, and hemorrhage in brain.
 Late stage schizonts of P. falciparum secretes protein on the  Common to P. vivax and P. ovale infections, as result from the
surface of RBC to form knob-like deformities. This knob reactivation of hypnozoite forms of the parasite in the liver
produces specific adhesive proteins, which promote  Suffering deterioration after a period of improvement.
aggregation of infected RBC to other non-infected RBC and  Pre mature stage of organism resides in the body that are in
capillary endothelial cells. dormant stage and will cause disease after recovering completely
 Blackwater fever from the previous occurrence of the disease.
 Malarial hemoglobinuria is sometimes seen in falciparum
malaria. Clinical manifestation include bilious vomiting and Table 1.2 Recrudescence vs. Relapse
prostration, with passage of dark red or blackish urine (black Recrudescence Relapse
water). There is a massive intravascular hemolysis caused by Seen in P. falciparum and P. Seen in P. vivax and P. ovale
anti-erythrocyte antibodies, leading to massive absorption of malariae
hemoglobin by the renal tubules (hemoglobinuric nephrosis). Due to persistence of the parasite at Due to reactivation of
a subclinical level in circulation hypnozoites present in liver cells
Occurs within a few weeks or Occurs usually 24 weeks to 5
months of a previous attack years after the primary attack
Can be prevented by adequate drug Can be prevented by giving
therapy or use of newer antimalarial primaquine to eradicate
drugs in case of drug resistance hypnozoites

F. Pathological Process of the RBC H. Immunity
1. Poikilocytosis and Anisocytosis  Duffy negative RBCs

 Poikilocytosis – variation in shape  It has been found that persons, who lack the Duffy blood
 Anisocytosis – variation in size group (Fya and Fyb alleles) antigen, are refractory to infection
2. Altered RBC membrane transport by P. vivax. These genetically determined blood group
3. RBC stiffness and cytoplasmic viscosity antigen appears to be the specific receptor for P. vivax
 Receptor of P. vivax on the erythrocyte surface is the Duffy
protein.
 Nature of hemoglobin
 Since malaria infects RBC, any alterations to the hemoglobin,
which is essential to RBC function, generally protects the RBC
from the invasion of Plasmodium parasites or replication
within the RBC.
 Problem with hemoglobin – it will not sustain the life cycle of
malaria (resistance to the disease).
 Hemoglobin E provides natural protection against P. vivax. P.
falciparum does not multiply properly in sickled red cells
containing HbS. Sickle cell anemia trait is very common in
Africa, where falciparum malaria is hyperendemic and offers
a survival advantage. HbF present in neonates protects them
G. Morphology
against all Plasmodium species.
 G6PD deficiency
Table 1.3 Morphology of Plasmodium spp.  RBC - Bite cells (there is an abnormality on the morphology
of RBC)
 Innate immunity to malaria has also been related to G6PD
deficiency found in Mediterranean coast, Africa, Middle East,
and India
 HLA-B53
 HLA-B53 is associated with protection from malaria. There is
some evidence that severe malnutrition and iron deficiency
may confer some protection against malaria
I. Diagnosis
a. Microscopy
 (Gold Standard)
 "Thick and Thin Blood Smear"
 stained with Giemsa or Wright's stain
 perform multiple sets of blood films (blood collected every 6 to 12
hours for up to 48 hours)
 Thin smear- absence or presence of parasite
Manner of Reporting
 Qualitative
 += 1-10 parasite/100 thick field
 ++= 11-100 parasite/100 thick field
 +++= 1-10 parasite/thick field
 ++++ = more than 10/thick field
 Quantitative
 Malaria parasite/uL = no. of parasites x 8,000
WBC
 Tally the parasite against WBC until you have counted 500
parasites or 1000 WBC whichever comes first.
 Express the result as parasites/uL of blood

b. Quantitative Buffy Coat (QBC)  Artemether-Lumefantrine (Coartem TM ) - first line drug for
confirmed P. falciparum cases. Not recommended in
 uses a special capillary tube with acridine orange pregnancy, lactation and infants.
 (+) bright green and yellow under fluorescent  Quinine (plus Tetracycline or Doxycycline) - second line
microscope drug for confirmed P. falciparum cases which AL fail or not
available.
 Quinine IV drip - drug of choice for complicated or severe P.
falciparum malaria.
 Chloroquine- anti-malarial drug used in P. falciparum before
but it is resistant now. Sensitive with P. vivax
c. Preventive
 Gametocidal: Objective is to destroy gametocytes to prevent

mosquito transmission and thereby reducing human reservoir.
c. Rapid Diagnostic Test (RDT)  In addition to AL and Q+T,D, Primaquine is given on the
4th day as single dose to prevent transmission
 Use test kits if (-) with microscopy and you are suspecting a
malaria K. Prevention
 detects Plasmodium-specific antigens in finger prick sample
 Histidine-rich protein Il (HRP Il) - water soluble CHON  Use of mosquito repellant
produced by trophozoites and young gametocytes (e.g.,  Use of insecticide treated nets (lTN)
Paracheck Pf test, ParaHlT f test)  Take prophylactic medication
 Plasmodium LDH - produced by both sexual and asexual  Wearing of light-colored clothing which cover most of the body
stages. Can distinguish between P. falciparum and non-P.
falciparum (DiaMed OptiMAL IT)
L. Control
 Environmental cleanliness (stream cleaning to speed up water flow

and exposing to sunlight)
 Indoor residual spraying
 Zooprophylaxis - use of carabao to deviate mosquitoes
 Use of biologic control methods
 Bacillus thuringiensis – larvicidal
 Larviparous fishes (e.g., Oreochromis niloticus)
III. Plasmodium knowlesi

 Anti-malaria antibody and control: Non-falciparum or it is
caused by other spp.  A primate malarial parasite common in South East Asia
 Anti-falciparum and anti-malaria antibody: Pure or mixed  Causes malaria in long tailed macaques (Macaca fascicularis)
infection with P. falciparum  May also infect humans
 The appearance of P. knowlesi is similar to that of P. malariae
d. Serologic Tests (IHA, FAT, ELISA)  PCR assay and molecular characterization are the most reliable
methods for detecting and diagnosing P. knowlesi infection
 (IHA, FAT, ELISA)  However, P. vivax appears to interfere PCR testing (cross-
reactivity)
e. Molecular Methods
IV. Babesia spp.
 through PCR (low cases and mixed infection  Babesia microti (Rodent strain)
 Babesia divergens and Babesia bovis (cattle strain)
J. Treatment  First described to cause "Texas cattle fever or red water fever”
 Blood parasites that cause malaria-like infections
 Anti-malaria drugs are used with various objectives like clinical  "Babesiosis" - pathology due to Babesia spp.
cure, prevention of relapse, prevention of transmission and
 Parasites divide through binary fission or budding
prophylaxis.
 Cycle in the tick is still uncertain
a. Protective 1. Vector
 Chemoprophylaxis: Objective is to prevent infections in non-  Ticks (Ixodes scapularis)

immune person visiting endemic areas (Mefloquine and
 Hard ticks
Doxycycline)
 Scapularis - capable of carrying Borrelia burgdorferi (CA of
Lyme disease)
b. Curative
 Action on established infection

 Therapeutic: Objective is to eradicate the erythocytic cycle and
clinical cure
 Radical cure: Objective is to eradicate the exoerythrocytic cycle
in liver to prevent relapse

2. Definitive host C. Diagnosis
 Ixodid ticks  Microscopy of the Giemsa-stained peripheral blood smear

 Merozoites in Maltese cross arrangement
3. Intermediate host  Ring form most frequent intraerthrocytic form found
 PCR (gold standard)
 Man or other mammals  Immunofluorescent assays (IFA)
 Immunochromatographic test (OCT)
4. Infective form
 Sporozoites
 bite of the nymphal stage of Ixodid ticks

 Other modes of transmission
 Blood transfusion
 Organ transplantation
 Transplacental route
6. Diagnostic stage
 "Maltese cross" arrangement of the merozoites and ring-form

trophozoite
D. Treatment
 Clindamycin - Drug of choice

 Drug combination: Clindamycin and Quinine or Azithromycin and
Atovaquone
 Chloroquine - former drug of choice (it only improve the symptoms
but not the degree of the parasitemia)
 In the Philippines: human babesiosis is not yet reported however,
A. Life Cycle of Babesia spp. it could be present in dogs (Babesia canis).
 Sporogony occurs in final host or definitive host (tick) E. Prevention and Control
 Humans are dead end host. (Merozoite form only). Trophozoites
are not developing into gametocytes.  avoidance of places where ticks are usually found
 But may develop in other animals like mouse. (Merozoite >  wearing of light-colored pants tucked into one's socks
gametocyte)  tick check (especially for children)
 Rodent population should be controlled – rodents are the major
carriers and reservoir of the parasite.
References:
 Belizario, V. and De Leon, W. (2015). Philippine Textbook

of Medical Parasitology. Third Edition. University of the
Philippines Manila. Ermita, Manila.
 Peter L. Chiodini BSc MBBS PhD MRCS FRCP
FRCPath FFTMRCPS(Glas), Anthony H Moody, and D.
W. Manser (2001) . Atlas of Medical Helminthology and
Protozoology. The London School of Hygiene & Tropical
Medicine. London, United Kingdom.
 Mikhail A. Valdescona, RMT, MPH. PAR313 Lecture.
Our Lady of Fatima University. Valenzuela City.
 Lecture Sidenotes of Prof. Sherlyn Joy Isip, RMT, MST –
OLFU VALENZUELA
B. Pathology
 Associated with excessive pro-inflammatory cytokines such as the

tumor necrosis factor (TNF)
 Most cases are subclinical and may occur as self-limiting
 Headache, high-grade fever, chills, vomiting, myalgia, DIC,
hypotension, respiratory distress and renal insufficiency.

OLFU Coccidian Parasites
CLINICAL PARASITOLOGY LEC 5 2021 – 2022
1st Semester
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
 Infection is usually asymptomatic among the immunocompetent.
May present a self-limiting gastroenteritis.
 Oocysts of Cystoisospora belli are elongated ovoid and measure
 Symptomatic: diarrhea, fever, malaise, abdominal pain and
25 um x 15 um.
 Each oocyst is surrounded by a thin smooth 2 layered cyst wall. flatulence
 Immature oocyst seen in the feces of patients contain two  Disease is common to children and male homosexuals with AIDS
sporoblasts.  In AIDS patients, reports on dissemination of parasite to other
 The oocysts mature outside the body. On maturation, the organs are present. (Opportunistic pathogens)
sporoblast convert into sporocysts. Each sporocyst contain 4  The stool may contain fatty acid crystals and charcot-leyden
crescent shaped sporozoites. cystals. There is a flattened mucosa and damaged villi causing
 There is a need of environmental contamination for the cyst to high fecal fat content in the stool (steatorrhea). These findings are
develop and become mature. 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.

[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
 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

 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
B. Infective Stage
E. Sources of Infection
 Oocyst
 Faulty water purification system
C. Life Cycle of Cryptosporidium hominis  Swimming in contaminated recreation water
 One person to another: infected food handlers
 Thick-walled oocyst is infectious when ingested. Sporozoites will  Nosocomial infection
attach to the surface of epithelial cells of the GIT.
 Sporozoites will develop to become small trophozoites, and the F. Diagnosis
trophozoites will divide (schizogony) producing merozoites.
Gametocytes are produced  Sheather's sugar floatation, Zinc sulfate floatation technique and
 Gametocytes > zygote > oocyst (both sporulated) Formalin ether/ethyl acetate concentration technique.
 Thin walled oocyst will infect other enterocytes > autoinfection  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

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
 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

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.

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.
2. Antibody Detection
 Acute infection with T. gondii can be made by detection of the

simultaneous presence of lgM and lgG antibodies.
3. Ocular Toxoplasmosis  Tests for detecting lgG antibody include: Enzyme linked
immunosorbent assay (ELISA), Indirect fluorescent antibody test
 It may present as uveitis (eye inflammation affects the middle (IFAT), Latex agglutination test and Sabin Feldman dye test.
layer of the tissue in the eyewall called uvea), choroiditis, or  Sabin Feldman dye test- special test incorporated to diagnose T.
choriorentinitis. 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. Toxoplasmosis in Immunocompromised Patients
4. Skin test of Frenkel
 Most serious and often fatal in immunocompromised patients,

 Diluted toxoplasmin is injected intradermally and delayed positive
particularly in AIDS, whether it may be due to reactivation of latent
reaction appears after 48 hours. This test is not very reliable for
infection or new acquisition of infections.
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

F. Diagnosis (CT) scan are used to diagnose toxoplasmosis with central
nervous system involvement.
1. Microscopy  Ultrasonography (USG) of the fetus in utero at 20—24 weeks of
pregnancy is useful for diagnosis of congenital toxoplasmosis
 Tachyzoites and tissue cysts can be detected in various
specimens like blood, sputum, bone marrow aspirate, G. Treatment
cerebrospinal fluid (CSF), amniotic fluid, and biopsy material from
lymph node, spleen, and brain.  Congenital toxoplasmosis: pyrimethamine and sulfadiazine
 Smear made from above specimens is stained by Giemsa, PAS,  Ocular toxoplasmosis: pyrimethamine plus either sulfadiazine or
or Gomori methenamine silver (GMS) stain. Tachyzoites appear clindamycin.
as crescent shaped structures with blue cytoplasm and dark  Immunocompromised patients: Trimethoprim sulfamethoxazole
nucleus. is the drug of choice, dapsone-pyrimethamine is the
 Gomori methenamine silver (GMS) stain- special stain used in recommended alternative drug of choice.
histopathology particularly in CNS.  Adverse effect of pyrimethamine- lowers the blood count. It
should be taken together with leucovorin or folic acid.

