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CLINICAL PARASITOLOGY

Introduction (WEEK 1 / LEC)


2nd SEM, 2021

Sporozoa Plasmodium spp.


(Plasmodium spp and Babesia spp)  Plasmodium falciparum
 Plasmodium vivax
Classification of Protozoan Parasites  Plasmodium malariae
Phylum Sarcomastigophora  Plasmodium ovale
Subphylum Acathamoeba  Plasmodium knowlesi
Sarcodina Endolimax nana
Babesia spp
Entamoeba coli
Iodamoeba butschlii  Babesia microti

Entamoeba dispar  Belong to the class of parasite that have no


Entamoeba gingivalis obvious structures for the purpose of
Entamoeba histolytica motility, known as “sporozoa”
Naegleria fowleri (sporozoan’s parasite)
Subphylum Chilomastix mesnili
Mastigophora Dientamoeba fragilis Malaria
Giardia lamblia  From Italian word “mal’aria” which means
Trichomonas vaginalis “bad air”
Trichomonas hominis  Considered to be the most important parasitic
Trichomonas tenax disease affecting man (Belizario, 2004)
 Historical development of the theories of
Trichomonas vaginalis casualty
Leishmania braziliensis
 It is one of the three major infectious disease
Leishmania donovani
along with HIV and tuberculosis causing 2.5M
Leishmania tropica
Trypanosoma cruzi deaths each year
Trypanosoma brucei complex Vector: female Anopheles mosquito
(Hemoflagellates)  Primary:
Phylum Balantidium coli –pathogenic
o Anopheles minimus var. Flavirostris
Ciliophora
 Others:
Phylum Babesia spp.
Apicomplexa Cryptosporidium hominis o Anopheles litoralis
Cyclospora cayetanesis o Anopheles maculates
Isospora belli o Anopheles mangyamus
Plasmodium spp. o Anopheles balacensis
Toxoplasma gondii o Anopheles Philippinensis
Phylum Enterocytozon bineusi
Microspora Encephalitozoon spp.  Final Host: / Definitive host- harbors the
Vittaforma cornea parasite on its mature stage
Pleistophora spp. o female Anopheles mosquito
Brachiola vesicularum  Intermediate Host:
Microsporidium spp. o Man
 Infective stages:
o Sporozoites (man)
o Gametocytes (mosquito)
 Microgametocytes (male)
 Macrogametocytes (female)

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CLINICAL PARASITOLOGY
Introduction (WEEK 1 / LEC)
2nd SEM, 2021

 Vector Biology:  The trophozoites in the bloodstream


o Anopheles flavirostris leave the blood vascular system
 Aquatic Habitat: within 30 to 60 minutes and
o slow flowing streams; shaded streams subsequently invade the parenchymal
 they don’t like the direct sunlight and cells of the liver
continuously flowing water  Once the sporozoites are in the liver,
 Adult biting: it will now undergo asexual
o Night biting (indoor and outdoor) multiplication called “Schizogony”
 Adult resting: o Schizogony- happens inside
o inside walls parenchymal cells of our liver
 resulting in the production of tiny
LIFE CYCLE OF PLASMODIUM MALARIA merozoite, rapture of the infective
hepatic cell releases merozoites into
Complex life cycle
the circulation
o if the schizont can’t contain
the number of merozoites, it
will rupture. Releasing the
schizont into the bloodstream
 Once merozoite is release into
bloodstream, the erythrocytic cycle
will start

B. Erythrocytic cycle
 The merozoites after schizont
rupture, will now invade the red
blood cells
 The migrating merozoites targets the
age and size specific RBC to invade
and thereby initiate the phase of
ADDED NOTES: production involvement ( it depends
 intermediate host: man on what kind of plasmodium that
enters the body of intermediate host;
o it have two stages:
if plasmodium ovale or plasmodium
 erythrocytic cycle
vivax, they target young RBC; if
o happens in the red cell
malaria, old or senescence; if
 exo-erythrocytic cycle or pre-
plasmodium falciparum infections,
erythrocytic cycle
young and old RBC)
o happens inside the liver
 After getting into liver, it can either go
to 3 paths:
A. Exo-erythrocytic cycle or pre-erythrocytic
cycle- happens in red cells  Some RBC infected with merozoites
rupture releasing this form target and
 Mosquito bites the host injecting
infect new RBC. this part of life cycle
sporozoites to man
repeat itself
 Once the sporozoites are in the
 infected RBC that contains merozoites
bloodstream it will infect the liver
develop into gametophyte( it can
basically the parenchymal cells of the
either be microgametocyte (male) or
liver
macrogametocyte (female)
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CLINICAL PARASITOLOGY
Introduction (WEEK 1 / LEC)
2nd SEM, 2021

 Once merozoites is released to the


SPOROGONY/GAMETOGONY
liver, it can be destroyed by immune
 Microgamete + Macrogamete to Zygote to
system otherwise with a healthy
Ookinete to Oocyst to Sporozoite
individual ( destroyed by immune
system) ADDED NOTES:
 In all the species, asexual
 Microgametocytes+Macrogametocytes
multiplication takes place within the
 Infective stage: mosquito
liver cells (plasmodium ovale,
o in mosquito, as the blood
plasmodium vivax, plasmodium
temperature falls the maturation of
malaria.
the male microgametes happen
Schizogony producing the microgametes or
A. Pre-erythrocytic or exo-erythrocytic cycle “exflagellation”
o The macrogametocytes it matures
 Sporozoite infect liver parenchymal cells to
and it became macrogametes
Schizont to Liver cells rupture releasing the
 it may be fertilized by the
merozoites to B. Erythrocytic cycle
microgametes and form the
zygote
o After the formation of the zygote, it
becomes elongated and active. now
called the Ookinete
o Ookinete penetrate the cells of the
stomach walls of the mosquito and
rounds up just beneath the outer
covering of the organ to become
oocyst
o Oocyst will ruptured and then
releasing the sporozoites (Infective
stage: man)

B. Erythrocytic Cycle

 Merozoites invade RBC to Ring Form (young


trophozoite) to Mature Trophozoite to
Schizont to Rupture of RBC releasing the
merozoites to Develop into a micro or
macrogamete.

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CLINICAL PARASITOLOGY
Introduction (WEEK 1 / LEC)
2nd SEM, 2021

ADDED NOTES: TO REMEMBER:

 Sporogonic cycle  FALCIPARUM


o sexual multiplication also known as o Most distinct
sporogony o Ferdinand Marcos
 Prepatent Period  VIVAX
o Parasites are visible o Star for all season
o the time between the sporozoites o Vilma Sanros
inoculation in the appearance of the  MALARIA
parasites in the blood o Manila zoo
 Incubation period  OVALE
o Between an infection and onset of the o Orange Juice
disease symptoms. recovery when
treated correctly

Intervals
Species Prepatent Incubation
Period Period
Plasmodium 11-14 days 8-15 days
falciparum (P.
falciparum)
Plasmodium 11-15 days 12-20 days
vivax (P. vivax)
Plasmodium 3-4 weeks 18-40 days
malariae (P.
malariae)
Plasmodium 14-26 days 11-16 days
ovale (P. ovale)

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CLINICAL PARASITOLOGY
Introduction (WEEK 1 / LEC)
2nd SEM, 2021

 high temperature (40-41˚C), headache,


palpitations, epigastric discomfort, thirst,
nausea and vomiting
 patient is confused and delirious
 may last for 2 to 6 hours
3. Sweating stage (Defervescence or Diaphoresis)

 profuse sweating, temperature lowers and


symptoms diminishes
 may last for 2 to 4 hours

Pathology

1. Recrudescence
 renewal of parasitemia or its clinical features
arising from persistent undetectable asexual
Pathology parasitemia in the absence of exo-erythrocytic
CLASSICAL MALARIA PROXYSYMS cycle
1. Cold stage
2. Relapse
 sudden coldness and apprehension
 Renewed asexual parasitemia following a
 mild shivering turns to teeth chattering and
period in which the blood contains no
shaking of the whole body
detectable parasites.
 may last for 15 to 60 minutes
 common to P. vivax and P. ovale infections, as
o The typical patient remains
result from the reactivation of hypnozoite
asymptomatic following the initial
forms of the parasite in the liver
mosquito bite and exo-erythrocytic
 happens with plasmodium vivax and
cycle of the malarial infection.
plasmodium ovale after a period of weeks or
however, once the erythrocytic phase
months reactivation of the hypnozoite Initiate
initiate and large number of rupturing
asexual division ( resting stage of sporozoites)
rbcs simultaneously occur, the
resulting merozoites and species toxic
3. Cerebral Malaria
waste by-products in the blood
 Diffuse symmetric encephalopathy, retinal
system produce the first clinical
hemorrhages, bruxism, mild neck stiffness. If
symptoms which is the paroxysm
left untreated may lead to coma and death.
 due to incomplete or inadequate treatment
o Bruxism-teeth grinding
as a result of drug resistance or improper
choice of medication Periodicity/ Febrile Cycle
 happens with plasmodium vivax and Species Febrile Interval Common
plasmodium ovale after a period of weeks or Cycle (hours) Victims
months reactivation of the hypnozoite Initiate P. Malignant 36-48 All
asexual division ( resting stage of sporozoites) falciparum tertian
P. vivax Benign 48 Young
2. Hot stage/ flush phase: best stage to collect blood tertian
sample P. malariae Quartan 72 Adult
P. ovale Ovale 48 Young
 Due to incomplete or inadequate treatment
tertian
as a result of drug resistance or improper
choice of medication
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CLINICAL PARASITOLOGY
Introduction (WEEK 1 / LEC)
2nd SEM, 2021
DIAGNOSIS 2. Rapid Diagnostic Test (RDT)

• Detects Plasmodium-specific antigens in


finger prick sample

A. Histidine-rich protein II (HRP II)

- Water soluble CHON


produced by
trophozoites and
young gametocytes

- e.g., Paracheck Pf
test, ParaHIT f test

B. Plasmodium LDH
1. Microscopy (Gold Standard) - Produced by both sexual and
 “Thick and Thin Blood Smear” asexual stages and can
 stained with Giemsa or Wright’s stain distinguish between P.
falciparum and non-P.
falciparum
Manner of Reporting - eg. Diamed Optimat IT
A. Qualitative DIAGNOSIS
+ = 1-10 parasite/100 thick field

++ = 11-100 parasite/100 thick field

+++ = 1-10 parasite/thick field

++++ = more than 10/ thick field

B. Quantitative

Malaria parasite/ uL = no. of parasites x 8, 000

200 WBC

Diagnosis

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CLINICAL PARASITOLOGY
Introduction (WEEK 1 / LEC)
2nd SEM, 2021

RESISTANCE TO MALARIA
3. Quantitative Buffy Coat (QBC)
1. Most Africans and American Blacks
• uses a special capillary tube with
o Duffy antigen negative: Fy(a-b-) 
acridine orange
Resistant to P.vivax and P. knowlesi
• (+) bright green and yellow under
2. Those with Sickle Cell Anemia
fluorescent microscope
3. G6PD deficient individuals
4. Serologic Tests (IHA, IFAT, ELISA)

5. Molecular Methods through PCR (low cases and


mixed infection)

TREATMENT

1.Protective (Prophylactic)
2.Curative (Therapeutic)
3.Preventive
 Arthemether-Lumefantrine (Coartem TM) Plasmodium knowlesi
o first line drug for confirmed P.  A primate malarial parasite common in SEA
falciparum cases.  Causes malaria in long tailed macaques
o Not recommended in pregnancy, (Macaca fascicularis)
lactation & infants  May also infect humans
 Quinine (plus Tetracycline or Doxycycline)  The appearance of P. knowlesi is similar to
o second line drug for confirmed P. that of P. malariae.
falciparum cases which AL fail or not  PCR assay and molecular characterization are
available the most reliable methods for detecting and
 Quinine IV drip diagnosing P. knowlesi infection
o drug of choice for complicated or
severe P. falciparum malaria Babesia spp.
o In addition to AL and Q+T,D, (Babesia microti)
Primaquine is given on the 4th day as
single dose to prevent transmission Blood parasites that cause malaria-like infections
Chemoprophylaxis: Mefloquine & Doxycyline  “Babesiosis” – pathology due to B. microti
 Parasites divide through binary fission or
PREVENTION budding
1. Use of mosquito repellant  Cycle in the tick is still uncertain
2. Use of Insecticide treated nets (ITN)
3. Take Prophylactic medication Vector: Ticks (Ixodes scapularis)
CONTROL Infective Stage: sporozoites
1. Environmental cleanliness
o (stream cleaning to speed up water Diagnostic stage:
flow and exposing to sunlight) - “Maltese cross” arrangement of the
1. Indoor residual spraying merozoites and ring-form trophozoite
2. Zooprophylaxis
o use of carabao to deviate mosquitoes
3. Use of biologic control methods
a. Bacillus thuringiensis
 larvicidal
b. Larviparous fishes
 (e.g., Oreochromis niloticus)

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CLINICAL PARASITOLOGY
Introduction (WEEK 1 / LEC)
2nd SEM, 2021

TREATMENT

 Clindamycin – Drug of choice


 Chloroquine – former drug of choice

In the Philippines: human babesiosis is not yet


reported however, it could be present in dogs. (B.
canis)

PREVENTION AND CONTROL


 Avoidance of places where ticks are usually
found
PATHOLOGY  wearing of light-colored pants tucked into
 Associated with excessive pro-inflammatory one’s socks
cytokines such as the tumor necrosis factor  Tick check (especially for children)
(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.