H. Prevention and Control C. Pathology
 Good sanitation and hygiene  Sarcosporidiosis and sarcocystosis

 Proper food preparation  Gastroenteritis, diarrhea, myalgia, weakness, fever
 Pregnant women should avoid contact with cats  For intermediate host, brain, muscle and kidney tissues may be
damaged.
VI. SARCOCYSTIS HOMINIS & SARCOCYSTIS SUIHOMINIS  May cause abortion to cows
 Sarcocystis species produce cyst in the muscle of the D. Diagnosis

intermediate hosts. These cysts are called Sarcocysts, contain
numerous bradyzoites  Fecal floatation methods: sporocysts will be seen
 Sarcocystis hominis from cattle  Fecal floatation wet mount using Bright Field Microscopy
 Sarcocystis suihominis from pigs  Floatation methods- based on high-density solutions
 Definitive host: Humans
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
A. Life Cycle of Sarcocystis spp.  Trimethoprim-sulfamethoxazole is seen as potentially effective
in treating intestinal infections
 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
B. Mode of Transmission
 acquired by eating raw or undercooked beef/pork

OLFU
Introduction to Nematodes
2021 – 2022
Date: November 12, 2021 TRANS 7 PARA311
LEC
OUTLINE

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  Phasmid nematode- with caudal chemoreceptors
considered as the prototype of the worms.  Aphasmid nematode- without caudal chemoreceptors
 Ex. of aphasmid nematode: Trichuris trichiura, Trichinella
A. General Characteristics 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.

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

 http://www.cdc.gov
 Lecture Sidenotes of Prof. Sherlyn Joy Isip, RMT, MSMT –
OLFU VALENZUELA

OLFU
Filarial Worms
2021 – 2022
LEC
OUTLINE
d. Covering and Habitat
 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)

[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

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. b. Occult Filariasis
 Lower limbs are commonly affected but upper limb and male
genitalia may be involved. Breast and genitalia of females may be  Synonyms: Weingartner's syndrome, Meyer's-Kouwenaar
affected but relatively uncommon. 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.
4. Hydrocoele
 Accumulation of fluid occurs due to obstruction of lymph vessel of c. Tropical pulmonary eosinophilia
the spermatic cord and also by exudation from the inflamed test
and epididymis.  Manifestation: low-grade fever, loss of weight, and pulmonary
 The fluid is usually clear and straw colored but may sometimes be symptoms
cloudy, milky, or hemorrhagic.  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.

 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

h. Demonstration of Antibody
 Complement fixation, indirect hemagglutination (IHA), indirect

fluorescent antibody (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).

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

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:

OLFU VALENZUELA

OLFU
Nematodes I
2021 – 2022
LEC
OUTLINE

I. Ascaris lumbricoides
A. Morphology
B. Life Cycle
C. Pathology
D. Diagnosis
F. Integrated Helminth Control Program (DOH)
II. Trichuris trichiura
III. Enterobius vermicularis
I. ASCARIS LUMBRICOIDES
 Common name: Giant intestinal/round worm

 Final Host: man
 Habitat: small intestine
 Diagnostic stage: fertilized and unfertilized egg
 Infective stage: embryonated egg
 Source of ex. to inf.: soil-transmitted helminth
 MOT: Ingestion
 Pathology: Ascariasis
 Diagnosis: Stool Exam, Concentration technique
 Drug of choice: Albendazole
(Mebendazole and Pyrantel Pamoate)
*Ascaris suum - Ascaris of Pigs
 Most common intestinal nematode of man (occurs most

frequently in tropics)
 Its specific name “lumbricoides” is derived from its
resemblance with the earthworm.
 Lumbricus – means earthworm in Latin.
 Soil-transmitted helminth (along with T. trichiura and
hookworms)
 The soil plays a major role in the development and
transmission of the parasite.
 The children are particularly vulnerable since they are at b. egg
risk in ingesting the embryonated Ascaris eggs while
playing in soil contaminated with human feces.
 Fertilized eggs
 Soil-transmitted helminth - considered as disease of the  laid by females, inseminated by mating with a male
poverty and may contribute to malnutrition and impairment  embryonated and develop into the infective eggs
of cognitive performance.  round or oval
 always bile-stained, golden brown in color
A. Morphology  surrounded by thick smooth translucent shell with an outer
coarsely mamillated albuminous coat, a thick transparent
a. Worm middle layer and the inner lipoidal vitelline membrane
(covering-corticated egg, no covering-decorticated egg)
 Adult Worm  Unfertilized eggs
 Large cylindrical worms, with tapering ends, the anterior end  laid by uninseminated female
being more pointed than the posterior  non-embryonated and cannot become infective
 Pale pink or flesh colored when freshly passed in stools but  Elliptical in shape, narrower and longer
become white outside the body.  has a thinner shell with an irregular coating of albumin
 The mouth at the anterior end has 3 finely toothed lips, 1
dorsal and 2 ventrolateral (trilobate lips)
 Male Worm
 Smaller than female, measures 10-31 cm in length
 Posterior end is curved ventrally to form a hook and carries 2
copulatory spicules.
 copulatory spicules- used for mating
 Female
 Larger than male, measuring 22-35 cm in length
 Posterior extremity is straight and conical
 Vulva is situated mid-ventrally
 A distinct groove is often seen surrounding the worm at the
level of the vulvar opening (genital girdle or vulvar waist)

[PARA311] 2.05 Nematodes I I Prof. Sherlyn Joy P. Isip, RMT, MSMT
b. Due to adult worm
 Spoliative or nutritional effects: enormous numbers occupying a

large part of the intestinal tract interferes with proper digestion and
absorption of food. Ascariasis may contribute to protein-energy
malnutrition and vitamin A deficiency.
 Toxic effects: due to hypersensitivity to the worm antigens and
may be manifested as fever, urticaria, angioneurotic edema,
wheezing, and conjunctivitis.
 Mechanical effects: most important manifestations of ascariasis,
worms may be clumped together into a mass, filling the lumen,
leading to worm bolus, intestinal obstruction and intestinal
perforation.
 Ectopic ascariasis (Wanderlust): worms may wander causing
acute biliary obstruction or pancreatitis, liver abscesses, respiratory
obstruction or lung abscesses and obstructive appendicitis. The
wandering is enhanced when the host is ill (If the temperature is
above 39C it may provoke the worms to wander around).
 Erraticity: if worm migrates to ectopic sites (gallbladder,
hepatobiliary tree, appendix and pancreas), maybe regurgitated
and vomited, may escape through the nostrils or inhaled to the
trachea maybe due to medication, spicy-diet and fever. *Usually
observed in male worms.
B. Life Cycle
 Does not need intermediate host.

 When embryonated eggs are ingested > it will hatch in the lumen
of small intestine releasing the larvae > larvae will migrate to the
cecum or proximal colon where they penetrate the intestinal wall >
they enter the venules and will go to the liver through portal vein,
to the heart or to pulmonary vessels.
 Female A. lumbricoides produces about 200,000 eggs per day. The
eggs are deposited into the soil, and it takes about 2-3 weeks for
the eggs to develop under favorable condition with suitable
temperature, moisture and humidity.
 Can survive the acidity of the stomach because of pepsin inhibitor
3 (protein).
D. Diagnosis
 The clinical diagnosis should be confirmed or established by

microscopic examination of stool sample.
 Direct fecal smear is less sensitive compare to Kato-thick and Kato-
katz.
 Stool Examination
 Direct Fecal Smear
 Kato-thick (qualitative)
 Kato-katz (provides a quantitative diagnosis in terms of
intensity of the helminth infection in eggs/gram of the stool.
Usefull in monitoring the efficacy of the treatment in the clinical
trials)
 Concentration Technique
 Formalin Ether/Ethyl Acetate Concentration Technique
C. Pathology (FECT)
 Merthiolate Iodine Formaldehyde Concentration
technique (MIFCT)
a. Due to larva
 Brine floatation
 Zinc sulfate floatation technique
 Ascaris pneumonitis or Loeffler's Syndrome: occurs during lung  X-ray (extra-intestinal ascariasis: lungs)
migration resulting in allergic reactions such as lung infiltration,  CBC (demonstrate eosinophilia)
asthmatic attacks and edema of the lips, similar symptoms of
pneumonia, vague abdominal pain. Eosinophilia is present
 Sputum- often blood-tinged and may contain Charcot-Leyden E. Prevention and Control
crystals.
 The larvae may occasionally be found in the sputum but are seen  Sanitary disposal of human feces
more often in gastric washing  Health education
 Mass chemotherapy

 Avoid using night soil A. Morphology
 Proper food preparation
a. Worm
F. Integrated Helminth Control Program (DOH)
 Adult Worms
a. Target and Doses  Flesh-colored
 Resembles a whip with the anterior three-fifth thin and thread-
1. Children aged 1 year to 12 years old like and the posterior two-fifth is thick and fleshy, appearing
like the handle of a whip.
 Attenuated anterior portion, which contains the capillary
For children 12 —24 months old
esophagus is embedded in the mucosa
 Albendazole - 200 mg, single dose every 6 months. Since the
preparation is 400mg, the tablet is halve and can be chewed by the
child or taken with a glass of water or
 Mebendazole - 500 mg, single dose every 6 months
For children 24 months old and above

 Albendazole - 400 mg, single dose every 6 months or
 Mebendazole -500 mg, single dose every 6 months
Note: If Vitamin A and deworming drug are given simultaneously during
the GP activity, either drug can be given first.
2. Adolescent females
 It is recommended that all adolescent females who consult the

health be given anthelminthic drug
 Albendazole -400 mg once a year or
 Mebendazole -500 mg once a year
3. Pregnant women
 It is recommended that all pregnant women who consult the health

be given anthelminthic drug once in the 2nd trimester of pregnancy. Table 2.0 Comparison of Male and Female worm of T. trichiura
 In areas where hookworm is endemic: Where hookworm prevalence MALE FEMALE
is 20 — 30% 30-45 mm 35-50 mm
 Albendazole - 400 mg once in the 2nd trimester Or Coiled posterior with a single Rounded/blunt posterior
 Mebendazole - 500 mg once in the 2nd trimester spicule and rectractile sheath 3,000-20,000 eggs/day
Where hookworm prevalence is > 50%, repeat treatment in the 3rd
trimester
 Attenuated anterior 3/5 - slender, hair-like, transversed by a
narrow esophagus resembling "string of beads" - used for
4. Special groups, e.g., food handlers and operators, soldiers, attachment
farmers and indigenous people  Robust posterior 2/5 - contains the intestines and single set of
reproductive organs
 Selective deworming is the giving of anthelminthic drug to an
individual based on the diagnosis of current infection. However, b. egg
certain groups of people should be given deworming drugs
regardless of their status once they consult the health center.
 Special groups like soldiers, farmers, food handlers and operators,  brown in color being bile-stained
and indigenous people are at risk of morbidity because of their  triple shell, the outermost layer of which is stained brown
exposure to different intestinal parasites in relation to their  barrel-shaped with a projecting mucus plug at each pole containing
occupation or cultural practices. an unsegmented ovum
 resembles Capillaria philippinensis- peanut shape ova with
 For the clients who will be dewormed selectively, treatment shall be
flattened bipolar plug
given anytime at the health centers
II. TRICHURIS TRICHIURA
 Common name: Whipworm

 Final Host: man
 Habitat: large intestine
 Diagnostic stage: egg
 Infective stage: Embryonated egg
 Source of ex. to inf.: soil-transmitted helminth
 MOT: Ingestion
 Pathology: Rectal prolapse, IDA, diarrhea
 Diagnosis: Stool exam, Concentration technique
 Drug of choice: Mebendazole (Albendazole as
alternative drug)
*Usually observed occurring together with Ascaris lumbricoides

B. Life Cycle III. ENTEROBIUS VERMICULARIS
 The worms inhabit the cecum and colon. It secrets pore-forming  Common name: Pinworm, Seatworm, Society worm*
protein called TT47 which allows them to embed their entire whip-  Final Host: man
like portion into the intestinal wall.  Habitat: (cecum) large intestine
 The female worms lay eggs, which are passed out with the feces  Diagnostic stage: ova
and deposited in the soil, under favorable conditions the eggs will  Infective stage: embryonated egg
develop and become embryonated. If swallowed, the infective  Source of ex. to inf.: contact-borne
embryonated eggs will go to the intestine and undergo four larva  MOT: Ingestion, inhalation
stages to become adult. No heart-lung migration.  Pathology: Enterobiasis or oxyuriasis
 Diagnosis: Scotch tape swab
 Drug of choice: Pyrantel pamoate (Mebendazole and
Albendazole as alternative)
*Familial disease-extremely contagious and can easily spread
among the members of the family or institution.
 Can cause autoinfection and retroinfection

 Retroinfection- migration of newly hatched larvae from the
anus back to the rectum.
A. Morphology
a. Worm
 Adult Worms
 short, white, fusiform worms with pointedalae ends, looking
like bits of white thread
 mouth is surrounded by 3 wing-like cuticular expansions,
which are transversely striated esophagus has a double-bulb
C. Pathology structure, a feature unique to this worm
 Male Worm
1. Rectal prolapse  posterior end is tightly curved ventrally, sharply truncated and
 Condition in which the rectum (the lower end of the colon, carries a prominent copulatory spicule
located just above the anus) becomes stretched out and  Female Worm
protrudes out of the anus. Weakness of the anal sphincter  posterior third is drawn into a thin pointed pin-like tailand
muscle is often associated with rectal prolapse at this stage, straight
resulting in leakage of stool or mucus.  vulva is located just in front of the middle third of the body
2. Appendicitis and granulomas

 Due to irritation and inflammation brought by the worms.
3. Blood streaked diarrheal stools, abdominal pain, tenderness,
anemia (associated with IDA) and weight loss
D. Diagnosis
 Flotac technique- more sensitive in diagnosing
 Direct Fecal Smear
 Kato-thick (highly recommended)
 Kato-katz
 Concentration Technique
 FECT
 MIFCT
 Brine floatation
 Zinc sulfate floatation technique
 Treatment of infected individuals

 Sanitary disposal of human feces, construction of toilets
 Washing of hands
 Health education (sanitation and hygiene)
 Proper food preparation practices

to the intestinal tract and they exit through the anus to deposit the
eggs on the perianal skin.
 After egg deposition, the female usually dies.
 Eggs are resistant to disinfectants.
 Best time to collect sample: morning
Table 3.0 Comparison of Male and Female E. vermicularis

MALE FEMALE
2 to 5 mm 8-13 mm
Curved tail and has a single long pointed tail
spicule 5,000-17,000 eggs/day
*rarely seen because they die
after copulation
b. egg
C. Pathology
 Mild catarrhal inflammation of the intestinal mucosa

 Nocturnal pruritus ani- "perianal itching" which may lead to
secondary bacterial infection and lack of sleep
 Other complications: appendicitis, vaginitis, endometritis and
peritonitis.
 Poor appetite, weight loss and abdominal pain.
D. Diagnosis
 Graham’s scotch adhesive tape swab (Perianal cellulose tape

swab)
 Provides the highest percentage of (+) results
B. Life cycle
 Infection occurs via self-inoculation or through exposure to the
eggs in the environment.  Personal cleanliness and hygiene are essential
 Following the ingestion of infective eggs, the larvae will hatch in the  Hand washing
small intestine and the adults will establish themselves in the colon  Boiling of linen and clothing
usually at cecum.
 The gravid females will migrate nocturnally outside the anus and
oviposit while crawling on the skin of perianal area. > migrate down

References:

OLFU VALENZUELA

OLFU
Nematodes II
2021 – 2022
Date: December 18, 2021 TRANS 10 PARA311
LEC
OUTLINE

I. Trichinella spiralis
A. Morphology
B. Life Cycle
C. Pathology
D. Diagnosis
II. Capillaria philippinensis
III. Hookworms
IV. Strongyloides stercoralis
V. Angiostrongylus/Parastrongylus cantonensis
VI. Anisakis spp.
VII. Toxocara spp.
VIII. Dirofilaria immitis
I. TRICHINELLA SPIRALIS
 Common name: Trichina worm, muscle worm

 F.H or I.H: Man, rat, dogs, pigs, bears, foxes or any B. Life Cycle
carnivore or omnivore
 Habitat: Small intestine (adult), skeletal muscle  Optimum host: pigs, Alternate host: humans
(larva)  Man is the dead end host of the parasite.
 Diagnostic Stage: Encysted larva
 Infective Stage: Encysted larva
 Source of ex. to inf: Food borne (insufficiently cooked pork
meat)
 MOT Ingestion
 Pathology Trichinosis/Trichinellosis, Muscle tissue
destruction, muscular dystrophy
 Diagnosis: Muscle biopsy, Beck's Xenodiagnosis,
BFT (Bentonite Flocculation Test),
Bachman Intradermal Test
 Drug of Choice: Mebendazole, Albendazole
 “Trichos” – hair, “ella” – diminutive, “spiralis” spirally coiled

appearance of the larvae in the muscle.
 Infective stage (larva) - seen in skeletal muscle
 Beck's Xenodiagnosis – feeding the meat (muscle biopsy) to
albino rats > observe for 14 days > check for the presence of
female worm.
 Bachman Intradermal Test – an extract of Trichinella larvae is
suspended in saline > inject intradermally. An immediate
wheal and flare or delayed response indicates infection.
 In mild cases of trichinosis, supportive treatment such as
bedrest, analgesic and antipyretic is given (infection is self-
limiting if mild).
C. Pathology
A. Morphology
a. Enteric Phase
 Adult Worm
 small white worm just visible to the naked eye, one of the
 malaise, nausea, vomiting, diarrhea, abdominal cramps
smallest nematodes infecting humans
 similar to attack of food poisoning
 The posterior end of the male has a pair of pear-shaped
clasping papillae (claspers), one on each side of the cloacal
orifice that it uses to hold the female worm during mating. b. Invasion Phase
 The female worm is viviparous and discharge larva instead of
eggs.  myalgia, periorbital edema and eosinophilia
 Severe cases: gastric hemorrhages, myocardial and neurological
Table 1.0 Comparison of Male and Female T. spiralis complications (eg., pericardial effusion, congestive heart failure,
MALE FEMALE meningoencephalitis and cerebral lesions)
1.5 by 0.04 mm 3.5 by 0.06 mm
Single testis Single ovary c. Convalescent Phase
Near its cloaca, there’s a pair of Viviparous
caudal appendages and two  fever, weakness and pain
pairs of papillae  all symptoms subside

[PARA311] 3.01 Nematodes II I Prof. Sherlyn Joy P. Isip, RMT, MSMT
* Self-limiting but some ailments may persist
D. Diagnosis
 Muscle biopsy- definitive diagnostic exam (deltoid, biceps,

gastrocnemius and pectoralis muscle)
 Biochemical Tests (increased creatine phosphokinase, lactate
dehydrogenase, aldolase and myokinase levels) - evidence of
muscle damage
 Serological Tests (Bentonite Flocculation Test-BFT, Latex
agglutination test, FAT, ELISA)
 Beck's Xenodiagnosis
*ELISA is recommended for the diagnosis of Trichinellosis

*Confirmatory test – western blot technique
*In molecular characterization, we need to digest the muscle first
in order to isolate the larvae. Trypsin, pepsin and HCl are used
to digest the muscle. Digestion of muscle using these can
also be done to determine the number of larvae per gram of
muscle.
 Health Education
 Proper Food Preparation
 Meat Inspections
 Keeping pigs in rat-free pen B. Life Cycle
II. CAPILLARIA PHILIPPINENSIS  Unembryonated thick-shelled will become embryonated in the

water/environment > the infective larvae will develop in the tissue
 Common name: Pudoc worm of intermediate host > the adults will develop in the intestinal
 Final Host: man and other vertebrate host mucosa.
 Intermediate Host: Bagsang, Birot, Bagtu, Ipon (fresh  Females may produce two types of eggs: unembryonates eggs
water and brackish water fishes) (passed in the feces) and embryonated eggs lacking shells (hatch
 Habitat: Small intestine inside the definitive host).
 Diagnostic Stage: egg  Larvae will re-invade the small intestinal mucosa in auto infective
 Infective Stage: Filariform larva (L3) cycle.
 Source of ex. to inf. Food borne
 MOT: Ingestion
 Pathology: Borborygmi, diarrhea, malabsorption
 Diagnosis: Stool exam, Duodenal fluid exam
 Drug of Choice: Mebendazole, Albendazole
*Discovered by Nelia Salazar in 1963 (Barrio Pudoc, Ilocus Sur)
 Capillaria philippinensis was described as a mystery disease

in 1998 in Monkayo Compostela Valley Province, which
resulted in the death of villagers due to misdiagnosis.
A. Morphology
Table 2.0 Comparison of Male and Female C. philippinensis

MALE FEMALE
1.5 to 3.9 mm 2.3 to 5.3mm
Presence of single spicule and Typical: oviparous
unspined sheath Atypical: larviparous
 Some larvae are retained in the gut lumen and will develop into
adults, which leads to hyperinfection or autoinfection.
 Unembryonated shelled-egg requires environmental contamination. C. Pathology
 Some eggs are covered with vitelline membrane and does not have
a shell.  Borborygmus - gurgling sound of the stomach
 Abdominal pain
 Diarrhea
 Weight loss, malaise, vomiting
 Severe protein loss
 Malabsorption of fats and sugars (associated with flattened
intestine and duodenal villi)
*Capillariasis is endemic in Ilocos Sur, Cagayan Valley, Isabela,

Pangasinan, Zambales, Ilocos Norte, La Union

D. Diagnosis
 Kato-thick
 Kato-katz
 Duodenal aspiration
 Avoid eating raw fish

 Good sanitary practices
III. HOOKWORMS
 Necator americanus - human hookworm

 Ancylostoma braziliense - cat hookworm
 Ancylostoma caninum- dog hookworm
 Ancylostoma duodenale - human hookworm
Dental Pattern:
 a pair of semilunar cutting plates - Necator americanus  Delicate eggshell and may be easily disintegrated in kato-thick
 1 pair of teeth - Ancylostoma braziliense and kato-katz (not recommended).
 3 pairs of teeth - Ancylostoma caninum  Manner of reporting: presence of hookworm eggs/ova
 2 pairs of teeth - Ancylostoma duodenale
B. Life Cycle
 Habitat: Small intestine
 Diagnostic stage: Ova  Humans are the only natural host. No intermediate host is
 Infective stage: L3 required
 MOT: Skin penetration  The L3 will penetrate the skin and enter the venules. They will
migrate into heart, lungs and alveoli. The larvae will ascend to
 Considered as STH and blood sucking nematodes because trachea and it will pass down to small intestine. The worms will
they attach to the mucosa of small intestine. become sexually mature and the female will start to lay eggs.
 Necator americanus was identified in the specimen obtained
in Texas, USA. The name means American Murderer.
 Ancylostoma duodenale came from the Greek word “ankulos”
hooked and “stoma” mouth.
A. Morphology
Table 3.0 Comparison of A. duodenale and N. americanus C. Pathology

Parameter A. duodenale N. americanus
Common Name Old World New World  Due to adult:
Hookworm Hookworm  Epigastric pain, diarrhea, malnutrition, severe anemia
Body curvature C shaped S shaped (microcytic, hypochromic type, IDA)
Dental Pattern 2 pairs Semilunar cutting  Due to larva:
plates  Creeping eruptions or Cutaneous Larval Migration (CLM)
Male bursa Tridigitate Bidigitate  Ground itch or dew itch extra intestinal larval migration
(dorsal rays) (tripartite) (bipartite) or due to skin penetration
Copulatory spicule Plain, bristle-like Fused, barbed  most common cause is nonhuman species of
Habitat Small intestine Small intestine hookworm (A. braziliense and A. caninum)
Dx. Stage Ova Ova
Infective Stage L3 L3
 Wakana Disease
 Pneumonitis
 characterized by nausea, vomiting, dyspnea,
pharyngeal irritation, cough, and hoarseness of voice
*ingested larvae will develop into mature worms in the intestine without
migrating in the lungs
Table 4.0 Differences in morphology
D. Diagnosis L1 or Rhabditiform larva L3 or Filariform larva
Open mouth Closed mouth
 Stool exam - DFS Short and stout Long and slender
 Culture Technique: Harada Mori Technique Feeding Non-feeding
 Filter-paper culture method utilizes the water tropism of larvae Long narrow buccal cavity
to concentrate them. Fresh feces is deposited on the filter Flask-shaped esophagus
paper, which is soaked with water.
 Incubate for 10 days at 30C
 Check for the formation of larvae
 Proper Sanitation
 Personal hygiene
 Chemotherapy
IV. STRONGYLOIDES STERCORALIS
 Common name: Threadworm

 Final Host: Man Table 4.1 Rhabditiform larva
 Habitat: Small intestine Parameter Hookworm S. stercoralis
 Diagnostic Stage: L1 Buccal cavity Long Short
 Infective Stage: L3 Genital primordium Small Prominent
 Source of ex. to inf. STH
 MOT: Skin penetration Table 4.2 Filariform larva
 Pathology: Cochin China diarrhea, honey-comb Parameter Hookworm S. stercoralis
ulcer, Villi atrophy, malabsorption, Esophagus Short Long
pneumonitis, creeping eruption Tail-end Pointed Forked/notched
 Diagnosis: Stool exam, Enterotube test, Harada- Sheath Sheathed Unsheathed
Mori culture
 Drug of Choice: Mebendazole, Albendazole,
Thiabendazole
*females are capable of parthenogenesis (fertilization without the

benefit of the males)
 Came from the word “Strongylus” round, “eidos”

resembling, and stercoralis means fecal.
 Dogs can be definitive host.
A. Morphology
 Adult Worms
 Favorable conditions - free-living
 Unfavorable conditions - parasitic
 Males have no purpose (usually passed out in the feces after
development to L3)
 Females are ovoviviparous.
 The individual worm has a lifespan of 3 or 4 months, but
because it can cause autoinfection, the infection may persist
for years.