DIAGNOSIS
1. Microscopy of the Giemsa-stained peripheral
blood smear
a. Merozoites in Maltese cross
arrangement
b. Ring form
 most frequent
intraerthrocytic form
2. PCR (gold standard)
3. Immunofluorescent assays

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COCCIDIAN PARASITES Notes:


Coccidian parasites ISOSPORIASIS
- Under class Sporozoea (Phylum Apicomplexa)  NO INT. HOST (pigs and cattles appeared to
be)
In class Sporozoea, the life cycle is characterized by an  DEFINITIVE HOST: MAN (sexual and asexual
alternations of generation repro takes place)
1. Sexual : Sporogony  Ingest OOCYST (excyst)  SPOROZOITES
2. Asexual: Schizogony (small intestines)  asexual repro
(SCHIZOGONY)  MEROZOITES  MACRO/
 Isospora belli MICROGAMETOCYTE (unite) 
 Cryptosporidium hominis  oocyst (excreted in the stool) (consists of a
 Cyclospora cayetanensis sporoblast) divides into TWO SPOROBLASTS
 Toxoplasma gondii (matures)  SPOROCYST (consist of 4 sausage
 Sarcocystis hominis and Sarcocystis suihominis shaped
 sporozoites) (MATURE OOCYST)
Notes:
 COCCIDIAN LIFE CYCLE: 3 Sequential stages ISOSPORA BELLI
 SEXUAL (SPOROGONY) PATHOLOGY
o Producing oocyst • Infection is usually asymptomatic.
 ASEXUAL (SCHIZOGONY/MEROGONY) • Symptomatic: diarrhea, weight loss,
o Producing merozoites eosinophilia, fever, malaise, abdominal pain
 GAMETOGONY and flatulence
o Devt of micro/macro gametocytes • In AIDS patients, reports on dissemination of
 Asexual reproduction occurs outside a human parasite to other organs are present.
host.
 SEXUAL REPLICATION DIAGNOSIS
o INSIDE a human host 1. Direct microscopy
ISOSPORA BELLI 2. Concentration technique (FECT, ZnSO4 and sugar
MORPHOLOGY floatation)
Infective stage: oocyst 3. Staining techniques (Iodine, Kinyoun, Auramine-
MOT: ingestion of oocyst (contains 2 sporocyst with 4 Rhodamine)
sporozoites each) 4. Enterotest and duodenal aspirate
5. Molecular testing
Disease is common to children and male homosexuals
with AIDS  CHARCOT-LEYDEN CRYSTALS

TREATMENT
 Asymptomatic: bland diet and bed rest
 Symptomatic: Trimetroprim Sulfamethoxazole

PREVENTION AND CONTROL


• Good sanitary practices
• Thorough washing and cooking of food
• Provision for safe drinking water

Cryptosporidium hominis
MORPHOLOGY
Infective stage: oocyst

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NOTES:
CRYPTOSPORIDIOSIS
 DIARRHEA  self-limiting (2weeks)
 fluid loss because of diarrhea and vomiting
may be fatal in children
 Gallbladder  LEADING TO ACUTE
GANGRENOUS CHOLECYSTITIS
 SPECIMEN OF CHOICE FOR RECOVERY: STOOL

TREATMENT
• No acceptable treatment yet
• Nitazoxanide – said to be effective in
preliminary studies
• Bovine colostrum, paromycin and
clarithromycin treatment of severe diarrhea

PREVENTION AND CONTROL


• Chlorination is NOT effective
• Use of multiple disinfectant and combined
water treatment
• Proper disposal of human and animal excreta
NOTES:
Cryptoporidosis CYCLOSPORA CAYETANENSIS
 Mature oocyst consist of four small MORPHOLOGY
sporozoites surrounded by a thick cell wall. Infective stage: oocyst
 The oocyst of cryptosporidium do not contain
sporocyst unlike the isospora belli
 Mot: ingestion of mature oocyst
 All stages  completed in the git:
 Oocyst  sporozoites (attach to git) 
Schizogony  prod merozoites 
micro/macro  fertilized and prod zygote 
thin (infect other enterocytes- autoinfection)
and thick cell wall (passed in feces) 
contaminate food and water Disease is usually self-limiting
 Autoinfection: thin-shelled MOT: ingestion

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 land excessive fluid loss
• AIDS patient: severe form of diarrhea,
progressively worse and life-threatening

DIAGNOSIS
1. Sheather’s sugar floatation or FECT
2. Kinyoun’s modified acid-fast stain (oocyst appear as
red-pink doughnut-shaped circular organisms) –
cheapest and simplest method of diagnosis
3. IFA
4. DNA probe

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Notes:
 Symptoms are Similar with cryptosporidium,
but duration of diarrhea with CAYETANENSIS IS
LONGER
 OOCYST sporulate best at ROOM TEMP.
 Addition of 5% POTASSIUM DICHROMATE
allows sporocyst to BECOME VISIBLE.

TREATMENT
• No treatment needed
• If pharmacologic treatment is warranted,
Cotrimoxazole is given

PREVENTION AND CONTROL


• Good sanitary practices
• Access to safe and clean drinking water
• Proper food preparation

TOXOPLASMA GONDII
MORPHOLOGY
Infective stages: tachyzoite,
bradyzoite and the oocyst

Notes:
 Originally called: cyanobacterium-like body
(clb)  but found to be a coccidian parasite
 Sporulated oocyst  w/c contains 2 sporocyst
 w/ 2 sporozoites  sporozoites invade the
epi cells of small intestines  merozoites 
 Micro/macro  fertilize  oocyst (feces) 
complete sporulation within 7-12 days in
warm environment

PATHOLOGY
• Chronic and intermittent watery diarrhea
occurs in early infection
• Fatigue, anorexia, weight loss, nausea,
abdominal pain, flatulence, bloating and
dyspnea may develop.
• Infections are usually self-limiting
• D-Xylose malabsorption has been found to
develop
• No death is associated

DIAGNOSIS
1. DFS
2. Concentration techniques
3. Kinyoun stain
4. Fluorescent microscopy
5. Safranin staining
6. PCR

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 Definitive host: Cats NOTES:


 Complete life cycle occurs in cats  Mimic infect. Mononucleosis: fatigue,
 Clinical manifestation is apparent if immune lymphadenitis, chills, fever, headache and
system is suppressed  AIDS patient myalgia
NOTES:  Congenital toxoplasmosis: fetus is infected via
 Toxoplasmosis, congenital toxoplasmosis, transplacental means sever eye and brain
cerebral toxoplasmosis damage, retinochoroiditis, microcephaly,
 2 morph forms: jaundice, hydrocephaly, epileptic seizures
o Tachyzoites  Death of newborn
o Bradyzoites o due to anemia w/ pneumonia
 Infective stage for humans: oocyst  Still births
 Oocyst is similar with i.belli but smaller o when mother acquire infection during
 Tachyzoites: crescent shape, actively the 1st trimester of pregnancy
multiplying
 Complete life cycle TREATMENT
o occur n cats (definitive host) • Pyrimethamine and sulfadiazine
 Typical coccidian life cycle  Schizogony,
gametogony, sporogony in the intestinal PREVENTION AND CONTROL
epithelium • Good sanitation and hygiene
 The extraintestinal stages • Proper food preparation
o are the asexual stages
 tachyzoites and bradyzoites SARCOCYSTIS HOMINIS
& SARCOCYSTIS SUIHOMINIS
 In intestinal epi of cats merozoites multiply
• S. hominis from pigs
diff into macro/micro fertilizaton oocyst
• S. suihominis from cattle
(feces)
• Definitive host: humans
 Ingestion of oocyst
o Release of sporozoites:
 Cats:
o merozoites
o micro/macro
o oocyst
 Man/ other intermediate host: sporozoites
o invade nucleated cells (macrophage)
transform into  tachyzoites (fast
multiplying) immunity
 Slow multiplying bradyzoites  form cyst

PATHOLOGY
• Toxoplasmosis commonly asymptomatic , if
immune system is good
• Encephalitis-most common manifestation
• CONGENITAL TOXOPLASMOSIS

DIAGNOSIS
1. Biopsy- stained through hematoxylin and eosin
stain
2. Serodiagnostic methods- positive titer or a four-
fold rise in the titer
3. Sabin-Feldman methylene blue dye test – very
specific and sensitive
4. IHAT
5. ELISA
6. PCR

_____________________________________________________________________________________ 4
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CLINICAL PARASITOLOGY
Introduction (WEEK 1 / LEC)
1st SEM, 2021

Notes:
 Sarcocyst  identifiable with hematoxylin and
eosin stain
 Confirmatory staining  pas (walls stain
positively)
 Wall of s. hominis  6um thick, radially
striated from villar protrusions that are 7um
long
 Walls of s. suihominis  4-9um thick, with
villar protrusions up to 13um long

TREATMENT
• No effective treatment is known
• Corticosteroids were found to be useful in
muscular inflammation
• Trimethoprim-sulfamethoxazole – seen as
potentially effective in treating intestinal
infections

PREVENTION AND CONTROL


Notes: • Uncooked animal carcass should not be fed to
 Sporocyst and oocyt in feces ingested by other animals
cows ruputures releasing sporozoites
merozoites penetrate muscles and
develope into
 Sarcocysts w/ bradyzoites ingested in
undercooked meat bradyzoites (become
motile after wall digestion) released enter
intestinal cells micro/macro oocyst -feces

PATHOLOGY
• Sarcosporidiosis and sarcocystosis
• Gastroenteritis, diarrhea, myalgia, weakness,
fever
• For intermediate host, brain, muscle and
kidney tissues maybe damaged
• May cause abortion to cows

DIAGNOSIS
Definitive: biopsy of an infected muscle
1. Fecal floatation methods sporocysts will be seen
2. Necropsy schizonts will be seen
3. Western blot
4. Serologic tests (IFA, ELISA)
5. PCR

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BANCROFTIAN FILARIASIS
FILARIAL WORMS Vector Biology:
FILARIAL WORMS – also known as vector borne  Anopheles flavirostris
nematodes  Aedes poecillus
1. Sheathed microfilaria- retains embryotic sheath Aquatic habitat: axils of abaca and banana plant
 Wuchereria bancrofti Adult biting: day and night biting, indoor and outdoor
 Brugia malayi Adult resting: base of abaca plants, cool, shady area

2. Unsheathed microfilaria- does not retain


embryotic sheath
 Onchocerca volvulus
 Mansonella perstans
 Mansonella ozzardi

3. Dracunculus medinensis

LYMPHATIC FILARIAL PARASITES


Wuchereria bancrofti
Brugia malayi
• One of the “most debilitating disease” in
tropical countries
• most debilitating disease- will make
the person very weak
• Filariasis – parasitic infection caused by
microscopic threadlike worms acquired
through a mosquito bite (vector borne)
• Has its social and economic impact