B. Life Cycle  It is known to cause eosinophilic meningoencephalitis
 In some countries, (China, Thailand, Taiwan) mebendazole
and albendazole have been demonstrated to effectively treat
Angiostrongylus cantonensis infection.
A. Morphology
Table 4.0 Comparison of Male and Female Angiostrongylus/

Parastrongylus cantonensis
MALE FEMALE
16 to 19 mm 21 to 25 mm
Kidney shaped, single-lobed "barber's pole" uterine
bursa tubules
(uterine tubules wound spirally
around the intestines)
C. Pathology
B. Life Cycle
 Cochin China Diarrhea or Vietnam Diarrhea (intermittent diarrhea
characterized by numerous episodes of water and bloody stool)
 In humans, the larvae may remain in the brain for a longer period
 Honey comb ulcer
and do not develop into adult stage. Dead end host is man.
 Skin allergy due to larval penetration
 May infect the brain and eye chamber.
 Larval migration > pneumonia
D. Diagnosis
 Kato-thick
 Kato-katz
 Concentration Techniques
 Harada-Mori culture
 Baermann Funnel Gauze Method (a muslin bag containing the
sample is submerged in water in a funnel. Being heavier than
water, the nematodes pass through the muslin and sink to the
bottom)
 Proper Sanitation
 Personal hygiene
 Chemotherapy
V. ANGIOSTRONGYLUS/PARASTRONGYLUS CANTONENSIS VI. ANISAKIS SPP. (ANISAKIS SIMPLEX, ANISAKIS

PHYSETERIS)
 Common name: Rat lung worm
 Common name: Codworm, Herring worm, Anisakine
 Final Host: Rattus rattus var. rattus, Rattus
norvegicus  Final Host: Marine mammals (sea lion, sperm whale,
 Intermediate Host Achantina fulica (giant African snail), dolphin)
(slugs and snails): Hemiplecta macrostoma, Vaginilus  Intermediate Micro crustaceans (Cyclops)
plebeius, Veronicella altae Host: A wide variety of fishes
 Accidental host: Man  Accidental host Man
 Habitat: CNS-brain  Habitat: alimentary canal and tissues
 Diagnostic Stage: adult worms  Infective Stage: third larval stage
 Infective Stage: L3  Source of ex. to food borne
 Source of ex. to inf. food borne inf.
 MOT: Ingestion  MOT: Ingestion of raw or semi-raw fish (sashimi)
 Pathology: Acute severe intermittent occipital or  Pathology: Herring's disease, Eosinophilic granuloma,
bitemporal headache Gastrointestinal Anisakiasis
 Diagnosis: Travel history, CSF analysis, CT scan  Diagnosis: Gastroscopic/Endoscopic examination,
 Drug of Choice: Anthelminthic treatment is not ELISA and Radioallergosorbent test
recommended, as the disease is due to  Morphology Smaller than Ascaris (trilobite lips) may be
dead larvae. seen macroscopically

 Curing techniques may not be effective because some
Anisakis can still survive.
Ocular larva migrans
 Visceral Larva Migrans – there is eosinophilic granuloma in the

tissues of liver, lungs, CNS and eyes.
 Ocular larva migrans may cause unilateral visual impairment,
B. Life Cycle strabismus, invasion of retina and blindness.
 Neurological Toxocariasis can cause encephalitis
B. Life Cycle
 The infection is acquired in puppies by transmission of larvae

transplacentally or lactogenically.
VIII. DIROFILARIA IMMITIS
 Common name: Dog heart worm

 Final Host: Dogs
 Accidental host: Man
VII. TOXOCARA SPP. (TOXOCARA CATI AND TOXOCARA  Habitat: Heart and lungs of dogs
CANIS) Blood vessels
 Infective stage: 3rd larval stage
 Common name: Cat or Dog Ascaris aka Ascarids  Source of ex. to inf.: vector borne
 Accidental host: Man  Vector: Mosquito
 Pathology: Visceral Larva Migrans (VLM), Ocular  Pathology: Coin lesions in the lungs, obstruction
Larva Migrans (OLM), Covert of the heart
Toxocariasis (CoTOX)  Morphology: Microfilaria is unsheathed, no terminal
 MOT: ingestion of embryonated eggs nuclei
 Diagnosis: detection or larvae from biopsy tissues,
Commercial lgG ELISA for the detection of  In humans, the worm lodges in the heart or in the branches of
Toxocara excretory antigens (TES) and pulmonary artery.
Western Blot  The dead worm becomes an embolus blocking a small branch
 Treatment: Albendazole or Mebendazole of the pulmonary artery producing pulmonary infarcts.
 Paratenic host: other mammals and birds
 Toxocara cati – cats, Toxocara canis – dogs

B. Life Cycle
References:

OLFU VALENZUELA

OLFU
Trematodes (Flukes)
2021 – 2022
Date: December 28, 2021 TRANS 11 PARA311
LEC
*There is a presence of two muscular cup-shaped suckers

OUTLINE called as distomata (other term for the suckers). The oral sucker is
surrounding the mouth at the anterior part of the parasite, while the
ventral sucker/acetabulum is in the middle part. The third sucker is
I. Trematodes
II. Fasciola hepatica and Fasciola gigantica called as genital sucker or gonotyl (unique characteristic of
III. Clonorchis sinensis, Opistorchis Felineus, Heterophyes)
Opistorchis viverrini
IV. Fasciola lanceolata (Dicrocoelium dendriticum)
V. Euretrema pancreaticum
VI. Fasciolopsis buski
VII. Echinostoma ilocanum (Eupharyphium ilocanum)
VIII. Heterophyes heterophyes
IX. Paragonimus westermani
X. Schistosoma spp.
I. TREMATODES (CLASS TREMATODA OR DIGENEA)
 Another set of helminths

 Primary characteristic of trematodes - they are unsegmented
helminths, which are flat and broad. They resemble the leaf a tree
or flat fish.
 Classified according to their habitat inside the human body:
Table 1.0 Difference between Schistosomes and other

Trematodes
Schistosomes Other Trematodes
dioecious monoecious
One IH two IH
cercaria metacercaria
skin penetration ingestion
elongated leaf like
II. FASCIOLA HEPATICA AND FASCIOLA GIGANTICA
F. hepatica F. gigantica
Common name Sheep liver fluke Giant liver fluke
Final host Sheep Local cattle,
herbivores
1st IH Lymnaea philippinensis, lymnaea auricularia
rubiginosa (snails)
2nd IH Ipomea obscura (kangkong) and Nasturtium
officinale (water cress)
Habitat Liver parenchyma, gall bladder
A. General Characteristics Infective Stage Metacercaria
Pathology Fascioliasis, or liver rot, liver atrophy,
(Except for Schistosomes) Halzoun
 Monoecious (hermaphroditic) Laboratory Stool exam, liver biopsy, PCR
 Has a primary and secondary intermediate host Diagnosis
 Metacercaria is the infective stage Drug of Choice Bithionol, Triclabendazole
 Ingestion is the mode of transmission
 Eggs are operculated A. Morphology
 Leaf-like
 Has 2 suckers (oral sucker and ventral bladder sucker or
"acetabulum").
*hermaphroditic – these organisms have complete or partial

reproductive organs and produces gametes normally associated with
both male and female sexes (2 in 1 parasite). In other words,
hermaphroditic flukes have both male and female structures; they
contain testes and ovary so that self-fertilization takes place.
*Intermediate host - they pass their larval stage in fresh
water mollusk or snails. Their second IH requires fishes or crabs for the
encystment in some trematodes (it varies, but most of them have  F. hepatica has a prominent cephalic cone and shoulders
primary and secondary IH) (distinguishing feature to F. gigantica).
*operculated- provided with a lid or cup-like in the end. They  They both have highly branched testis and dendritic ovary.
resemble as oval-shaped mostly.

[PARA311] 3.02 Trematodes (Flukes) I Prof. Sherlyn Joy P. Isip, RMT, MSMT
b. "Halzoun" or "Marrara" (pharyngeal suffocation)
 "Halzoun" term used in Lebanon, "Marrara" used in Sudan.

 suffocation as a result of temporary lodgment of the fluke in the
pharynx
D. Diagnosis
 Stool exam (since we are dealing with eggs)

 Recovery of adult flukes in duodenal contents and bile
 Liver biopsy
 Molecular methods PCR, ELISA and Western Blot
B. Life Cycle  Radiologic examination: Sonography, Computed Tomography,
Endoscopic Retrograde Cholangiopancreatography (ERCP)
 There are different larval forms in the life cycle of the trematodes.
The various larval forms are the following: miracidium, cercariae, E. Prevention and Control
rediae, metacercariae, and sporocyst. They vary in their life cycle.
 (Take note what is being passed in the feces, whether it is  Proper food preparation and handling
embryonated/mature or unembryonated/immature egg).  Killing of parasite in reservoir host through chemotherapy
 In this cycle, the unembryonated eggs become mature in the  Vaccination of animals with defined Fasciola antigens: fatty- acid
environment, particularly in the water. binding protein (FABP) termed Fh12, glutathione-S-transferase
 In the water, the eggs will hatch and miracidia will seek out the (GST), cathepsin L (CatL) proteinase, and hemoglobin (Hb).
snail intermediate host. Inside the snail, it will develop into series  Apart from reducing the fluke burden in the animals. Some of
of larval formation (sporocyst > rediae > cercariae). the vaccines have elicited concurrent reduction in the parasite
 The free-swimming cercariae will encyst on aquatic vegetation egg production in the animals (safe in the animals but not in
(the 2nd IH or the parasite) humans).
 Cercariae will develop to become metacercariae.(will ingest by  Health education
definitive host)
 Inside the human body, immature flukes excyst in duodenum, III. CLONORCHIS SINENSIS, OPISTORCHIS FELINEUS,
penetrate the intestinal wall, and migrate through liver OPISTORCHIS VIVERRINI
parenchyma to billary ducts.
 Aside from cattles and sheep, human can also be the definitive C. sinensis O. felineus
host.
Common name Oriental liver fluke Cat liver fluke
Chinese liver fluke
Final Host Man and other fish-eating vertebrate
1st IH Genera Parafossarulus, Genus Bithynia
Bulimus, (snail)
Semisulcospira,
Alocinma and
Melanoides (snail)
2nd IH Family Cyprinidae (fishes)
Habitat Liver parenchyma
Infective stage Metacercaria
Pathology Bile duct obstruction, live CA and gallbladder
CA
Laboratory Stool Exam, serological tests, molecular test
Diagnosis
Drug of Choice Praziquantel, Albendazole
A. Morphology
C. Pathology
a. Human fascioliasis
1. Acute or invasive phase
 may appear to be asymptomatic, or may produce fever,

abdominal pain and hyper eosinophilia
 migration of juvenile parasite from the intestine to the liver
 traumatic and necrotic lesions are produced when the parasite
burrows through the liver parenchyma
2. Chronic phase
 may only be diagnosed through surgical operation

 period where the parasites reached the bile ducts
 obstruction due to the adult worm may happen stimulating
inflammation and subsequently cause fibrosis