MOT: Skin penetration through a vector


Habitat: Lymphatic vessels (lymph nodes)
Vector: Aedes spp., Culex spp. and Anopheles spp. (W.
bancrofti) Mansonia spp. eg. M. bonnae and M.
uniformis (B. malayi)
Infective stages: L3 larva or filariform larva (man)
microfilariae (mosquito)
Diagnostic stage: microfilariae
Definite host: man
Notes:
Parameter Wunchereria Brugia malayi  Wunchereria bancrofti
bancrofti o Lower elephantiasis
Common name Bancroft’s Malayan filarial
 Brugia malayi
filarial worm worm
o Upper elephantiasis
Vector Anopheles, Mansonia spp.
aedes, culex  Mosquito is part of the life cycle
spp.  Mosquito ingested microfilariae (diagnostic
Area affected Lower Upper stage)
lymphatics lymphatics  Microfilariae will shed sheaths and penetrate
Periodicity Nocturnal Subperiodic mosquitos midgut and it will migrate to the
(8pm-2am) (12nn-8pm thoracic musculature for a period of growth
 Larvae will grow and become infective larvae
(L3larvae) (infective stage)
 Infective larvae will now enter the proboscis
of the mosquito
 Mosquito bites a person, larvae will enter
humans skin and will go to lymphatic

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 Lymphnodes blood channels (where they PATHOLOGY


mature)
“Expatriate Syndrome”
 Male and female worm is present in the same
area they will going to mate and they will – occurs to migrants who got infected from endemic
produce microfilariae which is now the regions
diagnostic stage; and infective stage for
mosquito  Characterized by clinical and immunologic
 Sexual maturity time- several months hyper-responsiveness to maturing worms
 Adult worms- year  Acute manifestations + allergic reactions
 Happens in lymphatics (hives, rashes and blood eosinophilia)

“Tropical Pulmonary Eosinophilia” (TPE)


PATHOLOGY – due to the microfilaria
Lymphatic Filariasis  “Weingartner’s syndrome”
 Immune response (cell-mediated and  Marked increase of IgE and IgG antiparasite
humoral) Ab as well as hypereosinophilia
Adult or •Causes lymphatic dilation  Nocturnal coughing, breathlessness, wheezing
Larval worm

•Causing mechanical damage to the lymphatics

•Elicit the most severe inflammation


Dead worms

•Calcification of necrotizing granulomas

•LYMPHATIC OBSTRUCTION

DIAGNOSIS
A. Acute Filarial Disease 1. Microscopy
 Adenolymphagitis (ADL) or
Dermatolymphangiodenitis (DLA) a. “wet smears”
 Pain, tenderness & swelling of affected areas,  demonstrate motile microfilariae
with or without fever b. “thick blood smears”
 Epididymo-orchitis in males may occur  Giemsa stain
o Inflammation in testes  Demonstration of the microfilaria
(most practical diagnostic
procedure)
B. Chronic Filarial Disease – more commonly
encountered than its acute form

 Lymphedema- swelling of arms and legs


 Elephantiasis- enlargement and hardening
of lymph due to fluid surrounding the
testicles
 hydroecele
 Kidney damage – “milky urine” due to
reflux of intestinal lymph to the renal
lymphatics (proteinuria and hematuria)
o Protein and blood

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Differences in microfilariae LOA LOA


Parameter Loa loa
Parameter Wuchereria Brugia
bancrofti malayi
common African eye worm
name
mean length 290 222
(µm)
vector Chrysops spp. – deerflies

cephalic space/ 1:1 2:1 (aka mango flies or


breadth mangrove flies)

sheath affinity Unstained Pink area Subcutaneous tissue


to Giemsa affected

body nuclei regularly irregular periodicity diurnal


spaced and
overlapping
Pathology:
terminal nuclei none 2 nuclei
 Loaisis, Fugitive swellings or Calabar swellings
 *causes localized subcutaneous edema as the
appearance in smoothly kinky microfilaria die in the capillaries around the
blood film or gracely eye.
curved

DIAGNOSIS

2. Knotts Concentration Method – for low


intensity infection
Filtration method (Swinney filter) – use of
nucleopore filter
3. Diethylcarbamazine provocative test (3 mg
per Kg DEC single dose)
 stimulates microfilariae to come
out to peripheral circulation
4. RDT/Immunochromatography (ICT) – detects
circulating filarial antigens (CFA)
5. Molecular methods – PCR
6. Ultrasonography – may demonstrate the live
worms in the lymphatics

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Notes: TREATMENT

 Happens in subcutaneous tissue happens 1. Diethylcarbamazine citrate (DEC) – drug


 Usually adults produced sheathed choice for Bancrotian filariasis and TPE
microfilariae that are found in spinal fluid,
2. Ivermectin – found to be as effective as 12
urine, sputum, peripheral blood and lungs.
days of DEC in clearing microfilaremia
UNSHEATHED MICROFILARIA
PREVENTION AND CONTROL
• Onchocerca volvulus
WHO targeted lymphatic filariasis to be eliminated by
– “Blinding worm”, Gale filarienne”, 2020
“Craw craw”
 Development of microfilaricidal regimens
– causes Onchocerciasis, River
(Moxidectin)
blindness, Roble’s disease
– destroys optic nerve  Goal for endemic areas: Eliminate presence of
• Mansonella perstans microfilariae in blood

– old name: Acathocheilonema perstans 1. Personal protective measures (use of


– rare parasite of man mosquito nets)

• Mansonella ozzardi 2. Residual spraying

– rare parasite of man 3. Health education

DRACUNCULUS MEDINENSIS
Parame O. volvulus M. M. ozzardi  “Guinea worm”, “Worm of Medina”, “Dragon
ter perstans worm” or “Fiery serpent”
 Longest nematode to man (1 meter)
Vector Black flies Small Small flies  Causes “dracunculiasis” or “Guinea worm
flies (gnats) disease” (GWD)
Simulium
(gnats)  No symptoms for one year
damnosum Culicoides
Culicoid furens  Common symptoms: rashes, fever, nausea,
es vomitting, diarrhea, dizziness
austeni  Until there is formation of blister and causes a
burning sensation
Habitat Subcutaneo Body Subcutane Complications: cellulitis, abscess, sepsis, lock jaw
us tissue cavities ous tissue (tetanus)

Patholo Onchocercia Non- Non-


gy sis, River pathoge pathogenic
blindedness nic

Specime Skin
n shadings/ni
ps

 I.S. to man : 3rd stage larva (L3)


 I.S. to vector : microfilaria
 Covering : unsheathed
 Periodicity : non-periodic

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TREATMENT AND MANAGEMENT

1. Immersion of affected body part to water

2. Wound is cleaned

3. Worm extraction

4. Topical antibiotics are given to prevent


infection

5. Aspirin and Ibuprofen are given to ease the


pain

PREVENTION AND CONTROL

1. Surveillance and Case containment

2. Provision for safe drinking water

3. Vector control – use of a chemical larvicide


(Abate™)

4. Health Education

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INTRODUCTION TO PARASITOLOGY ● Spurious/Coprozoic parasites


● Parasitology ○ Free-living organisms that passes
○ Area of biology concerned with the through the digestive tract without
phenomenon of dependence of one infecting the host.
living organisms on another. ● Temporary parasites
○ Parasites that lives on the host only
● Medical Parasitology for a short period of time.
○ concerned primarily with parasites of ● Permanent parasites
human and their medical significance. ○ Parasites that remains on or in the
body of the host for its entire life.
Host-Parasite Relationship (Biological Relationship) ● Saphrophytes
● Symbiosis ○ Microorganisms that lives on dead or
○ Living together of unlike organisms. It decaying organic matter.
may also involve protection or other
advantages to one or both partners. Types of Host
○ The primary function of the host is to
carry on the parasite’s life cycle. a. Definitive host
● Where parasites attain its sexual maturity
Different forms of Symbiosis: ● A host in which a parasite develops to an adult
1. Commensalism or sexually mature stage.
● Is a symbiotic relationship in which ● Also called Final host
two species benefit from the
relationship without harming or b. Intermediate host
benefiting the others. ● Harbors the asexual or larval stage of the
2. Mutualism parasite.
● Is a symbiosis in which two organisms ● The host in which a parasite undergoes
mutually benefit from each other. development but does not reach sexual
3. Parasitism maturity.
● Is a symbiotic relationship where one
organism, the parasite, lives in or on c. Reservoir
another, depending on the latter for ● They allow the parasite’s life cycle to continue
its survival and usually at the expense and become additional sources of human
of the host. infection.
● Pigs: Balantidium coli
Types of Parasites according to the mode of living ● Rats: Paragonimus westermanii
● Ectoparasites ● Cats: Brugia malayi
○ Parasite that lives outside the body of
a host d. Paratenic host
● Endoparasites ● Host in which the parasites does not develop
○ Parasites living inside the body of a further to later stages. However, the parasites
host. remains alive and is able to infect another
● Facultative parasites susceptible host.
○ Exist in free-living state or may ● An intermediate host whose presence may be
become parasitic when the need required for the completion of a parasite's life
arises cycle but in which no development of the
● Obligate parasites parasite occurs.
○ Parasites that need a host to complete
their development and to propagate
their species.
● Incidental/ Accidental parasites
○ A parasites, which establishes itself in
a host where it does not ordinarily live

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CLINICAL PARASITOLOGY
Introduction (WEEK 1 / LEC)
1st SEM, 2021
VECTORS LIFE CYCLE ACCORDING TO NUMBER OF HOST
● Vectors are responsible for transmitting the
parasite from one host to another 1. Monoxenous
● Only one host
1. Biological Vector ○ Ex. Ascaris
● transmits the parasite only after the latter has 2. Heteroxenous
completed its development within the host, ● Requires 2 or more host in its entire
therefore it is an essential part of the life cycle
parasite’s life cycle. ○ Ex. Trematodes

2. Mechanical or phoretic vector According to set of sex organ


● Only transport the parasite, not part of the
parasite’s life cycle 1. Monoecious
● Parasites that contains the male and
EXPOSURE AND INFECTION female sex organs in one body.
○ Ex.Hermaphrodites-
1. Carrier Trematodes and Cestodes
● harbors a particular pathogen without 2. Dioecious
manifesting any signs and symptoms. ● Sexes are separate
2. Incubation period ○ Ex. Nematodes
● is the period between infection and
evidence of symptoms. Epidemiologic Measures
3. Autoinfection
● results when an infected individual ● Epidemiology is the study of patterns,
becomes his own direct source of distribution, and occurrence of disease.
infection.
● Incidence is the number of new cases of
SOURCES OF INFECTION infection appearing in a population in a given
period of time
● Contaminated soil and water (most common .
source) ● Prevalence is the number (usually expressed
● Lack of sanitary toilets as percentage) of individuals in a population
● Use of night soil or human excreta as fertilizer estimated to be infected with a particular
● Food containing immature infective stage of parasite species at a given time
the parasite .
● Blood sucking insects ● Cumulative prevalence is the percentage of
● Domestic and wild animals individuals in a population infected with at
● Another person least one parasite
.
PARASITIC LIFE CYCLE ● Intensity of infection refers to burden of
infection which is related to the number of
Modes of Transmission worms per infected person
● Mouth/ Fecal oral route
● Skin Penetration Classification of disease according to distribution
● Bites (vector borne) 1. Endemic
● Congenital Transmission ● Always present in a given location
● Transmammary 2. Epidemic
● Inhalation ● Sudden increase in a given location;
outbreak
Morphologic Forms: 3. Hyperendemic
● Infective stage ● Very high number of cases (already
● Diagnostic stage high, then it becomes higher)