C. Pathology
 Periductal fibrosis- fatigue, weakness, weight loss and altered

appetite
 Gallbladder and liver carcinoma
 Pancreatitis
D. Diagnosis
 Stool exam (eggs)

 Serologic tests (ELISA, EIA)
 Molecular method (PCR)
 Cholangiography

 eggs are almost the same phenotypically, reported as C.
sinensis/O. felineus  Health education
 Has shoulders  Proper waste disposal
 Fish irradiation at a dose of 0.15 kGy (kilogray- unit of
measurement in radiation, metacercaria may be killed)
IV. FASCIOLA LANCEOLATA (DICROCOELIUM DENDRITICUM)
Common name Lancet fluke

Final host Sheep, cattle
1st IH Cionella lubrica, Hellicella candibula
(snails)
2nd IH Formica fusca (ants)
Habitat Biliary tree of herbivores
Morphology Blade-like, lancet like shaped,
 Adult fluke are leaf-like and elongated compared to Fasciola Aspinous body, Large ventral sucking
disc
Laboratory diagnosis Stool exam (eggs)
B. Life Cycle
 Same life cycle A. Morphology

 The adults are found in the biliary duct of the definitive host.
 Embryonated eggs are being passed in the feces
 Eggs are ingested by the snails. Miracidia will liberate in the
embryonated eggs and will develop to become sporocysts > rediae
> cercariae.
 Free-swimming cercariae will encyst in the skin or flesh of
freshwater fish.
 The metacercariae in the flesh of skin of fresh water fish are
ingested by the definitive host

B. Life Cycle B. Life Cycle
 The adults inhabit the bile duct.  Host becomes infected by ingestion of infected ants.
 Embryonated eggs are shed in the feces  Adults are seen in the bile dust.
 Eggs are ingested by a snail IH. Miracidia will liberate in the eggs  Embryonated eggs are shed in the feces
and it will develop to become sporocyst > cercariae.
 The cercariae are released from the snail via respiratory pore in a
slime ball.
 Cercariae encyst to metacercariae after being eaten by ant IH.
VI. FASCIOLOPSIS BUSKI
Common name Giant intestinal fluke

V. EURETREMA PANCREATICUM Final Host Man
1st IH Semetina spp., Hippeutis spp., Gyraulus
Common name Pancreatic fluke spp. (snails)
Final host Hogs (pancreatic ducts), Sheep and 2nd IH Trapa (water caltrop), Eichhornia (water
cattle (biliary ducts) hyacinth), Eliocharis tuberosa (water
1st IH Bradybaena similaris, Macrochlamys chestnut), Zizania (water bamboo)
indica (snails) Habitat Small intestine (duodenum and jejunum)
2nd IH Technomyrmex deterquens (ants) Morphology Largest intestinal fluke, fresh colored,
Habitat Pancreas, Duodenum, Bilary duct larger ventral sucking disc, no cephalic cone
Morphology Larger oral sucker, 2 notched testes, 1 Laboratory Stool exam (operculated eggs)
notched ovary diagnosis
Laboratory diagnosis Stool exam (eggs) Eggs “Hen’s egg shape”, yellowish brown, small
Eggs Similar to F. lanceolata, Thick shelled operculum, resembles F. hepatica (no
and dark brown shoulders)
Pathology Destruction of the pancreas, chronic Pathology Fasciolopsiasis
granulomatosus pancreatitis,
enlargement of the pancreas
A. Morphology
A. Morphology
 Fresh in color, macroscopic

 To further diagnose the trematodes spp., since their ova are

almost the same, we need to isolate the adult worm as well (for
the definitive diagnosis)
VII. ECHINOSTOMA ILOCANUM (EUPHARYPHIUM ILOCANUM)
Common name Garrison’s fluke

Final Host Hogs (pancreatic ducts), sheep and
cattle (bilary ducts)
1st IH Gyraulus convexiusclus and Hippeutis
umbilicalis (snails)
2nd IH Pila luzonica (kuhol), VIII. HETEROPHYES HETEROPHYES
Vivipara angularis ("susong pampang")
(snails) Common name Von Siebold's fluke, Heterophyid fluke
Habitat Small intestines Final host Man
Morphology Two lobed testes, Oviviparous 1st IH Pironella conica (snails)
Laboratory Diagnosis Stool exam (eggs) 2nd IH Mugil cephalus (fish)
Eggs Straw colored, less prominent cephalic Habitat Small intestines
operculum than Fasciola, Immature Morphology Smallest trematode, pear-shaped/
when released avocado shaped with genital sucker
(gonotyl)
A. Morphology Laboratory Stool exam (eggs)
Diagnosis
Eggs Embryonated when released, resembles C.
sinensis ova, Oviparous
Pathology Heterophyiasis- can be fatal (migration of
eggs to the heart or brain causing
granuloma)
A. Morphology
B. Life Cycle
 Unembryonated eggs are passed in the feces, then it will

become mature in the water
 Miracidia will hatch from the eggs and will seek out snail host
 Miracidium penetrates the snail host, and will develop to become
sporocyst > rediae > cercariae.
 Free-swimming cercariae will invade the 2nd IH.
 Cercariae > metacercariae (ingested by definitive host)

B. Life Cycle
 Embryonated eggs with fully-developed miracidium are

passed in the feces
 Snail host ingests the eggs, miracidia will emerge from the eggs
and penetrate the intestine. Then it will develop to become
sporocyst > rediae > cercariae
 Cercariae will penetrate the skin of fresh/brakish water fish and
encyst as metacercariae.
 The host becomes infected by ingesting undercooked fish
containing metacercariae. The metacercariae excyst in the small
intestine.
B. Life Cycle
 Unembryonated eggs are passed in the feces > embryonated in

the environment
 Miracidia hatch and penetrate the snail. Inside the snail it will
develop to become sporocyst > rediae > cercariae.
 Cercariae will invade the crustacean and encyst into
metacercariae.
 Humans ingest inadequately cooked or pickled crustaceans
containing metacercariae > excyst in duodenum
 Adults in cystic cavities in the lungs may lay eggs, which are
excreted in sputum. Alternatively, eggs are swallowed and passed
with stool.
IX. PARAGONIMUS WESTERMANI
Common name Oriental lung fluke, Pulmonary

distomiasis
Final host Man
1st IH Brotia asperata (Antemelania asperata)
(snail)
2nd IH Sundathelphusa philippina,
Parathelpusa mistia and P. grapsoides
(crab)
Habitat Lungs
Infective stage Metacercaria
Pathology Paragonimiasis
Laboratory Diagnosis Sputum exam, Serologic Test, X-ray
exam, Stool exam
Drug of Choice Praziquantel
*Paragonimus siamensis - identified only in cats
A. Morphology
C. Pathology
 Granulomatous formation in the lungs

 fibrotic encapsulation, dry cough, chest pains, dyspnea,
hemoptysis
 Erratic paragonimiasis
 worm migration in the abdominal wall, lymph nodes,
omentum, pericardium, myocardium, intestinal wall and the
brain > Cerebral paragonimiasis: conglomerated, multiple,
ring-enhancing lesions ("grape-cluster" appearance) with
surrounding edema

D. Diagnosis
 Radiography (X-ray)
 Sputum examination- definitive diagnosis (treat the sputum
prior to examination with 3% NaOH because it is mucoid and sticky)
 Intradermal test — used as screening test
 Serologic Test (Complement fixation, Immunoblotting and ELISA)
 Proper food preparation and handling

X. SCHISTOSOMA SPP.
 Blood flukes  during copulation, the female is trapped inside the male parasite
 Dioecious
 Presence of gynecorphoral canal or groove — holds the male penis
during copulation
 In perpetual copulation (occurring repeatedly)
 Ova is non-operculated (we can diagnose it using the unique
spines that are being observed in the ova)
 Infective stage: cercaria (last larval stage)
Species:
 Schistosoma japonicum
 Schistosoma mansoni
 Schistosoma haematobium
 Schistosoma mekongi
 Schistosoma intercalatum
 Check the spines to differentiate the ova

 S. japonicum has a small lateral spine
 S. mansoni has a prominent lateral spine
 S. haematobium has a large terminal spine
A. Morphology
B. Life Cycle
 The free-swimming cercariae will penetrate the skin.

 Cercariae will lose their tails during penetration and become
schistosomulae > they will go in the blood circulation (that’s why
they are called as blood flukes)
 Migration to portal blood in the liver and maturation into adults.
 The paired adult worms will migrate into mesenteric venules of
bowel/rectum; eggs shed in stool or venous plexus of bladder;
eggs shed in urine.
 Eggs will shed from the infected human > it will hatch and release
the miracidia
 Miracidia will penetrate the snail tissue, developing into sporocyst
and cercariae.
 cercaria has forked tail

 Chemotherapy
 Health Education
 Control of Oncomelania snails
 Chemical control
C. Pathology
 Early Schistosomiasis
 Itching, chills and fever
 Colonic Schistosomiasis
 Deposition of eggs in the colon (dysentery or diarrhea)
 Hepatosplenic Schistosomiasis
 Most serious consequence
 Characterized by hepatosplenomegaly and ascites
 Pulmonary Schistosomiasis
 Larval migration to the lungs
 Cerebral Schistosomiasis
 Meningoencephalitis, headache, confusion, lethargy and
coma
Schistosomal Cercarial Dermatitis
 Swimmer's itch
 Gulf Coast itch
 Clam digger's itch
 Cercarial itch
D. Diagnosis
 Stool exam (we can incorporate kato-katz to know the intensity of

infection)
 Immunodiagnosis
 Intradermal test
 IHA
 Circumoval Precipitin Test (COPT)
 Method of choice for definitive diagnosis, (+) bleb or References:
septate precipitates attached to one or more points on
the egg surface after incubation of schistosome eggs in  Belizario, V. and De Leon, W. (2015). Philippine
patient serum Textbook of Medical Parasitology. Third Edition.
 ELISA University of the Philippines Manila. Ermita, Manila.
 Faust-Meleney Egg Hatching Technique
 Zeibig, Elizabeth A. (2013). Clinical parasitology: a
practical approach. (2nd ed.) Singapore: Elsevier.
OLFU VALENZUELA

OLFU
Cestodes (Tapeworms/Flatworms)
2021 – 2022
Date: January 7, 2022 TRANS 12 PARA311
LEC
OUTLINE

I. Cestodes
II. Diphyllobothrium latum
III. Taenia solium and taenia saginata
IV. Taenia saginata asiatica
V. Dipylidium caninum
VI. Echinococcus granulosus
VII. Echinococcus multilocularis
VIII. Hymenolepis diminuta and Hymenolepid nana
IX. Raillientina garrisoni
I. CESTODES
 Multi segmented whose sizes vary from few millimeters to several

meters. They are tape-like and flatworm.
 The adults are normally found in the small intestine of humans
 2 orders of cestodes that are medically important:
 Apolysis – the gravid segments are detached from the main body
of the worm and the eggs are eventually released. Evident in
Cyclophyllidea (since they don’t have uterine pore).
 Oncospheres- “hook ball” (spherical in shape with hooklets
inside). The oncospheres of human tapeworm typically have 3
pairs of hooklets (that’s why it is called hexacanth).
II. DIPHYLLOBOTHRIUM LATUM
Common name Broad fish tapeworm

Final host Man
A. General Characteristics
Intermediate host 1st IH: Cyclops (copepods)
2nd IH: Fish
 Ribbon like or tape-like, segmented Infective stage Plerocercoid larva (sparganum)
 Hermaphroditic (both sexes present in one body) Pathology Larva: Sparganosis
 Require intermediate host(s) Adult: Bothriocephalus anemia (B12
 Ingestion is the mode of transmission deficiency) - similar to Megaloblastic
 Usual habitat is the small intestine anemia
 They are oviparous Lab diagnosis Stool exam
Treatment Praziquantel
B. Important structures
 Criterion for the cure: recovery of scolex after the treatment. If not
 Scolex: hold-fast organ, organ for attachment (head) recovered, a repeat stool examination is done after 3 months to
 Neck: region of growth be certain that the patient is no longer infected.
 Proglottids or Segments
 Immature A. Morphology
 Mature - trunk (strobila)
 Mature segments
*Rostellum
 If the segments or uterus is filled with eggs, it is called gravid

segments.
 Some of the cestodes contain the rostellum, it is a knob-like
protrusion at the extreme anterior end of a tapeworm, as an
extension of the tegument. It is globular, spiny structure
when it protrudes, and a circular hollow pit when retracted. It
is structurally composed of a number of concentric rows of
hooks.
 The rostellum may be armed (the globular protrusion
contains hooks) or unarmed (no hooks).
 Ivory colored when passed out in the feces

[PARA311] 3.03 Cestodes (Tapeworms/Flatworms) I Prof. Sherlyn Joy P. Isip, RMT, MSMT
 Very long, considered as largest tape-worm inhabiting the small E. Prevention and Control
intestine of the humans (up to 10 meters or more)
 Head – 2 sucking grooves or bothria  Proper food preparation and handling
 Centrally located rosette-shaped uterine structure with uterine
pore (where ova is being released)
 Freezing of fresh water fishes for 24 to 48 hours under -180C
III. TAENIA SOLIUM AND TAENIA SAGINATA
Parameter T. solium T. saginata

Common name Pork tapeworm Beef tapeworm
Final host Man Man
Intermediate host Pig Cattle
Infective stage Cysticercus Cysticercus bovis
cellulosae
Pathology Taeniasis (adult) Taeniasis (adult)
Cysticercosis (larva)
Lab diagnosis Stool exam, recovery of the ova
Treatment Praziquantel, Niclosamide
 When the oncospheres hatches in the duodenum, they are

 Ova – not infective to humans. But it is being passed in the feces. spreading to different organs through the blood stream, this result
Ova is similar with P. westermani (one way to differentiate them is in human cysticercosis. One of the most serious manifestation is
based on the specimen you will use. P. westermani - sputum or in the neurocysticercosis (most serious zoonotic disease worldwide).
bronchial washing, D. latum – stool)  Not necessary to recover the scolex unless spp. specific
diagnosis is needed. (Recovery of scolex or segments for spp.
B. Life Cycle specific diagnosis)
 Report as presence of Taenia eggs.
 The eggs embryonate in the water.  Criteria for the cure: recover scolex or (-) stool exam after 3 mos
 After hatching, there are three stages of larva developmet. after the treatment
(coracidia > procercoid > plerocercoid)
A. Morphology
C. Pathology
 Infections are usually limited to one worm. (one worm may release
up to 1 million eggs)
 Some may experience nervous disturbances, digestive disorders,
abdominal discomfort, weight loss, weakness and anemia
 D. latum infection results in hyperchromic, megaloblastic
anemia. May be mistaken for Pernicious anemia.
D. Diagnosis
 Stool exam – presence of the egg or proglottid

 Kato thick
 Examination of gastric juice (PA is associated with achlorhydria-
no HCl in gastric juice)

 Ova of T. solium is infective to humans alongside with
cysticercus
B. Life Cycle
 Humans acquire the parasite by ingesting a raw or undercooked

infected meat.
 The adults reside in small intestine.
 Ova of T. saginata is NOT infective to humans.
C. Pathology
 Mild irritation (epigastric pain, hunger pangs, weakness, loss

of appetite, pruritus ani)
 Intestinal obstruction due to tangled proglottid
*pruritus ani - scotch-tape method can isolate the Taenia spp.

*the site of actively motile proglottids in the perianal area and in
the undergarments may result in anxiety or distress.
*perianal swabs may also be useful because the eggs are left in
the perianal skin as the gravid segments squeeze out into the
opening. (associated to apolysis)
D. Diagnosis
 Stool exam, Kato-Katz, Kato-thick

 FECT
 Perianal swabs
 Cysticercosis: Computed axial tomography (CAT) scans and
nuclear magnetic resonance imaging (MRI), CSF ELISA and
Western blot
 Case Finding

B. Life Cycle
IV. TAENIA SAGINATA ASIATICA
 Definitive host is infected by ingesting the fleas containing
Parameter T. asiatica cysticercoids.
Common name Asian Taenia
Intermediate host Pig (mostly), cattle, goat
Infective stage Cysticercus larva located primarily
in liver of the pig (not muscle).
Morphology Similar to T. saginata only that it has
a sunken rostellum with 2 rows of
hooklets
Pathology Abdominal pain, nausea, weakness
and weight loss
Lab diagnosis Stool exam *multiple adults maybe
present
Treatment Praziquantel
V. DIPYLIDIUM CANINUM
Common name Dog or cat tapeworm, double pored

tapeworm, pumpkin seed tapeworm
Final host Dog
Intermediate host Ctenocephalides canis,
Ctenocephalides felis (fleas)
C. Pathology
 Infection is rarely multiple and symptoms are minimal.

 Slight intestinal discomfort, epigastric pain, diarrhea and some
allergic reactions
Infective stage Cysticercoid larva
Pathology Dipylidiasis D. Diagnosis
Lab diagnosis Stool exam
Treatment Praziquantel  Stool exam
 Common tape worm of dogs and cats  Recovery of the proglottids
 MOT: INGESTION of fleas
A. Morphology
 Periodic deworming of pet cats and dogs
 Insecticide dusting of dogs and cats against fleas
VI. ECHINOCOCCUS GRANULOSUS
Common name Dog tapeworm, Hydatid tapeworm

Final host Dog
Intermediate host Herbivores (sheep, ox)
Accidental Host Man (serves also as dead-end host)
Infective stage Embryonated egg, hydatid cyst
Habitat tissues or lymphatics "extraintestinal
cestode"
Pathology Hydatid disease, Cysticercosis
involving soft tissue organs (may have
liver and lung involvement)
Lab diagnosis Biopsy, X-ray, MRI
Treatment Praziquantel, Surgical removal of the
cyst

A. Morphology B. Life Cycle
VIII. HYMENOLEPIS DIMINUTA AND HYMENOLEPID NANA
B. Life Cycle
A. Morphology
VII. ECHINOCOCCUS MULTILOCULARIS
Epidemiology Cause of hydatid cyst in the Subarctic as

well as central Europe and Indi
Final Host Foxes
Intermediate Host Rodents (mice and voles)
Pathology  Disease manifestation similar to E.
granulosus
 Oncospheres are released in the
intestine and cysts develop within in the
liver. Metastasis or dissemination to
other organs (e.g., lungs, brain, heart,
bone).

A. Morphology
B. Life Cycle
B. Life Cycle
 The eggs may be ingested by the insects or by the humans from

contaminated food, water or hands.
 If the eggs are ingested by the insects, it will develop into
cysticercoid. Humans and rodents are infected when they ingest
the cysticercoid-infected arthropods.
 Autoinfection can occur.
C. Pathology
 Patients are usually asymptomatic. Children are brought for

medical consultation when proglottids are passed out with their
feces
D. Diagnosis
 Stool exam (recovery of the proglottids or ova in stool)

IX. RAILLIENTINA GARRISONI
Common name Madagascar worm
Final Host Rat  Elimination of rodents from households
Intermediate Host Tribolium confusum (Flour beetle)  Proper storage of grain products
Infective stage cysticercoid larva  Sanitary waste disposal can help preventive infection
Morphology Armed rostellum with 2 alternating
circular rows of 90-140 "hammer
shaped hooks"
Ova Egg pockets with 1-4 "spindle-shaped"
ova
Gravid segment "rice grain appearance"
With 200-400 egg capsule where each
capsule has 1 to 4 spindle shaped eggs
References:

practical approach. (2nd ed.) Singapore: Elsevier.
OLFU VALENZUELA

OLFU Atrial and Reproductive Flagellates
2021 – 2022
CLINICAL PARASITOLOGY LAB 5
RMT 2023
1st Semester
Instructor: Prof. Sherlyn Joy P. Isip, RMT, MSMT
LAB
Outline b. Trichrome stain permanent staining

At the end of the session, the student must be able to learn:  Trophozoites appear as pear-shaped organisms, measuring 12 to
I. Diagnosis of Giardia lamblia 15 um (range: 10 to 20 um).
A. Basic Guidelines  Trophozoites contain two anteriorly placed nuclei and 8 flagella
B. Stool Examination (rarely seen because they stain poorly).
C. Antigen detection  Cysts appear ovoid to ellipsoid in shape.
 Nuclei and intracytoplasmic fibrils are visible.
D. Molecular method
II. Diagnosis of Trichomonas vaginalis
symmetrically bilateral trophozoite
III. Diagnosis of Dientamoeba fragilis
IV. Diagnosis of Chilomastix mesnili
V. Non-pathogenic Atrial Flagellates
I. DIAGNOSIS OF GIARDIA LAMBLIA
A. Basic Guidelines
 Multiple stool samples (at least 3) should be tested before a

negative result is reported.
 To maximize recovery of cysts, stool samples in formalin, or other
fixatives, should be concentrated prior to microscopic examination
 In microscopic examination, it is okay to concentrate the sample.
 (e.g., 10 min at 500 g when using the formalin-ethyl acetate
Immunological based reactions:
concentration procedure). Exception: Specimens to be used for c. Direct fluorescent antibody (DFA) assay
EIA or rapid cartridge assays should NOT be concentrated
because antigens are lost during the procedure.  Detects antigen. The reagent is antibody conjugated with
fluorescent tag.
 The antibody with fluorescent tag is added directly to unknown
Formalin ethyl acetete concentration antigen fixed in microscope slides.
technique  Antigens are typically visualized as bright apple green or orange
Compatible only in microscopic exam yellow objects against a dark background.
-Exception:
Enzyme immunoassay  This technique offers the highest combination of sensitivity and
rapid cartridge assay specificity and it is considered as the gold standard by many
test kits laboratories.
-must not be concentrated  For commercial DFA kits, it is recommended that a concentrated
stool specimen be used to increase the probability of detection
of low numbers of cysts.
 However, special equipment (fluorescence microscope) and
. commercially available test kits are required, and it does not
provide a permanently stained slide that can be archived.
appearance of cyst
with flourescent
microscopy
d. Enzyme immunoassay (EIA)
a. Direct Fecal Smear/Wet mount  The EIA does not rely on microscopy and is useful for
screening large numbers of specimens. Borderline positives and
 In bright-field microscopy, cysts appear ovoid to ellipsoid in shape questionable negatives obtained with this technique should be
and usually measure 11 to 14 um (range: 8 to 19 um). further confirmed by DFA.
 Immature (2 nuclei) and mature cysts (4 nuclei).  Antigens of Giardia are detected in the feces using this method;
 Intracytoplasmic fibrils are visible in cysts therefore, specimens should not be concentrated prior to
testing. However, special equipment (microplate reader) and
commercially available test kits are required. microtiter plate reader
 The substrate (contains chromophore) and enzyme bonding will
produce a color reaction.read within 5 mins
1. microtiter plate contains capture antibodies which is
used to detect antigen by binding to ab.
2. AntiGiargia antibody that will also bind to capture antigen (sandwich)
3. secondary antibody conjugated to an enzyme (substrate)
observing color formation
unstained cyst: use NSS
stained cyst:iodine ; stained trophozoite with iodine Gurrea, A.N - Transcriber
[PARA311] 2.02 I Atrial and Reproductive Flagellates I Prof. Sherlyn Joy P. Isip, RMT, MSMT
cyst wall protein I uninucleated

-particular antigen detected in stool sample no cyst
a. Microscopic examination
 Microscopic examination of wet mounts may establish the

diagnosis by detecting actively motile organisms.
 This is the most practical and rapid method of diagnosis (allowing
immediate treatment), but it is relatively insensitive.
jerky-tumbling motility
e. Rapid immunochromatographic cartridge assays twitching motility
 The rapid cartridge assays may be used with preserved

specimens and are quick and easy to perform. Antigens of
Giardia are detected in the feces using this method; therefore,
specimens should not be concentrated prior to testing.
 Borderline positives and questionable negatives obtained with this
technique should be further confirmed by DFA. No special
equipment is needed.
 Cyst wall protein 1- antigen of G. lamblia being detected in stool.
b. Direct immunofluorescent antibody staining
 More sensitive than wet mounts, but technically more complex.