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CLINICAL PARASITOLOGY
Introduction (WEEK 1 / LEC)
1st SEM, 2021
4. Sporadic HOST-PARASITE INTERACTIONS
● Occasional; only few cases
5. Pandemic ● NATURAL PHYSICAL BARRIERS
● Worldwide - Skin (First line of defense)
- Mucous membranes lining the
Pathophysiology and Symptomatology of Parasitic respiratory, gastrointestinal and
Infections genitourinary tract
- Low pH of vaginal secretions and
Major body areas associated with infections: gastric juices
● CHEMICAL COMPINENTS OF BOSY FLUIDS
● Gastrointestinal tract - Breast milk
● Urogenital tract - Tears and saliva
● Blood and tissue ● PHYSIOLOGIC FUNCTIONS
● Liver - Peristalsis
● Lung - Motion of cilia
● Miscellaneous locations (CSF, Eye, skin and - Coughing
extremities - Flushing of urine
Symptoms associated with parasitic disease process:
HOST-IMMUNE RESPONSES
● Diarrhea
● Fever ● INNATE IMMUNITY
● Chills - Phagocytosis
● Abdominal pain - Toll-Like receptors (TLR’s)
● Abdominal cramping - Natural killer cell
● Anemia - Blood cells
● Vitamin deficiency ● ACQUIRED IMMUNITY
- Major histocompatibility complex
PREVENTION AND CONTROL - Parasite antigens: IgE, IgG, IgM and
IgA
● Morbidity Control
● Information-education communication Nomenclature
● Environmental management
● Environmental sanitation ● Animal parasites are classified according to
● Sanitation the International Code of Zoological
Nomenclature
IMMUNOLOGY OF PARASITIC ● Each phylum is divided into Classes, which are
INFECTIONS further subdivided into Orders, Families,
genera and species.
● Parasite fails to become established in the ● Scientific names are latinized
host ● The scientific names of parasites are written in
● Parasite becomes established and the host italics and consist of two components:
eliminates the infection - genus (pl., genera)
● Parasites become established and the host - species.
begins to overcome the infection but is not
totally successful Classification of Parasites
● Parasites become established and the host,
trying to eliminate the organism, becomes 1. Subkingdom Protozoa (unicellular)
damaged itself
● Parasites become established and kills the a. Phylum Sarcomastigophora
host ➢ Subphylum Sarcodina (Amoeba)- organ of
movement through :pseudopods

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CLINICAL PARASITOLOGY
Introduction (WEEK 1 / LEC)
1st SEM, 2021
Acanthamoeba castellani ● Intestinal Nematodes
Endolimax nana
Entamoeba coli Ascaris lumbricoides
Entamoeba dispar Capillaria philippinensis
Entamoeba gingivalis Enterobius vermicularis
Entamoeba histolytica Hookworm
Iodamoeba butschlii Strongyloides stercoralis Trichuris trichiura
Naegleria fowleri
● Extraintestinal Nematodes
Subphylum Mastigophora (flagellates)
Lymphatic filarial
● Atrial flagellates Parastrongylus cantonensis
Trichinella spiralis
Chilomastix mesnili b. Phylum Platyhelminthes
Dientamoeba fragilis
Giardia lamblia ● Class Trematoda (flukes)
Trichomonas hominis Artyfechinostomum malayanum
Trichomonas tenax Trichomonas vaginalis Clonorchis sinensis
Echinostoma ilocanum
● Hemoflagellates Fasciola hepatica
Fasciolopsis buski
Leishmania braziliensis Heterophyids
Leishmania donovani Opisthorchis felineus
Leishmania tropica Opisthorchis viverrini
Trypanosoma brucei complex Paragonimus westermani
Trypanosoma cruzi Schistosoma haematobium Schistosoma japonicum
Schistosoma mansoni
b. Phylum Ciliophora (ciliates)
● Class Cestoda (tapeworms) Cyclophyllidea
● Balantidium coli Dipylidium caninum Echinococcus spp.
Hymenolepis diminuta
c. Phylum Apicomplexa Hymenolepis nana
Raillietina garrisoni
● Babesia spp. Taenia saginata
● Cryptosporidium hominis Taenia solium
● Cyclospora cayetanensis Pseudophyllidea
● Cystoisospora belli Diphyllobothrium latum Spirometra sp.
● Plasmodium spp.
● Toxoplasma gondii 3. Kingdom animalia

d. Phylum Microspora ● Phylum Arthropoda Class


● Enterocytozoon bieneusi
● Encephalitozoon spp. Arachnida
● Vittaforma cornea Mites
● Trachipleistophora hominis Scorpions
● Pleistophora spp. Spiders Ticks
● Anncaliia vesicularum Microsporidium spp
Class Crustacea
2. Subkingdom Metazoa (multi cellular) Capepods
a. Phylum Nemathelminthes Crabs
(Nematodes)

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CLINICAL PARASITOLOGY
Introduction (WEEK 1 / LEC)
1st SEM, 2021
Class Chilopoda
Centipedes

Class Pentastomida
Tongue worm

Class Insecta
Flies
Flea
Beetle
Bees
Lice
Wasp
Bugs
Mosquitoes

References
Belizario, Vicente Y., Jr. (2015). Medical
parasitology in the Philippines. Quezon City :
The University of the Philippines.

Zeibig, Elizabeth A. (2013). Clinical


parasitology: a practical approach. (2nd ed.).
Singapore : Elsevier.

MAIN #1

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CLINICAL PARASITOLOGY
Introduction (WEEK 2 / LEC)
1st SEM, 2021

PARASITIC AMOEBA GENERAL RULES FOR AMOEBA

 PATHOGENIC ● All amoeba are commensal except for


○ Entamoeba histolytica Entamoeba histolytica
● With pseudopodium (false feet): finger-like
 NON-PATHOGENIC structures for movement
○ Entamoeba dispar ● Undergoes ENCYSTATION except for E.
○ Entamoeba hartmanii gingivalis and Dientamoeba fragilis
○ Entamoeba coli ● Inhabits the large intestine except for E.
○ Entamoeba gingivalis gingivalis (gums)
○ Entamoeba polecki ● Amoebiasis – presence of amoeba in any part
○ Entamoeba moshkovskii of the body (exclusively applied to E.
○ Endolimaxnana histolytica)
○ Iodamoeba butschlii ● Asexually multiplies through Binary fission
○ Blastocystis hominis
Entamoeba histolytica
 PATHOGENIC AND FREE-LIVING
○ Naegleria fowleri Morphologic Forms:
○ Acanthamoebaspp. 1. Trophozoite – divides through “binary
○ Hartmanellaspp. fission”, irregular in shape, motility:
○ Balamuthiamandrillaris unidirectional, flask-shaped ulcers
2. Precyst
 CILIATA 3. Cyst –1 to 4 nucleus, cigar/rod shaped
○ Balantidium coli chromatoidal body, centrally located
karyosome
 OTHER INT. PROTOZOAN 4. Metacyst
○ Dientamoeba fragilis
❖ Infective stage: Tetranucleated/mature cyst
Protozoan Development and ❖ MOT: ingestion of contaminated food and/or
Reproduction water with E. histolytica cyst

● 2 stage of development: TROPHOZOITE CYST


○ Cyst – Non-motile, Non-Feeding Vegetative & motile Non-motile, non-feeding
stage, Resistant to acid stage
stage (feeding stage)
○ Trophozoite – Motile, Feeding stage,
Fragile
Found in watery, soft Found in soft to formed
● 3 stages of reproduction: or stool
○ Excystation – development of cyst Semi-formed stool
into trophozoite Resistant to acidic pH
Fragile
○ Encystation – development of
trophozoite into cyst
ADDED NOTES:
○ Binary Fission – mode of
● Entamoeba Histolytica- first describe by a
reproduction of trophozoite
young Russian physician LOSCH
● trophozoite
○ Motility of trophozoite: unidirectional,
progressive
○ Characteristic of Ulceration: flask-
shaped ulcers.

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○ Found mostly in tropical and ✔ Presence of Charcot-Leyden crystals
subtropical areas with high found microscopically in the stool in
prevalence in areas with work, cases of Amoebic dysentery
sanitation, and overcrowding
○ Should be tested if the sample is
watery, 30 minutes after the passage
( watery)
○ Should be tested within/ after 1 hour
after the passage (soft or semi-
formed)
● CYST
○ 1-4 nucleus- mature cyst
○ 1-4 nucleus- immature cyst
○ chromatoidal body- Preserved food
goes
○ Has the ability to pass through the
stomach acidity.

1. Intestinal Amebiasis

a. Amebic colitis / Amebic dysentery:


abdominal pain, diarrhea (w/ or w/o
mucus & blood)
b. Characteristic ulcer: FLASK SHAPE
ULCER
c. Ameboma – mass-like lesion with
abdominal pain and dysentery (<1%)

ADDED NOTES:

● Amoebic colitis/ amoebic dysentery


○ Most serious complication is the
perforation And secondary bacterial
peritonitis
○ Perforation- there's a formation of
hole
■ If left untreated and can kill
Pathogenesis the patient or can cause
severe organ damage
● Symptoms 2. Extraintestinal Amebiasis
✔ Gradual onset of abdominal pain
✔ Diarrhea (with or without blood and a) Hepatic amebiasis:
mucus) o Amebic Liver Abscess: ANCHOVY
✔ In children, bloody diarrhea, fever and SAUCE-LIKE EFFUSION
abdominal pain b) Pulmonary amebiasis
✔ Abscess formation ---- Amoebic liver c) Cerebral amebiasis
absces. d) Amebic pericarditis
e) Cutaneous amebiasis
f) Genital amebiasis

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Extraintestinal amoebiasis ○ this will insert the cells inform a tiny
● Through the portal vein (liver), trophozoite hole that result in the lysis of target
reach other parts of the body (liver, brain, cells
lungs, kidneys) ● Cysteine proteinase: Tissue invasiveness
✔ Amoebic liver abcess (ALA)
▪ fever and right upper ○ Degrade the host proteins which
quadrant pain enables the attachment to the gut by
▪ Formation of an abscess in degrading the mucus and the debris.
the right lobe of the liver
▪ anchovy sauce-like materials
▪ MOST COMMON
● Assymptomatic carriers: cysts becomes
unnoticed

ADDED NOTES:

● Amoebic liver abscess (ALA)


○ it can also cost hepatomegaly (30%
concurrent diarrhea, 72% harbor
protozoa in stool and 1% mortality)
○ most common complication of ALA is
rapture pericardium with 70%
mortality, rapture in pleura with
15% to 30% mortality)

 Superinfection - infection after an earlier


infection m
o Second most common intraperitoneal
rupture
o 2% to 7.5% of the cases not as serious Mode of transmission
as colonic perforation ( hole in the
✔ Ingestion of contaminated food and/or water
colon)
Diagnostic Stage
Pathology
● Can cause ulceration “flask-shaped ulcer” in ✔ Identification of the cyst or trophozoite
the intestines (cecum, ascending colon and Sample for ID
sigmoid)
✔ Stool (examined within 30 minutes from
Pathogenic determinants / Virulence factors: collection)
1. Suppressor factor: neutralizes stomach pH
2. Gal/Gal Naclectin: cytoadherence
3. Amebapores: poreformers
4. Cysteine proteinase: Tissue invasiveness

ADDED NOTES:

● Amebapores: poreformers
○ It forms ion channels in the
phagocytize cells

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Morphologic Comparison between E. histolytica and Laboratory Diagnosis
Escherichia coli 1. Direct Fecal Smear

saline solution trophozoite motility

Entamoeba spp. stain


blue
saline +

methylene blue

saline + iodine
nucleus of E. histolytica
can

be observed

ADDED NOTES:

● Direct fecal smear- standard method for


microscopic detection of cyst
● three times in 10 days
○ Collection of stool for identification
● Saline+iodine
○ Observe pathogenic and non-
pathogenic amoeba
● Saline methylene blue
○ Entamoeba histolytica will stained
blue

2. Concentration Techniques
✔ Formalin Ether Concentration Technique
(FECT)
✔ Merthiolate Iodine Formalin Concentration
(MIFC) MORE SENSITIVE
✔ 33 % ZnSO4 Floatation Technique (SP 1.18-
1.20)

3. Culture: Robinson’s and Inoki medium


✔ More sensitive than stool microscopy)

4. Serologic Testing:
✔ ELISA, IHAT (can detect past infection), CIE,
AGD, IFAT
5. Molecular Testing: PCR
6. CT-SCAN, MRI

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Treatment (Drug of Choice) 2. Entamoeba dispar
 Metronidazole
● Morphologically similar to E. histolytica, but
✔ drug of choice for invasive amoebiasis
with different DNA and RNA
 Diloxanide furoate
3. Entamoeba hartmanni
✔ drug of choice for asymptomatic cyst passers

Prevention and Control ● Similar to E. histolytica except much smaller


and no RBC inclusions
● Proper hygiene ● “small-race E. histolytica”
● Provision for sanitary disposal of human feces
● Improve access to clean and ● Smaller compared to entamoeba histolytica
safe drinking water Non-Pathogenic Species
● Good food preparation practices
● Avoid using “night soil” 1. Entamoeba polecki
● Health education and promotion

ADDED NOTES: ● Parasite of the pigs and monkeys (rarely infect


humans)
● Two objectives ● Cyst contains one nucleus
○ to cure both intestinal and ● Chromatoidal bars with pointed or angular
extraintestinal amoebiasis ends are often present
○ to eliminate the passage of cyst from
intestinal lumen 2. Entamoeba chattoni
Commensal Amoebas
● Found in apes and monkeys
1. Entamoeba coli 3. Entamoeba gingivalis
● Harmless inhabitant of the colon
o Tropozoite: Karyosome is eccentrically ● Can be found in the mouth (gum and teeth
located, motilitysluggidh/non surfaces)
directional ● Abundant in cases of oral diseases
Cyst: 1-8 nucleus, witchbroom stick/splinter shape ● No cyst stage
chromatoidal body. ● Transmission through kissing, droplet spray,
sharing utensils
Epidemiology Geographic areas that have poor
hygiene and sanitation 4. Entamoeba moshkovskii
practice
Treatment No specific drug is needed ● morphologically indistinguishable from those
to treat the infection of the disease causing species E. histolytica
and the non-pathogenic E. dispar
Prevention Proper disposal of human ● Physiologically unique
feces
Proper personal hygiene 5. Endolimax nana
practices
Protection of food and
● “Smallest amoeba”
drinks from flies and
● “Cross eyed cyst” – 4 eccentric nuclei
cockroaches

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6. Iodamoeba butschlii

● “iodine-cyst” because of its affinity to iodine


● Large glycogen vacuole/ body which stains
deeply with iodine
● Chromatoidal bars are absent
● Uninucleated cyst

● It has a large glycogen vacuole

Free Living Pathogenic Amoeba

ACANTHAMOEBA

MOT:

● Direct invasion of the parasite via


contaminated contact lens solution, aspiration
or nasal inhalation via lower respiratory tract
or thru ulcers in the mucosa or broken skin.

Pathogenesis:

● Causative agent of Granulomatous Amoebic


Encephalitis (GAE)
o destructive encephalopathy and
associated meningeal irritation
● Amoebic keratitis (contact lens users)

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Acanthamoeba TREATMENT:
● Cases of Acanthamoeba keratitis have
successfully been treated with several
medications that include itraconazole,
ketoconazole, miconazole, propamidine
isethianate, and rifampin
● Few patients show good responses with
combinations of Amphotericin B,
Cotrimoxazole and rifampin

Free Living Pathogenic Amoeba

Naegleria
Parasite Biology
● Two vegetative forms:
o Amoeboid (trophozite form)
o Amoeboflagellate (swimming form)
Amoebic keratitis ● Cyst
● Thermophilic organisms
✔ Severe ocular pain and blurring vision
✔ Corneal ulcerations with progressive corneal
infiltration
✔ Progression of infection may lead to Scleritis
and Iritis
o Vision loss

Granulomatous Amoebic Encephalitis

✔ Destruction of brain tissue and associated


meningeal irritation
✔ Fever, malaise and anorexia
✔ Neurologic symptoms
✔ Hemiparesis
✔ Blurring of vision
✔ Cranial nerve deficits Naegleria
✔ Ataxia and increased intracranial pressure MOT:
● Oral and intranasal routes while swimming in
DIAGNOSIS contaminated pools, rivers and lakes
● Histopathologic techniques (biopsy) ● Inhalation of dust contaminated with
o demonstration of cyst and N.fowleri
trophozoite in neural tissue ● The ameboid trophozoites transform into
● PCR flagellate trophozoites in vitro after being
transferred to water from a tissue or culture.
Specimen ● The flagellate trophozoites do not divide but
rather lose their flagella and convert back into
● Discharges
the ameboid form, in which reproduction
● exudates, tissue secretions
resumes.
● CSF (specimen of choice)
● The cyst form is known to exist only in the
● Corneal scrapings: specimen
external environment.
● of choice for recovery of eye infections
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● Amphotericin B and miconazole damage the
cell wall of Naegleria
● Rifampicin inhibits RNA synthesis in the
amoeba
● A person can survive if signs are recognized
early but, if not, PAM almost always results in
death

CILIATES

Naegleria Phylum Ciliophora


Pathogenesis: Balantidium coli
● Fatal Primary amoebic encephalitis (PAM) ● Causative agent of “balantidiasis or balantidial
o fever, nausea, vomiting, headache, dysentery”
mental status changes, rapid ● Similar to amoebic dysentery
progression to coma and death ● Largest protozoan parasite
● Kernig’s sign ● Only parasitic ciliate www.southampton.ac.uk
Diagnosis: ● Primarily associated with pigs
● PCR
● ELISA

Specimen
● CSF (specimen of choice)
● Post mortem of infected brain

Prevention:
● Frequent cleaning Morphology:
● Chlorination ● Has trophozoite and cyst stage
● Salination Parts:
● cytostome : entry of food
TREATMENT: ● cytophage/cytopyge: excretes waste
● In rare cases, amphotericin B in combination ● 2 disimilar nucleus:
with rifampin, Clotrimoxazole or miconazole o macro- and micronucleus
has also proved to be an effective treatment.

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● 2 contractile vacuoles
❖ encystation doesn’t result in increase in nuclei

MOT:
● Ingestion of food/water contaminated with
Balantidium coli cyst

BALANTIDIUM COLI

Pathogenic determinant:
● Hyaluronidase: causes the ulceratio
● Ulceration: is described as flask-shaped with
wider neck and round base

BALANTIDIASIS:
● Asymptomatic
● Fulminant Balantidiasis
● chronic Balantidiasis

Specimen:
● stool

Diagnostic Stage: cyst and trophozoite in stool


● Direct examination or Concentration
techniques
● Sigmoidoscopy

Infective Stage: cyst


Treatment: Metronidazole
Prevention: same with amoeba

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OTHER INTESTINAL PROTOZOAN


o The parasite is isolated from both
asymptomatic and symptomatic
patients, so many still argues about
the pathogenicity of this parasite. New
studies shows its role as a pathogen.
o Symptomatic patients have
intermittent diarrhea and fatigue in
(fatiquein) young population [Irritable
bowel syndrome (IBS)]

ADDED NOTES:
 The stool ram gorilla and swine are found to
 Dientamoeba fragilis carry dientamoeba fragilis trophozoite. Thus,
o First describe by Jepps and Dobell the animal reservoir may also be potential
(1918) sources of human infection
o First seen by 1909 by Charles Wenyon
o Originally described as an ameba, but  Dientamoeba fragilis, not invade the tissues
molecular study, ultrastructure but present in intestine produces irritation of
observation through electron the mucosa with chronic infection of this
microscope and presence of no cystic organism It can mimic the symptoms of
stage determines that it is closely diarrhea
related to the trichomonads
(flagellate).
o Resembles Trichomonas
o Co-infection with Enterobius
vermicularis
 Simultaneous infection of a
host by more than 1 pathogen

 Morphology:
o Rosette shaped nuclei (1 to 2)
o Cytoplasm may contain vacuoles with Nuclei: 1 or 2 with chromatin granules
ingested bacteria and debris
o No cystic stage identified Table 4-5. Dientamoeba fragilis Trophozoite:
o Only trophozoite stage Typical Characteristics at a Glance
o Karyosome consist of 4-5 discrete PARAMETER DESCRIPTION
granules Size range 5-18 um
Shape Irregularly round
 Clinical Symptoms Motility Progressive, broad
o Life cycle is unknown. hyaline pseudopodia
o Exact transmission is not yet well Number of nuclei Two, each consisting of
understood; no fecal-oral, foodborne massed clumps of (4-8)
or waterborne transmission has been four to eight chromatin
documented, but transmission is granules
associated to helminthic eggs No peripheral chromatin
especially Enterobius vermicularis Cytoplasm Bacteria-filled vacuoles
(Pinworm) eggs. common
 Transmission: human to
human via fecal oral routes,
transmission of helminthic
eggs.

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 Diagnosis
1. Flagellum/Flagella
o NO available rapid test kit.
o Microscopic evaluation of freshly  locomotor apparatus- movement
passed liquid stool is still the standard 2. Kinetoplast – provides energy
procedure.  blepharoplast
 Consistency of stool: watery  parabasal body
and examine in 30 mins of 3. Cytostome – cell mouth
passage 4. Undulating membrane
o Fixed stool with polyvinyl alcohol or  a membrane laterally projecting from
o Schaudinn’s fixative the body of certain flagellates,
o Permanent stained smear: Iron participate in active motility of the
hematoxylin. flagella
o Molecular techniques: RT-PCR Giardia lamblia
5. Axostyle or axial rod
 Treatment:  for support in locomotion
o The treatment of choice for such 6. Costa
infections is iodoquinol.  rib-like structure within the
o Tetracycline and metronidazole have cytostome
also been found to be effective.
Pathogenic
 Prevention and Control GIARDIA LAMBLIA
o Proper sanitation  Old names:
o Proper disposal of human waste o Giardia intestinalis
o Giardia duodenalis
ATRIAL FLAGELLATES o Lamblia duodenalis
o Lamblia intestinalis
o Cercomonas intestinalis
 Habitat:
o Duodenum, jejunum and upper ileum
of humans

Phylum Sarcomastigophora
Subphylum Mastigophora
A. Pathogenic
 Giardia lamblia
 Trichomonas vaginalis
B. Non-pathogenic
 Trichomonas hominis
 Trichomonas tenax
 Chilomastix mesnili  It was first discovered in 1681 by Antoine van
 Retortamonas intestinalis Leeuwenhoek in his own stools
 First described in 1859 by French scientist Dr.
BASIC STRUCTURE OF FLAGELLATES F. Lambl and Czechoslovakian scientist Dr.
Giard: Cercomonas intestinalis
 In 1915 Stiles coined Giardia lamblia

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I. Morphology
A. Trophozoite Table 4-1. Giardia Intestinalis Trophozoite: Typical
 Pear/tear drop shaped, pyriform Characteristics at a Glance
 Bilaterally symmetrical, with distinct PARAMETER DESCRIPTION
medial line called axostyle Size range 8-20 um long
 “Old-man with eyeglasses” 5-16 um wide
o Old man with (whispers, Shape Pear-shaped, teardrop
cartoon character, monkey’s Motility Falling leaf
face) Appearance Bilaterally symmetrical
 with large ventral sucking disc – Nuclei Two ovoid-shaped, each
pathogenic determinant with a large karyosome
o Trophozoite used sucking disc No peripheral chromatin
by touching the sucking disc to Flagella Four-pairs, origination
mucosa (used in of each:
pathogenicity) One pair, anterior end
o sucking disc attached mucosa One pair, posterior end
to intestinal wall Two pair, central,
 4 pairs of flagella extending laterally
 2 nuclei with distinct karyosome Other Structures Two median bodies
(symmetrically bilateral)- looks like Two axonemes
eyes Sucking disk
 “falling leaf motility” - movement *uses micrometer for measuring
 Covered with variant-specific surface
proteins (VSPs) B. Cyst
o The resistance to intestinal  Ovoidal in shape
proteases  Thick shell (double wall)
o It attributes to the survival of  Nuclei:
the parasites o - 2 (young)
o 4 (mature)
GIARDIA LAMBLIA TROPHOZOITE  Presence of axoneme

II. Infective Stage:


 Mature cysts

III. Mode of Transmission


 Ingestion of contaminated food and
water

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GIARDIA LAMBLIA CYST TROPHOZOITE

CYST

IV. LIFE CYCLE OF GIARDIA LAMBLIA

Table 4-2. Giardia Intestinalis Cyst: Typical at a


Glance
PARAMETER DESCRIPTION
Size range 8-17 um long
6-10 um wide
Shape Ovoid
Nuclei Immature cyst, two
Mature cyst, four
Central karyosomes
No peripheral chromatin 1. Trophozoites are also
Cytoplasm Retracted from cell wall passed in stool but
Other structures Median bodies: two in they do not survive in
immature cyst or four in the environment
fully mature cyst (CYST) (Infective
Interior flagellar stage) (diagnostic
structures stage)
*twice as many in mature cyst as compared with 2. Contamination of
immature cyst water, food, or
hands/ fomites with
infective cysts.
(Infective stage)