 The DFA can be performed in a clinic within 30 min if a wet mount
is negative. The DFA is a useful alternative to the more time-
delayed culture method.
enterotest
(string test)
-any adherent fluid on the capsule
will be subjected to microscopic
analysis
B. Stool Examination
 Macroscopic examination fecal specimens: offensive odor, are

pale colored and fatty, and float in water (steatorrhea).
 Microscopic examination: cysts and trophozoites can be found in
diarrheal stools by saline and iodine wet preparations.
parasitic morphology c. Culture
C. Antigen Detection
 Gold standard
 Enzyme linked immunosorbent assay (ELISA) and indirect  Culture of the parasite is the most sensitive method, but results
immunofluorescent (IIF) tests using monoclonal antibodies have are not available for 3 to 7 days.
been developed for detection of Giardia antigens in feces.
D. Molecular Method
 DNA probes and polymerase chain reaction (PCR) have been

used to demonstrate parasitic genome in the stool specimen.
II. DIAGNOSIS OF TRICHOMONAS VAGINALIS
 In women, examination should be performed on vaginal and

urethral secretions. In men, anterior urethral or prostatic
secretions should be examined
 T. vaginalis in Modified Diamond culture (x40). Before

inoculation, the culture tubes were removed from -200 C and
incubated at 37 o c for 1 to 2 hours to bring prepared medium at
room temperature.
Gurrea, A.N - Transcriber
 Directly, the swab was inserted into the culture tubes containing IV. DIAGNOSIS OF CHILOMASTIX MESNILI
the modified Diamond's medium. The tubes containing the
inoculated medium were incubated vertically at 37 o c in 5% C02  Chilomastix mesnili is identified through the detection of cysts
 The culture was examined daily using binocular or inverted and/or trophozoites in stool specimens
microscope for the presence of T. vaginalis trophozoites.  Both concentrated wet mounts and permanent stained smears
Aseptically, drop of the deposit was removed using a sterile (e.g., trichrome).
pipette and placed on a slide and covered with a glass cover slip
for wet mount examination.
TYM: trypticase, yeast extact, maltose

d. lnPouchTM TV
 A highly specific and sensitive device allowing for simultaneous

growth and observation of Trichomonas vaginalis. It is selective nipple-like protruberance, clear hyaline knob
for the transport and growth of T. vaginalis and increases
specificity by inhibiting the growth of yeasts, mold, bacteria, and V. NON-PATHOGENIC ATRIAL FLAGELLATES
other commensal micro flora.
 No slide preparation is required to view T vaginalis in the  The flagellates Enteromonas hominis, Retortamonas intestinalis,
lnPouchTM . and Trichomonas hominis are considered non-pathogenic.
Presence in stool sample indicates exposure to fecal
contamination.
 These are less frequently encountered than Chilomastix mesnili,
another non-pathogenic flagellate. The presence of cysts and/or
trophozoites in stool indicates exposure to fecal contamination.
stool sample scrapings on mouth
III. DIAGNOSIS OF DIENTAMOEBA FRAGILIS
 Infection typically is diagnosed by detection of D. fragilis

trophozoites in fecal smears stained with trichrome or another
permanent stain. (usually, permanent staining is used in
diagnosing D. fragilis)
 The trophozoite stage of the parasite is not usually detectable if
stool concentration methods are used.
 Dientamoeba fragilis trophozoites can easily be overlooked or
misidentified because they are pale staining and their nuclei
sometimes resemble those of Endolimax nana or Entamoeba
hartmanni.
 The key point for identification of D. fragilis is the shape of nuclei.
(rosette shape chromatin granules)

References:

practical approach. (2nd ed.). Singapore : Elsevier
 Dr. Jose Jurel M. Nuevo. Diagnostic Parasitology
Laboratory Manual. Our Lady of Fatima University.
Valenzuela City.
 https://www.cdc.gov/dpdx
 Lecture Sidenotes of Prof. Sherlyn Joy Isip, RMT, MSMT-
OLFU VALENZUELA

OLFU Blood and Tissue Flagellates
2021 – 2022
RMT 2023
1st Semester
LAB
Outline  For other samples such as spinal fluid, concentration techniques

include centrifugation followed by examination of the sediment.
I. Diagnosis of Trypanosoma cruzi
II. Diagnosis Of Trypanosoma brucei gambiense and
Trypanosoma brucei rhodesiense
III. Laboratory diagnosis of trypanosomiasis
A. Microspcopy
B. Culture
C. Antibody detection
D. Antigen detection
IV. Diagnosis of Leishmania spp.
A. Microscopy
B. Isoenzyme analysis
C. Serology
D. Molecular Diagnosis III. LABORATORY DIAGNOSIS OF TRYPANOSOMIASIS
E. Montenegro’s Intradermal Test
V. Laboratory diagnosis of Kala-azar
A. Napier's aldehyde test
B. Chopra's antimony test
I. DIAGNOSIS OF TRYPANOSOMA CRUZI

Chaga's disease
 In the acute stage of American trypanosomiasis, diagnosis may be a. Microscopy
made by the finding of trypomastigotes in circulating blood or
cerebral spinal fluid (CSF). diagnostic stage  Wet mount preparation of lymph node aspirates, wet mount and
 During the chronic stage, trypomastigotes are usually not found stained smear of the CSF, Giemsa stained thick peripheral blood
circulating in blood and serologic testing is recommended. smears reveals the presence of the trypomastigotes.
 Amastigotes (intracellular) may be found in biopsy specimens
stained with hematoxylin-and-eosin (H&E) or Giemsa
b. Culture
cardiac muscle primarily affected
 The organisms are difficult to grow; hence, culture is not routinely

used for primary isolation of the parasite.
c. Antibody detection
 Almost all patients with African trypanosomiasis have very high

levels of total serum lgM antibodies and later, CSF lgM antibodies.
d. Antigen detection
 Antigens from serum and CSF can be detected by ELISA.
IV. DIAGNOSIS OF LEISHMANIA SPP.
a. Microscopy
 In the human host, only the amastigotes stage is seen upon

microscopic examination of tissue specimens. Amastigotes can be
visualized with both Giemsa and hematoxylin and eosin (H&E)
II. DIAGNOSIS OF TRYPANOSOMA BRUCEI GAMBIENSE AND stains. The amastigotes of Leishmania spp. are morphologically
TRYPANOSOMA BRUCEI RHODESIENSE indistinguishable from those of Trypanosoma cruzi. Amastigotes
are ovoid and measure 1-5 micrometers long by 1-2 micrometers
 The diagnosis rests upon demonstrating trypanosomes by wide. They possess both a nucleus and kinetoplast.
microscopic examination of chancre fluid, lymph node aspirates,
blood, bone marrow, or, in the late stages of infection,
cerebrospinal fluid.
 A wet preparation should be examined for the motile
trypanosomes, and in addition a blood smear (thin or thick) should
be fixed, stained with Giemsa (or Field), and examined.
 Concentration techniques can be used prior to microscopic
examination. For blood samples, these include centrifugation
followed by examination of the buffy coat; mini anion-
exchange/centrifugation; and the Quantitative Buffy Coat (QBC)
technique (uses capillete, to concentrate blood sample).
amastigote- seen in tissue
biopsy specimen
[PARA311] 2.03 I Blood and Tissue Flagellates I Prof. Sherlyn Joy P. Isip, RMT, MSMT
b. Isoenzyme analysis
 Isolation can be done using the biphasic medium which includes a

solid phase composed of blood agar base (e.g., NNN medium),
with defribinated rabbit blood. After isolation, parasites can be
characterized to the complex and sometimes to the species level
using isoenzyme analysis, which is the conventional diagnostic
approach for Leishmania species identification. Diagnostic
identification of Leishmania using this approach may take several
weeks.
 NNN Medium was developed by Novy, McNeal and modified by
Nicolle . NNN medium consists of two phases, blood agar base and
Lockes solution. This medium consists of a blood agar and an
overlay medium. The blood agar base is a highly nutritious medium
that supports the growth of fastidious organisms like Leishmania
and Trypanosoma. The specimens are inoculated into the liquid
phase of the biphasic medium and incubated. The amastigotes
e. Montenegro’s Intradermal Test
transform to promastigotes.
 Check for the growth of organism or possible fungal
contamination after 4 days.  MST, also known as leishmanin skin test, evaluates the late cellular
hypersensitivity response. The test consists of an intradermal
injection of a solution containing an antigenic preparation of
promastigotes. It tends to show positive results within 3 months of
infection, not having however frequent positivity in acute infections
and in anergic forms as disseminated cutaneous leishmaniasis.
 A result is considered positive with the appearance of a hardened
papule, equal or greater than 5mm after 48 hours of application on
the anterior forearm. It is a test of high sensitivity, low cost and
minimally invasive.
c. Serology
 Antibody detection can prove useful in visceral leishmaniasis but is

limited value in cutaneous disease, since most patients do not
develop a significant antibody response. In addition, cross
reactivity can occur with Trypanosoma cruzi, a fact to consider
when investigating Leishmania antibody response in patients who
have been in Central or South America.
 Using Western blot for diagnosis of leishmaniasis adds greater
sensitivity to the process, sometimes reaching close to 100%.
However, it is a more costly exam that requires greater technical
laboratory infrastructure, thus hindering its implementation as
routine.
V. LABORATORY DIAGNOSIS OF KALA-AZAR
d. Molecular Diagnosis
 Molecular approaches have the potential to be more sensitive and a. Napier's aldehyde test
rapid; e.g., the results can be available within days versus weeks.
CDC has incorporated molecular methods in the algorithm for the  1 ml- of clear serum from the patient is taken in a small test tube, a
laboratory diagnosis of leishmaniasis. The method is based on drop of formalin (40% formaldehyde) is added, shaken, and kept in
PCR amplification using generic primers that amplify a segment of a rack at room temperature.
the rRNA internal transcribed spacer 2 (ITS2) from multiple  A positive reaction is jellification and opacification of the test
Leishmania species. serum, resembling the coagulated white of egg appearing within 3-
 DNA sequencing analysis is performed on the amplified fragment 30 minutes.
for species identification.  Aldehyde test is always negative in cutaneous leishmaniasis.
 The test merely indicates a greatly increase serum gamma globulin
(IgM). not specific
 indirect evidence and supporting test

[PARA311] 2.03 I Blood and Tissue Flagellates I Prof. Sherlyn Joy P. Isip, RMT, MSMT
b. Chopra's antimony test
 It is done by taking 0.2 rnL of serum diluted 1:10 with distilled water
in a Dreyer's tube and overlaying with few drops of 4% solution of
urea stibamine.
 Formation of flocculant precipitate indicates positive test.
 Both Napier's aldehyde test and Chopra's antimony test are
nonspecific serum test (may have false positive reaction with
several diseases with hypergammaglobulinemia such as, multiple
myeloma, liver cirrhosis, tuberculosis, leprosy, schistosomiasis and
African trypanosimiasis).
 indirect evidence and supporting test
References:

Valenzuela City.
 Lecture Sidenotes of Prof. Sherlyn Joy Isip. Our Lady of
 Complementary Exams in the Diagnosis of American
Tegumentary Leishmaniasis.
https://www.researchgate.net/publication/265344897

OLFU Ciliate (Balantidium coli)
2021 – 2022
RMT 2023
1st Semester
LAB
Outline
Table 1.0: Balantidium coli Trophozoite and Cyst
At the end of the session, the student must be able to learn: Parameter Trophozoite Cyst
I. Ciliate 28 to 152 um in length
A. Diagnosis of Balantidium coli Size 43 to 66 um
40 um in width
subspherical to
Shape ovoid to sac-shaped
oval
Motility rotary, boring motility -
I. CILIATE micronucleus
Nucleus micronucleus and macronucleus and
A. Diagnosis of Balantidium coli macronucleus
largest protozoa; boring motility Cytoplasm
contain food vacuoles, as well as
-
 Diagnosis is based on detection of trophozoites in stool ingested microbes
samples from symptomatic patients or in tissue collected during two contractile
endoscopy. vacuoles, cyst
 When the stool examination is negative, biopsy specimen or Other two contractile vacuoles, wall,
the scrapings from intestinal ulcer may be examined for the features cytostome, cilia for locomotion mature cysts
presence of trophozoites or cyst. tend to lose
 Cysts are less frequently encountered and are most likely to be their cilia
recovered from formed stool
 Balantidium coli is passed intermittently and once outside the colon
is rapidly destroyed. Thus, stool specimens should be collected Table 1.1: Characteristics of Balantidium coli Visible in Different Types of
repeatedly, and immediately examined or preserved to enhance Fecal Preparations
detection of the parasite; concentration via sedimentation or
flotation can increase the probability of recovery.
 Lugol's iodine is sometimes used for staining but may obscure
internal morphological features
 Can also be cultured in in vitro, Locke’s egg albumin medium or in
NIH polygenic medium like E. histolytica
 Permanent stain- trichrome stain iodine may obscure internal morphologic

feature
References:

Valenzuela City.

OLFU Coccidia
2021 – 2022
RMT 2023
1st Semester
LAB
Outline

I. Diagnosis of Cystoisospora belli
II. Diagnosis Of Cyclospora, Cryptosporidium, and
Cystoisopora belli
III. Diagnosis of Sarcocystis hominis and Sarcocystis
suihominis
IV. Diagnosis of Toxoplasma gondii
acid fast staining

I. DIAGNOSIS OF CYSTOISOSPORA BELLI
A. Basic Guidelines
 Multiple stool samples (at least 3) should be tested before a Safranin stain
negative result is reported.
 To maximize recovery of oocysts, stool samples in formalin, or  Oocysts stain uniformly, red to reddish-orange.
other fixatives, should be concentrated prior to microscopic  The oocysts (25 to 30 um) will have the typical ellipsoidal shape
examination (e.g., 10 min at 500 x g when using the formalin-ethyl as in the wet mount; their internal structure may not be seen.
acetate concentration procedure). Some oocysts may appear collapsed or distorted to one side. This
technique requires heating, therefore additional equipment is
Wet mount necessary (e.g., microwave oven).
 Under bright-field microscopy, the oocysts are large (25 to 30

by 10 to 19 um) and have a typical ellipsoidal shape.
Sporulated oocysts containing two sporocyts can be observed if
the stool specimen is kept in potassium dichromate at room
temperature for more than two days.
 Under UV fluorescence microscopy, the oocyst wall auto
fluoresces. An intense blue fluorescence is obtained with the
preferred UV excitation filter set (330 to 365 nm). If this filter set
is not available, a less intense green fluorescence can be
obtained with blue excitation (450 to 490 nm). Other objects,
however, can also auto fluoresce. A fluorescence microscope is
required, and this procedure does not provide a stained slide that
can be archived. II. DIAGNOSIS OF CYCLOSPORA, CRYPTOSPORIDIUM, AND
 Both differential interference contrast (DIC) and UV CYSTOISOPORA BELLI
fluorescence microscopy are efficient and reliable approaches
for identification of this coccidian. Objects found by UV
microscopy should always be checked under DIC and vice versa.
Modified acid-fast stain
 A blue-green background, or contrasting counterstain, of fecal

debris allows the oocysts to stand out.
 They are variably stained: some will stain light pink to deep
purple, while others may be unstained. The oocysts (25 to 30
um) have the typical ellipsoidal shape as shown in the wet
mount; their internal structure will not be seen.
 Some oocysts may appear collapsed or distorted on one side.
This staining method is the easiest and most practical and
provides a permanent record.
 Almost the same in diagnosis. (Modified Acid fast stain or Safranin

staining)
 Bright field microscopy, DIC, UV fluorescence
 Report as presence or absence with coccidian

[PARA311] 2.05 I Coccidia I Prof. Sherlyn Joy P. Isip, RMT, MSMT
Flotation techniques
 Most frequently used: zinc sulfate or Sheather's sugar

 Use solutions, which have higher specific gravity than the
organisms to be floated so that the organisms rise to the top and
the debris sinks to the bottom.
 Since specific gravity of most parasite eggs is 1.05 to 1.23, you
must use a flotation solution with a specific gravity of at least 1.24.
 The main advantage of this technique is to produce a cleaner
material than the sedimentation technique.
 The disadvantages of most flotation techniques are that the walls
of eggs and cysts will often collapse, thus hindering identification.
Also, some parasite eggs do not float.
Antibody Detection of Toxoplasma gondii
Sheather’s Sugar Floatation
 The detection of Toxoplasma-specific antibodies is the primary
 Employs use of boiled sugar solution preserved with phenol. diagnostic method to determine infection with Toxoplasma.
 Sheather's sugar solution has a specific gravity of 1.27, which is  Toxoplasma antibody detection tests are performed by a large
high enough to float any ova. number of laboratories with commercially available kits.
 It is best for recovery of coccidian oocysts (Cryptosporidium,  The IFA and EIA tests for lgG and lgM antibodies are the tests
Cyclospora and Cystoisospora). most commonly used today. Persons should be initially tested for
 Better visualization can be appreciated through the use of a the presence of Toxoplasma-specific lgG antibodies to determine
phase-contrast microscope. their immune status. A positive lgG titer indicates infection with
the organism at some time.
III. DIAGNOSIS OF SARCOCYSTIS HOMINIS AND  If more precise knowledge of the time of infection is necessary,
SARCOCYSTIS SUIHOMINIS then an lgG positive person should have an lgM test performed by
a procedure with minimal nonspecific reactions, such as lgM-
 For intestinal sarcocystosis caused by S. hominis and S. capture EIA. A major problem with Toxoplasma-specific lgM
suihominis, diagnosis is made by the observation of oocysts or testing is lack of specificity.
sporocysts in stool. They are easily overlooked as they are often
shed in small numbers. Also, the two species cannot be
separated by oocyst or sporocyst morphology.
 When humans serve as dead-end hosts for non-human
Sarcocystis spp., diagnosis is made by the finding of sarcocysts in
tissue specimens.
 May be seen macroscopically
 Hematoxylin or eosin (staining)
*refer to Table 4.0
Sabin-Feldman dye test
 Specific test for T. gondii

 This test is based on the observation that live tachyzoites stain
blue with alkaline methylene blue dye. (Based on presence of
certain antibodies that prevent methylene blue dye from
entering the cytoplasm of organism)
 Live tachyzoites are mixed with different dilutions of the patient's
serum and the mixtures are then incubated for an hour, stained
Table 3.0: Characteristics of Coccidia Visible in Different Types of with dye, and examined with a microscope.
Fecal Preparations  Color formation of tachyzoites (negative)
 Colorless tachyzoites (positive) – there is a presence of
antibodies against Toxoplasma
 If antibodies to T. gondii are present in the patient's serum, they
will damage the organisms. The damaged organisms will not take
up the dye and appear as pale "ghosts" compared to undamaged
organisms.
 The test requires live tachyzoites and is difficult to perform, so
IV. DIAGNOSIS OF TOXOPLASMA GONDII
other serological tests are typically used. However, the test is very
sensitive and specific and remains the reference method.
The diagnosis of toxoplasmosis may be documented by:
 Observation of parasites in patient specimens, such as
bronchoalveolar lavage material from immunocompromised
patients, or lymph node biopsy.
 Isolation of parasites from blood or other body fluids, by
intraperitoneal inoculation into mice or tissue culture. The mice
should be tested for the presence of Toxoplasma organisms in the
peritoneal fluid 6 to 10 days post inoculation; if no organisms are
found, serology can be performed on the animals 4 to 6 weeks post
inoculation.
 Detection of parasite genetic material by PCR, especially in
detecting congenital infections in utero.
 Serologic testing is the routine method of diagnosis.

Principle
 The test is based on specific inhibition by antibody, of the staining

of trophozoites by alkaline methylene blue dye
Technique:
 Equal volumes of diluted patient's serum are incubated with
live trophozoites and normal human serum (accessory
factor) for an hour at 37C.
 Later, a drop of alkaline methylene blue dye is added to each
tube and are examined under microscope.
 If less than 50% of the tachyzoites first take up stain and the
cytoplasm remains colorless, the test is positive.
 The presence of 90-100% tachyzoites, deeply swollen and
stained with blue color, shows the test to be negative. It
denotes the absence of Toxoplasma antibodies.
 The highest dilution of the serum, which inhibits staining up
to 50% is the titer.
 Limitation: The test is reported to give false positive reaction in
Sarcocystis, Trichomonas vaginalis, and Trypanosoma lewisii
infections.

Table 4.0: Toxoplasmosis Laboratory Diagnosis
 Applicable to humans except for infants.

 Equivocal- the result interpretation indicates that the analyte being
detected in the system falls within range of positive and negative. The
analyte of interest is present but in small amount to be considered as
positive. (Cut off values must be reached) A second specimen should
be drawn and submitted for testing if equivocal.
References:

Valenzuela City.

Direct fecal Smear/ Wet Mount
Unstained cyst |Stained cyst with iodine | stained trophozoite with iodine
Trichrome Stain
Trophozoite Cyst Giardia lamblia

Left:
Direct fluorescent antibody
(DFA) assay
Right:
Enzyme Immunoassay (EIA)
GIARDIA ELISA
ColorPAC Giardia
Left:
Microscopic Examination
Right:
Direct immunoflourescent
Antibody staining
In Modified Diamon Culture
Differential Interference contrast microscopy (DIC) micrographs and Scanning electron microscopy
and Transmission electron microscopy of
Trichomonas vaginalis vitro culture, Giemsa | vaginal smear, Giemsa

InPOUCH TV
Dientamoeba fragilis trophozoite
Chilomastix mesnili
Left: trophozoite from stool specimen
Stained by trichrome
Middle: cyst in stool specimen,
Trichrome
Right: Cyst in concentrated wet mount
Of stool, iodine
Chilomastix mesnili
Left: Trichomonas hominis
Right: Trichomonas tenax
Enteromonas hominis
Retortamonas intestinalis
Trypanosoma cruzi
Left: trypomastigote in thin blood smear, Giemsa
Right: amastigote in heart tissue, H&E
Left: Positive IFA

Right: Triatomine bug
Tripanosoma brucei spp
Thin blood smear, Giemsa thin blood smear, Wright-Giemsa Tsetse fly
Leishmania tropica Leishmania spp Promastigote Sandfly

Amastigotes from from culture
Biopsy of skin lesion
NNN medium
Spleen aspiration or bone marrow
Biopsy or lymphnode aspiration
Leishmania + flouresence
Balantidum coli
Up: trophozoites in colon tissue, H&E
Cyst (left area)

Trophozoite (right part)
Balantidum coli
Cyst (upper area)

Trophozoite (lower part)
Balantidum coli trophozoite

Under microscope (Saline)
Cryptoisospora belli
Wet mount DIC UV fluorescence microscopy
Cystoisospora belli oocyst
Modified acid fast staining
Cystoisospora belli oocyst

Safranin stain
Oocysts in stool smears stained with

modified acid-fast stain:
A. Cryptosporidium spp.
B. Cyclospora cayetanensis
C. Cystoisospora belli
Oocysts in stool smears stained with

safranin stain:
D. Cryptosporidium spp.
E. Cyclospora cayetanensis
F. Cystoisospora belli
Sarcocystis spp
Toxoplasma gondii

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OLFU

I. PARASITOLOGY B. Parasites according to the Mode of Living

Gurrea, A.N, Ortiz, M.J - TRANSCRIBER

III. TYPES OF HOST

 Vector is responsible for transmitting the parasite from one host to

 Pathogens A. Biological vector

Gurrea, A.N, Ortiz, M.J - TRANSCRIBER

VIII. PORTAL OF EXIT

Gurrea, A.N, Ortiz, M.J - TRANSCRIBER

 Deprivation of the host’s essential nutrients and substances

Creeping eruption, a skin infection caused by hookworms

Gurrea, A.N, Ortiz, M.J - TRANSCRIBER

XVII. PREVENTION AND CONTROL

XVIII. ERADICATION AND ELIMINATION

Gurrea, A.N, Ortiz, M.J - TRANSCRIBER

OUTLINE B. Classification of Protozoan Parasites

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

 Proto ( first), Zoa (animals) Encystation

GURREA, A.N - TRANSCRIBER

 All Entamoeba are commensal except for Entamoeba histolytica.

II. Entamoeba histolytica

1. Tropozoite: divides through "binary fission", capable of encystation

 mature quadrinucleate cyst passed in feces

 Ingestion of contaminated food and/or water with E. histolytica

GURREA, A.N - TRANSCRIBER

Amoebic dysentery Bacillary dysentery

Onset Gradual Acute

 Common associated disease: Intestinal amebiasis, amebic

GURREA, A.N - TRANSCRIBER

 Microscopic detection of cyst and trophozoite is the standard

 To cure invasive disease at both intestinal and extraintestinal site

H. Prevention and Control

GURREA, A.N - TRANSCRIBER

 Not capable of encystation. Trophozoite form only

 Morphologically similar to E. histolytica, but with different DNA and

 Similar to E. histolytica except much smaller and no RBC inclusions

 Morphologically indistinguishable from those of the disease

GURREA, A.N - TRANSCRIBER

 "iodine-cyst" because of its affinity to iodine Acanthamoeba spp.

Iodamoeba butschlii Acanthamoeba spp. cycst

 Amoebic keratitis (contact lens users)

GURREA, A.N - TRANSCRIBER

 Causative agent of "balantidiasis or balantidial dysentery", similar

GURREA, A.N - TRANSCRIBER

GURREA, A.N - TRANSCRIBER

OUTLINE  Microscopy and direct fecal smear

1. Morphology of the trophozoite

 Rosette shaped nuclei (1 to 2)

 fecal-oral route via transmission of helminth eggs (eg., Enterobius

 Infections are asymptomatic because it does not invade the

 Observation of binucleate trophozoites in multiple fixed and stained

Gurrea, A.N - TRANSCRIBER

 Trophozoite: "Old-man with eyeglasses", "Monkey Face"

 Mature cysts (resistant to routine chlorination)

Gurrea, A.N - TRANSCRIBER

 The onset is between 1-4weeks on an average of 9 days. Half of  Pyriform shape

 Specimen: Stool and Duodenal contents

2. Infective and Diagnostic stage

Gurrea, A.N - TRANSCRIBER

 Male: urine sample, prostatic fluid or seminal fluid  Asymmetrical

 Oral Metronidazole (Tinidazole)

9. Prevention and Control

 Both the male and female must be treated