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ADDED NOTES: PATHOGENICITY


 Once the mature cysts are ingested (infective
stage) thick cell wall can penetrate and it can
pass through the acidity of the stomach
o because of the gastric acid of the
stomach it stimulate the cyst to exist
(Excystation will happen)
o exist in the duodenum developing
into trophozoite Which rapidly
multiply and attached in the intestinal NORMAL INTESTINAL VILLI FLATTENED INTESTINAL VILLI

villi  Upon the attachment to the intestinal cells of


 Giardia lamblia cyst exist in duodenum which Lamblia via sucking disc the structural
is stable for the excystation. it has a pH of changes in the intestinal villi causing villous
neutral or a slightly alkaline flattening and crypt hypertrophy Or shrinking
 Once trophozoite were Found in the jejunum and flattening of intestinal villi
they will multiply every 8 hours via
longitudinal binary fusion causing pathogenic VI. DIAGNOSIS
changes Non-invasive procedure
 As the feces enter the colon and dehydrates o Stool examination
the parasite will encyst o Enterotest
 After the encystation The mature cyst are  Invasive procedure
o Duodenal aspirate
passed out in the faces and the infective stage
o Biopsy
 Cyst are the infective stage
 Immunologic and Molecular methods
 In the diagnostic stage, trophozoite can be o Direct fluorescent antibody-gold
seen if the sample are watery or soft or semi standard
formed o EIA and ELISA
 Mode of Transmission: contaminated food, o Western Blot
hand fomites with infective cyst o PCR
ADDED NOTES:
Non-invasive procedure
GIARDIA LAMBLIA  Direct fecal stool examination
V. Pathology o DFS: trophozoite and cyst detected
 Causative agent of Giardiasis o trophozoite may be characterized as
(malabsorption syndrome) or having a floating leaf-like Motility or
Lambliasis falling leaf-like under microscope
 “Traveller’s diarrhea”
 Acute infections : “rotten eggs” odor  to detect cyst: concentration technique is
• Due to hydrogen sulfide recommended
 Chronic infections:
o Steatorrhea → passage of  Enterotest:
greasy, frothy stools that may o straight charge into trophozoite
float on toilet water o patient swallow a gelatin capsule
o Malabsorption of electrolyte, attached to a nylon string with the
glucose, fluid one and string attached to the patient
o Gay bowel syndrome cheeks
o stays in stomach 4-6 hours
o All liquid in the capsule will be used as
a sample for examination

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 Female: vulva (vagina)
 Male: prostate gland

Morphology of the trophozoite:


 Pyriform shape
 4 anterior flagella
 Prominent axostyle
 Presence of undulating membrane
 “Rapid jerky tumbling”- movement
 Siderophylic granules

Entero-tube Trichomonas vaginalis (Trophozoite)


PARAMETER DESCRIPTION
Size range 5-14 um long
Shape Ovoid, round or pear-
shaped
Motility Rapid jerky tumbling
Nuclei One, ovoid, nondescript
Flagella All originating anteriorly
3-5 extending anteriorly
one extending
posteriorly
Others structure Undulating membrane
Biopsy Extending half of body
length
GIARDIA LAMBLIA Prominent axostyle that
often curves around
VII. TREATMENT: nucleus granules maybe
 Metronidazole, Tinidazole, Furazolidone, seen along axostyle
Albendazole, Nitazoxanide
Trichomonas vaginalis
VIII. PREVENTION AND CONTROL
 Proper disposal of human excreta
 Proper use of night soil
 Improve access to clean and safe drinking
water
 Good food preparation practices
 Avoid using “night soil”
 Health education and promotion

TRICHOMONAS VAGINALIS
 Common sexually transmitted disease
among women, usually males are
asymptomatic
 The only pathogenic Trichomonas
 No cyst stage trophozoite stage only
 First observed by Donne in 1836 in
purulent secretions of male and female
urogenital tracts.
Size range: up to 30 um long
HABITAT: Urogenital tract Average length: 8-15 um

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Trichomonas vaginalis Trichomonas vaginalis

Infective and diagnostic stage 1. Trophozoite in vaginal and


 trophozoite prostatic secretions and
urine (diagnostic stage)
Pathology 2. Multiplies by longitudinal
 Trichomoniasis binary fission
3. Trophozoite in vagina or
Symptoms orifice of urethra
(intercourse) (infective
 Males:
stage)
o Asymptomatic (less persistent, self-
limiting) Specimen:
 Females:  Male: Urine sample
o Greenish-yellow discharge o Prostatic fluid or seminal fluid
o Edema, itching, burning sensation  Female: urine sample vaginal
o Vaginal pruritus o discharge cervical
o “strawberry cervix” o scrapings/swabs
 Infants: respiratory tract as well as in the
conjunctiva

Laboratory Tests:
A. Microscopy
 Wet smear or wet mount (SALINE)
 Quickest and most unexpensive and low
sensitivity
B. Culture
 Feinberg-Whittington, Diamond Modified
medium[
MOT:  Gold standard
 Sexual intercourse  2-5 days
 Can be passed through newborns through the  Best result seen in combination of rectal
birth canal swab and urine sediments
 Contaminated underwear or towels, or sitting C. Staining Methods
at contaminated toilet bowl  Giemsa, Papaniculao, Romanowsky and
Acridine orange
D. PCR- very expensive

Treatment:
 Oral Metronidazole
 Acidic Douche (10% vinegar)

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

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Non-pathogenic Atrial Flagellates

Chilomastix mesnili
Largest flagellate in man Habitat:
 Cecal region of the large intestine

Trophozoite
 Asymmetrical
Morphologic Comparison of the Trophozoite
 Pear-shaped
Point of Giardia lamblia Trichomonas
 Spiral groove on midportion
comparison vaginalis
 3 anterior flagella
Shape Pear, tear- pyriform
 1 flagellum within the cytostome →
drop, pyriform
Cystostomal fibril (shepherds crook)
Characteristics Round anterior, Prominent
 “Boring/spiral movement or Cork-screw
pointed axostyle,
movement”
posterior, with undulating
large sucking membrane
Chilomastix mesnili
disc
Trophozoite
(pathogenecity)
Flagella 4 pairs 4 anterior
(anterior, mid,
sucking disc,
extreme
posterior)
Nuclei 2 nuclei One
Symmetry Symmetrical Asymmetrical
Motility Falling-leaf Rapid jerky
tumbling
Pathogenicity Pathogenic Pathogenic

Morphologic Comparison of the Trophozoite


Point of Giardia lamblia Trichomonas
comparison vaginalis
Shape Ovoid No cyst stage
Characteristics Thick shell,
axostyle
present
Nuclei 2 to 4

Size range: 5-25 um by 5-10 um


Average length: 8-15 um

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Table 4-3. Chilomastix mesneli Trophozoite: Table 4-4. Chilomastix mesneli Cyst: Typical
typical characteristics at a glance characteristics at a glance
PARAMETER DESCRIPTION PARAMETER DESCRIPTION
Size range 5-25 um long Size range 5-10 um long
5-10 um wide Shape Lemon-shaped, with a
Shape Pear-shaped clear hyaline knob
Motility Stiff, rotary, directional extending from the
Nuclei One with small central anterior end
or eccentric karyosome Nuclei One, with large central
No peripheral chromatin karyosome
Flagella Four: three extending No peripheral chromatin
from anterior end Other structures Well-defined cytosome
One extending located on one side of
posteriorly from the nucleus
cytosome region
Other structures Prominent cytosome Chilomastix mesnili
extending 1/3 to ½ body
length
Spiral groove

Chilomastix mesneli Cyst


 Pear or lemon shaped
 Conical anterior with knob-like or nipple-
shaped proturbance

Size range: 5-10 um long


Average size: 7-10 um by 3-7 um

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Trichomonas hominis Trophozoite


Non-pathogenic Atrial Flagellates

Trichomonas hominis
 Usually found in the intestines
 Commensal
 Relatively smaller than T. vaginalis
 Specimen: Stool
 MOT: fecal contamination of food
and drinks
Trichomonas tenax
 Also known as Trichomonas buccalis
 Usually found in the mouth
 No cyst stage
 Specimen: Mouth Scrapings
 MOT: contaminated dishes and utensils,
kissing
 Trophozoites appear too durable: surviving
several hours in drinking water.
 Unable to survive in digestive tract
Size range: 7-20 um by 5-18 um width  Only will get in the mouth
Average length: 10-12 um  No cyst stage, only trophozoite stage present

Table 4-6. Trichomonas hominis trophozoite:


typical characteristics at a glance
PARAMETER DESCRIPTION
Size range 7-20 um long
5-18 um wide
Shape Pear-shaped
Motility Nervous, jerky
Nuclei One, with a small
central karyosome
No peripheral chromatin
Flagella 3-5 anterior
1 posterior extending
from the posterior end
of the undulating
membrane
Other structures Axostyle that extends
beyond the posterior
end of the body Size range: 5-14 um long
Full body length Average length: 6-9 um
undulating membrane
Conical cytostome cleft
in anterior region
ventrally located
opposite the undulating
membrane.

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Trichomonas tenax (trophozoite)
PARAMETER DESCRIPTION
Size range 5-14 um long
Shape Oval or Pear-shaped
Nuclei One, ovoid nucleus;
consist of vesicular
region filled with
chromatin granules
Flagella 5 total, all originating
anteriorly
4 extended anteriorly
1 extends posteriorly
Other structures undulating membrane
extending 2/3 of body
length with
accompanying costa
thick axostyle curves
around nucleus extends
beyond body length
Small anterior
cytostome opposite to
undulating membrane

11
CLINICAL PARASITOLOGY
Introduction (WEEK 5 / LEC)
1st SEM, 2021

Blood and Tissue Flagellates


Phylum Sarcomastigophora
Subphylum Mastigophora
Hemoflagellates - (arthropod borne)

A. Leishmania spp.
 Leishmania tropica
 Leishmania braziliensis
 Leishmania donovani

B. Trypanosoma spp.
 Trypanosoma gambiense
 Trypanosoma rhodesiense
 Trypanosoma cruzi

NOTES:
 arthropod borne- they need a vector to
transmit an infection

Morphologic froms:

1. Amastigote – “binary fission”


o Only morphologic form without
flagellum
o Also known as Leishmania stage Trypanosoma spp.
o Nucleus is more toward the edge Etiologic Disease Vector Stages
2. Promastigote agent exhibited
o Has an elongated spindle shape body Trypanos Chaga’s Assasin ALL
with free flagellum that arises from oma cruzi disease or bug,
kinetoplast at the anterior ends American Kissing
o Also known as leptomonads stage Trypanoso bug, Cone
o Front of nucleus miasis nose bug,
3. Epimastigote – “longitudinal fission” Triatomine
o Have flagellum and elongated spindle bugs
shape body Triatoma,
o Also known as Crithidia stage Rhodnius,
o Undulating membrane: half of the Panstrong
body length ylus
4. Trypomastigote Trypanos Gambian or Tsetse fly, Epimastigo
o Have flagellum and elongated spindle oma West Glossina te and
shape body gambiens African spp. Trypomasti
o Also known as Trypanosoma stage e Sleeping gote only
o The kinetoplast is near, the posterior Sickness
end of the body and the flagellum lyze Trypanos Rhodesian
attached to the cell body. oma or East
rhodesie African
nse Sleeping
Sickness

1
CLINICAL PARASITOLOGY
Introduction (WEEK 5 / LEC)
1st SEM, 2021
LIFE CYCLE OF TRYPANOSOMA CRUZI  Laboratory tests:
Intracellular parasite
1. Stained smear
o Giemsa staining
o Demonstration of Trypomastigote

2. Blood Cultures
o NNN medium (Novey-McNeal-Nicolle)
,
3. Xenodiagnosis
o use of laboratory animal

4. Serologic test (IFA, CFT, IHA, ELISA)


o Dot-immunobinding: small amounts of
sample is used

5. Molecular testing (PCR)


Trypanosoma cruzi o amplify DNA from kinetoplast

Pathology  Treatment:
 “Chagas’ disease” or American o Nifurtimox and benznidazole
trypanosomiasis  Prevention and Control
 usually serious and fatal in young children o vector control (insecticide spraying)
o screening and sterilization of
 “Chagoma”
transfusion blood
o inflammation at the site of inoculation
o health education
o small, painful, reddish erythamotous
nodule
LIFE CYCLE OF TRYPANOSOMA BRUCEI COMPLEX
1. Asymptomatic
2. Acute trypanosomiasis
 Generalized lymphadenopathy
 “Romaña’s sign” – conjuctivitis
and unilateral edema of the
eyelids
3. Chronic trypanosomiasis
 No characteristic symptom and
may last for 20 years or more
cardiomegaly, mega esophagus
and megacolon these advanced
conditions can lead to death

 Infective stage to vector:


o Trypomastigote Trypanosoma brucei complex
 Infective stage to man: Pathogenesis:
o metacyclic Trypomastigote
 Specimen: Chancre
o blood, CSF, fixed lymph node tissues o Earliest sign of African trypanosomiasis
and lymph juices. o Hard, painful lesion at the site of inoculation
o Surrounded by a white halo at the bite site

2
CLINICAL PARASITOLOGY
Introduction (WEEK 5 / LEC)
1st SEM, 2021

Trypanosoma brucei complex

Winterbottom’s Sign
A. Gambian trypanosomiasis
1. Acute:  Treatment: effective on earlier stages
o Fever, headache, joint and muscle pain, o Suramin and Pentamidine
tachychardia, dizziness and rashes o Melasorprol and tryparsamide (w/ CNS
o “Winterbottom’s sign” – enlargement of involvement)
the posterior cervical lymph node and o DL-alpha-difluoromethylornithine
have a ripe plum consistency. (DFMO, Eflornithine)

2. Chronic: with CNS invasion  Prevention and Control


o Severe headache, alternately morose and o Control of tsetse flies (traps, screens,
excitable and lack interest in work insecticides)
o Somnolence o Reduction of pool of human infection
o Tremors and “Kerandel’s sign” or (diagnose as many as individuals as
hyperesthesia and inversion of sleep cycle possible)
can be observed o Trimming of bushes

B. Rhodesian trypanosomiasis Leishmania spp.


o More rapid and fatal than Gambian
trypanosomiasis Etiologi Disease Vector Stages
o CNS involvement appear early c Agent exhibited
o Neurologic deterioration is rapid Leishma Cutaneous Sandfly I. Vector:
o Subsenquent kindey damage and ina leishmanias vectors Amastigote
myocarditis tropica is (Phleboto (reticuloendot
mus spp.) helial system)
 Specimen: Leishma American
o Blood, CSF and lymph juices nia or
 Laboratory tests: brazilie Mucocutan
nsis eous I. host:
1. Wet smear: presence of live parasite Leishmania Promastigote
2. Stained smear – Giemsa staining: sis (midgut and
demonstration of trypomastigote proboscis)
3. Serologic test: Leishma Visceral
a. IFA nia Leishmania
b. ELISA donova sis/ Kala-
c. Indirect hemeagglutination ni azar/
Dumdum
fever

3
CLINICAL PARASITOLOGY
Introduction (WEEK 5 / LEC)
1st SEM, 2021
ETIOLOGIC AGENT OTHER NAME
Leishmania tropica Old world leishmaniasis,
Oriental sore,
Cutaneous
leishmaniasis, Jericho
boil, Baghdad boil, Delhi
boils
Leishmania braziliensis New world
leishmaniasis, chiclero Leishmania braziliensis complex
ulcer, espundia, forest
yaws, uta Pathology
B. American or Mucocutaneous Leishmaniasis
Leishmania donovani Kala-azar, dum dum
o “Espundia”- metastatic spread of lesion to
fever
oronasal and pharyngeal mucosa
o “Tapir nose”– disfiguring leprosy-like tissue
LIFE CYCLE OF LEISHMANIA SPP.
destruction and swelling
o “Chiclero ulcer”– erosion of the pinna of the
ear

Leishmania tropica complex

Pathology Leishmania donavani complex


A. Cutaneous Leishmaniasis
o Skin ulcer (leaving an ugly scar on healing) Pathology
o Painless lesions C. Visceral Leishmaniasis
o Diffuse case: resembles “leprematous leprosy” • Kala-azar or Dumdum fever
o Lesions do not heal spontaneously and tend to • Twice-daily elevation of fever: prominent
relapse after treatment finding
• Hepatosplenomegaly and cachexia
• Parasites are numerous in reticuloendothelial
cells of the spleen, liver, lymph nodes, bone
marrow and other organs.
• Advanced stages of disease result in kidney
damage and granulomatous areas of skin
• FATAL in a matter of weeks

4
CLINICAL PARASITOLOGY
Introduction (WEEK 5 / LEC)
1st SEM, 2021
Leishmania spp.

 Infective Stage to Man:


o promastigote
 Infective Stage to vector:
o amastigote
 Specimen:
o Blood and Tissue sample

Diagnostic Tests
1. Biopsy
o Cutaneous: skin
o Visceral: bone marrow, spleen or bone
marrow
2. Giemsa-stained slides:
o aspiration fluid underneath the ulcer bed,
blood, bone marrow, lymphnode aspirates
3. Serologic Test
o Complement Fixation Test
o Montenegro’s intradermal test
o IFA
o Counter current electrophoresis
techniques

 Treatment:
 Pentavalent antimonials: sodium
stibogluconate and n-methyl-glucamine
antimonite
 Second line drugs
o Amphotericin B
o pentamidine (kala-azar)
o metronidazole
o nifurtimox

 Prevention and Control


o Skin lesions must be protected from
insect bites
o Health education

5
CLINICAL PARASITOLOGY
TREMATODES ( LEC & LAB)
1st SEM, 2021
TREMATODES (Flukes) ○
Schistosoma mansoni
General Characteristics: ○
Schistosoma haematobium
● Hermaphroditic (Except for Schistosoma spp.) ○
Schistosoma mekongi
● All eggs are operculated ○
Schistosoma interculatum
● Lack respiratory system Fasciola hepatica
● Excretory system are governed by flame cells Also known as “SHEEP LIVER FLUKE” or “TEMPERATE
and excretory tubules LIVER FLUKE”
● Incomplete digestive system Habitat liver and bile ducts
● Self fertilization
● ADULT WORM: Leaf like or lancet like Infective Stage Metacercaria
● Sexual organs are highy developed
● Oral suckers (used for feeding), Ventral sucker Diagnostic Stage Operculated ova
(used for attachment), Genital sucker
● Need 2 intermediate host Infection Fascioliasis
○ 1st IH: Snail
1st IH Lymnea spp (Lymnea
○ 2nd IH: Another snail, aquatic
philippinensis, Lymnea
vegetation/fruit, freshwater fish or
auricularia rubiginosa)
crustacean
● Do not possess anus 2nd IH Ipomea obscura, Nasturtium
● Adult stages are found in man & animals officinale (Water cress)
● Larval stages are found in the intermediate
host Final Host Sheep, cattle
● Nervous system is governed by ganglia
● INFECTIVE STAGE: Metacercaria Accidental Host Man
● MODE OF TRANSMISSION: Oral fecal route

Life Cycle
Operculated ova → Miracidium → Infect the snail (1st
IH) → Transforms inside the snail → Mother Redia
(Redia I) → Daughter Redia (Redia II) → Cercaria (will
go out the body of the snail → 2nd IH → Metacercaria
(INFECTIVE STAGE) → Man → Adult worms
For Schistosoma: Cercaria → Schistosomulum →
Adult worm
List of Trematodes
● LIVER FLUKES
○ Fasciola hepatica
○ Fasciola gigantica
○ Clonorchis sinensis
○ Opisthorchis felineus
○ Opisthorchis viverrini
● INTESTINAL FLUKES
○ Fasciolopsis buski PATHOLOGY
○ Echinostoma ilocanum ● ACUTE STAGE: Affect intestinal wall
○ Heterophyes heterophyes ○ SYMPTOMS: Necrotic lesions,
● PANCREATIC FLUKE Hepatomegaly, fever with eosinophilia
○ Eurytrema pancreaticum ● CHRONIC STAGE: Infect bile ducts
● LUNG FLUKE ○ SYMPTOMS: Severe jaundice,
○ Paragonimus westermani obstruction and abscess formation,
● BLOOD FLUKES (Schistosoma) can be ectopic.
○ Schistosoma japonicum
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CLINICAL PARASITOLOGY
TREMATODES ( LEC & LAB)
1st SEM, 2021
SYMPTOMS AND DIAGNOSIS Life Cycle
● Symptoms:
○ Biliary colic
○ Jaundice
○ Abdominal pain
○ Cholecystitis
○ Cholelithiasis
○ Bloody diarrhea
○ Liver cirrhosis
● Diagnosis:
○ Stool examination
○ Concentration Technique
○ Serological Test
○ Radiological test
○ PCR
Fasciola gigantica
Known as “GIANT LIVER FLUKE” or “TROPICAL LIVER
FLUKE” SYMPTOMS AND DIAGNOSIS
● Symptoms:
○ Fatigue
○ Weakness
○ Weight loss
○ Hepatomegaly
○ Liver cirrhosis
○ Eosinophilia
Clonorchis sinensis ○ Cholangiocarcinoma
Known as “CHINESE LIVER FLUKE” or “ORIENTAL LIVER ● Diagnosis:
FLUKE” ○ Stool examination
○ String test/ Entero test
Habitat Liver, bile ducts and gallbladder ○ Complement fixation
○ Intradermal test
Infective Stage Metacercaria

Diagnostic Stage Mature ova Opisthorchis felineus


Known as “CAT LIVER FLUKE”
Infection Clonorchiasis Final Host Cat
MOT Ingestion of 2nd IH Accidental Host Man
1st IH Bulimus fuchsiana, Alocinma 1st IH Bulimus tentaculata, Bithymia
sp., Parafossarulus sp.
2nd IH Freshwater fish (Tinca tinca,
2nd IH Ctenopharyngodon idaellus, Barbus barbus)
Cobitidae fishes

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CLINICAL PARASITOLOGY
TREMATODES ( LEC & LAB)
1st SEM, 2021
Opisthorchis viverrini Anterior end of adult Fasciolopsis buski
Known as “SOUTHEAST ASIAN LIVER FLUKE”
Can cause gallstone formation in man

Fasciolopsis buski
Known as “Large or giant intestinal fluke”
Egg of Fasciolopsis buski
Disease Fasciolopsiasis
(Eggs are ellipsoidal with a thin shell and a usually
Habitat Intestine (Duodenum & Jejunum) small, indistinct operculum. In this particular egg, the
operculum is open)
Definitive Host pig & humans SYMPTOMS AND PATHOLOGY
● Symptoms:
1st IH snail (Segmentina / Hippeutis) ○ Colic
○ Diarrhea
2nd IH water chestnuts & lotus (Trapa ○ Vomiting
bicornis, Eliocharis tuberosa, ○ Edema
Ipomea obscura) ● Pathology:
○ Intestinal obstruction
Infective Stage metacercariae ○ Intoxication
○ Vitamin B12 malabsorption
Lab. Diagnosis eggs in stool
Paragonimus westermani
Life Cycle Known as “Oriental Lung Fluke”
Disease Paragonimiasis, pulmonary
distomiasis, lung fluke disease,
Parasitic hemoptysis

Habitat Lungs
Portal of Entry Mouth

Definitive Host humans & a variety of carnivores

1st IH freshwater snail (Antemelania


aspirate, Antemalania ductylus)
Adult fluke of Fasciolopsis buski 2nd IH freshwater crab (Parathelphusa
philippina) or crayfish (Cambarus,
Astacus)

Source of consumption of raw or


Infection undercooked infected freshwater
crustaceans

Infective Stage metacercariae

Lab. Diagnosis eggs in sputum & stool

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CLINICAL PARASITOLOGY
TREMATODES ( LEC & LAB)
1st SEM, 2021
Morphology of Adult Paragonimus westermani BLOOD FLUKES (Schistosoma spp.)

Schistosoma japonicum
Also known as “ORIENTAL BLOOD FLUKE”
Disease Schistosomiasis, Katayama fever,
Yangtze Valley River fever,
Hankaw fever

Habitat veins of small intestine

MOT skin penetration

Definitive Host humans, dogs, cats, horses, pigs,


cattle, deer & rodents
Egg of P. westermani (The average egg size is 85 µm
by 53 µm (range: 68 to 118 µm by 39 to 67 µm). They Intermediate snail (Oncomelania hupensis
are yellow-brown, ovoidal or elongate, with a thick Host quadrasi)
shell, and often asymmetrical with one end slightly
flattened. At the large end, the operculum is clearly Infective Stage cercariae
visible. The opposite (abopercular) end is thickened.
Lab. Diagnosis eggs in stool and liver biopsy
The eggs of P. westermani are excreted
unembryonated)

(Adult: 2mm)
SYMPTOMS AND PATHOLOGY
● Symptoms: Oncomelania hupensis spp.
○ Chest pain
○ Hemoptysis
○ Eosinophilia
○ Sputum rusty brown
○ Fever
○ Sweating
● Pathology:
○ Lung abscess
○ Abscess in ectopic sites
( Subcutaneous Creeping Eruption)
○ Toxemia
○ Jacksonian epilepsy
DIAGNOSIS
● Stool examination
● Concentration exam
● Sputum analysis
○ 3% NaOH + Sputum → Centrifuge S. japonicum egg ( typically oval or subspherical, and
(vortex machine) à Examine sediment has a vestigial spine (smaller than those of the other
● Chest x-ray species)
● Serological test
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CLINICAL PARASITOLOGY
TREMATODES ( LEC & LAB)
1st SEM, 2021
CERCARIA Schistosoma mansoni
Also known as “MANSON’S BLOOD FLUKE”(smallest
blood fluke)
Disease Schistosomiasis, intestinal
schistosomiasis, bilharziasis “snail
fever”

Habitat veins of large intestine

MOT skin penetration

Definitive Host humans, baboons & rodents

Intermediate snail (Biomphalaria sp &


Host Tropicorbis sp)

Infective Stage cercariae

Lab. Diagnosis eggs in stool, rectal or liver


biopsy

SYMPTOMS AND PATHOLOGY


● Symptoms: Life Cycle
○ Dermatitis: Cercarial itch, Swimmer’s
itch, Gulf coast itch, Clam diggers itch\
○ Pneumonitis
○ Weakness
○ Trauma in the intestinal wall
○ Hepatitis
○ Eosinophilia
○ Toxemia 8. Adults in copula can lay
eggs in ectopic site (results in tubercle
formation)
○ Ascites
○ Hepatosplenomegaly

DIAGNOSIS
● Stool examination
● Kato-Katz
● COPT (Circum Oval Precipitin Test)
● Culture Technique (Faust and Meleney Egg
Hatching Technique)
● Serological Test
○ Complement Fixation
○ Cercarial Agglutination
○ ELISA Biomphalaria spp.
○ IHAT
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CLINICAL PARASITOLOGY
TREMATODES ( LEC & LAB)
1st SEM, 2021
Schistosoma haematobium
Disease Urinary schistosomiasis,
schistosomal hematuria, urinary
bilharziasis

Habitat veins of urinary bladder

MOT skin penetration

Schistosoma mansoni eggs (large (length 114 to 180 Definitive Host humans, monkeys & baboons
µm) and have a characteristic shape, with a prominent
LATERAL SPINE near the posterior end. The anterior Intermediate snail (Bulinus, Physopsis, and
end is tapered and slightly curved. When the eggs are Host Biomphalaria sp)
excreted, they contain a mature miracidium)
Infective Stage cercariae

Lab. Diagnosis eggs in urine; cystoscopy

Bulinus spp.

S. haematobium eggs (large and have a prominent


TERMINAL SPINE at the posterior end)

Male and female schistosomes

Adult male

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CLINICAL PARASITOLOGY
TREMATODES ( LEC & LAB)
1st SEM, 2021

S.haematobium (adult schistosomes live in pairs in


the pelvic veins (especially in the venous plexus
surrounding the bladder); males are 10-15 mm in
length by 0,8-1 mm in diameter, and have a ventral
infolding from the ventral sucker to the posterior end
forming the gynecophoric canal. Adult male with
female in the copulatory groove)

SYMPTOMS AND PATHOLOGY


● Lesions in urinary bladder (Hematuria)
● Burning sensation when urinating
● Develop Urogenital malignant tumor

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CLINICAL PARASITOLOGY
DIAGNOSTIC PARASITOLOGY ( LEC & LAB)
1st SEM, 2021
Laboratory Diagnosis
● accurate diagnosis of parasitic infections can
help decrease the prevalence and incidence of
a parasitic infection
○ Confirm clinical impression
○ Rule out diagnosis
○ Aid a clinician in the choice of proper
medication
○ Help in monitoring the effect of
treatment regimen
● Diagnostic parasitology is done by:
○ A. Demonstration of parasites (e.g.,
eggs, larvae, adults, cysts, oocysts,
trophozoites)
○ B. Detection of host immune
response to the parasites (e.g., Abs
and Ags)
Outline of Techniques
● Direct Fecal Smear No. of microns = (no. of stage micrometer units X
● Kato-thick Smear 1000) / (no. of ocular micrometer units)
● Concentration = (0.4 x 1000) / 60
○ Sedimentation Techniques = 6. 67 um or 7 um
○ Floatation Techniques Note: Suggested ranges of the micron value per ocular
● Stool Culture unit by magnification: (Zeibig, 2013)
● Egg counting procedures 10x: 7.5-10 um
● Perianal Swab 40x: 2.5-5 um
● Staining stool specimen 100x: 1 um
Macroscopic Examination of Stool Direct Fecal Smear (DFS)
● Consistency ● Routine method of stool examination
○ reflects the level of hydration ● Employs use of approx. 2 mg of stool and 0.
○ gives an indication as to which 85% NSS
organisms are present ● Primarily useful in detection of motile
● Color protozoan trophozoites
● Gross examination ● Trophozoites are pale and transparent
○ tapeworm proglottids ● Nair’s buffered methylene blue (BMB) –
○ adult nematodes (Ascaris or demonstrate nuclear morphology of
Enterobius) trophozoites
○ a. Entamoeba cytoplasm: light blue
Ocular micrometer ○ b. Entamoeba nucleus : dark blue
● specially designed ocular piece equipped with ● Lugol’s iodine – temporary stains nuclei of
measuring scale protozoan cysts
● Must be calibrated to ensure accurate ○ cytoplasm : golden yellow
measurement ○ nucleus: pale and refractile
● Expressed in microns (µ or µm) defined as ○ glycogen: deep brown
0.001 [10-3] millimeter, or 10-6 meter ● Light infections may not be detected
● Calibration is aided with the use of a stage
micrometer containing a calibrated scale
divided into 0.01-mm units.
● The ocular micrometer is a disk equipped with
a line evenly divided into 50 or 100 units

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CLINICAL PARASITOLOGY
DIAGNOSTIC PARASITOLOGY ( LEC & LAB)
1st SEM, 2021
Kato Thick Smear B. Floatation Procedures
● Employs use of 50-60 mg of stool (size of two ● Zinc Sulfate (ZnSO4) Floatation
mongo beans) ○ 33% ZnSO4 with specific gravity of
● Uses cellophane paper soaked in a mixture of 1.18-1.20
glycerine and malachite green solution ○ If parasites are exposed to high
● Simple and economical specific gravity, distortion and
● Very good in detecting eggs with thick shells shrinkage of protozoan cysts and
(e.g., Ascaris and Trichuris) but not thin shells thinwalled nematode eggs may occur.
● Usefulness is limited in diarrheic and watery ● Brine Floatation
stools ○ uses Table salt solution
● Not able to detect protozoan cyst and ○ no need for centrifugation since
trophozoite helminth eggs rise from the surface of
the solution.
○ Schistosoma become badly shrunken
○ NOT useful for operculated eggs like
Clonorchis, Opistorchis and
heterophyids because these do not
float in brine solution.
Concentration Techniques ● Sheather’s Sugar Floatation
● Useful in cases of light infections ○ employs use of boiled sugar solution
preserved with phenol
A. Sedimentation Procedures ○ best for recovery of coccidian oocysts
● Acid Ether Concentration Technique (AECT) (e.g., Cryptosporidium, Cyclospora
○ 40% HCl → dissolves albuminous and Isospora)
material ○ better visualization can be
○ Ether → dissolves neutral fats appreciated through the use of a
■ recommended for recovery phase-contrast microscope
Trichuris, Capillaria and
trematode eggs specially
Schistosoma.
● Drawbacks: loss of parasite to the plug of
debris and possible destruction of protozoan
cyst
● Formalin Ether Concentration Technique
(FECT) Stool Culture Methods
○ 10% Formalin as preservative ● Useful for hookworm identification
○ Ether → dissolves neutral fats (highly ● Stools positive for hookworm ova and/or
explosive and flammable) Strongyloides rhabditiform larva can be
● Ethyl acetate as alternative to ether (not as cultured until the filariform larvae develop
efficient as ether in the extraction of fat or ● Coproculture
mucoidal material from the stool) - more ○ positive stools mixed with moistened
efficient in recovering cestode eggs and soil and granulated charcoal
Giardia cysts ○ Larvae are harvested using Baermann
procedure

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CLINICAL PARASITOLOGY
DIAGNOSTIC PARASITOLOGY ( LEC & LAB)
1st SEM, 2021
Baermann Technique Kato- Katz Method or Cellophane Covered Thick
Smear
● Uses a measured amount of stool which has
been sieved through a wire mesh and pressed
under cellophane paper soaked in malachite
green solution
● Uniform amount of stool is examined using a
template with a uniform sized hole in the
middle
● Consistency is the main determinant of the
sensitivity of this technique
● For ID of Schistosoma ova, 1% eosin can be
layered over the cellophane paper

● Harada-Mori or the Test tube Culture Method


○ employs use of test tubes and filter
paper strips
○ also used for cultivation of intestinal
protozoan
○ Filariform larva will move downwards
against the upward capillary
movement of water and can be
recovered from the water at the
bottom of the tube
○ Strongyloides larvae move upwards
and accumulate at the upper end of
the filter paper strip

7cc of boiled water or distilled water

Egg Counting Procedures


● Used to correlate the severity of clinical
disease with the intensity of infection or
worm burden
○ Kato-Katz Method or Cellophane
Covered Thick Smear
○ Stoll Egg Count

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ARAULLO, BAIS, BALATBAT, BALUYUT, BRIONES, BUNDALIAN, DE CASTRO, DE LEON, DELOS TRINOS, DURAN, MAGDALERA, MENDOZA, RASING, RODRIQUEZ, TOLENTINO
CLINICAL PARASITOLOGY
DIAGNOSTIC PARASITOLOGY ( LEC & LAB)
1st SEM, 2021
Stoll Egg Count
● 0.1 N NaOH and a stool displacement flask
calibrated at 56 mL and 60 mL
● Sodium hydroxide serve as stool diluent, it
saponifies fat and free eggs from fecal debris
● Uses Stoll pipettes calibrated at 0.075 mL and
0.15 mL to measure amount of diluted stool

Perianal Swab (Cellulose Tape or Scotch Tape Method


● Used to recover eggs of E. vermicularis and
Taenia spp.
● In some laboratories, a drop of toluene or
xylene solution helps in the visualization of
eggs

Staining of Stool Samples


● Performed specifically for the examination of
the nuclear characteristics of amoeba.
● Also useful for ID of other intestinal
protozoans such as Balantidium coli and
Giardia spp.
○ Iron- hematoxylin
○ Trichome
○ Chlorazol Black E
○ Kinyoun staining for coccidians
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ARAULLO, BAIS, BALATBAT, BALUYUT, BRIONES, BUNDALIAN, DE CASTRO, DE LEON, DELOS TRINOS, DURAN, MAGDALERA, MENDOZA, RASING, RODRIQUEZ, TOLENTINO
CLINICAL PARASITOLOGY
CESTODES ( LEC & LAB)
1st SEM, 2021
CESTODES (Flukes) Diphyllobothrium latum
General Characteristics: Disease Diphyllobothriasis; fish
● Flat, ribbon-like, chalk-white tapeworm infection; broad
● Hermaphrodite tapeworm infection
● Do not possess circulatory system
● Do not possess digestive tract Site in host small intestines
● Acquire food by means of osmosis
● Voracious appetite Portal of entry mouth
● Excretory system governed by flame cells
● Nervous system governed by ganglia Definitive host human, dogs, cats

TAPEWORM STRUCTURE 1st IH crustaceans (Cyclops or


Diaptomus)

2nd IH freshwater fish (carp, salmon)

Infective stage plerocercoid larvae

Sources of plerocercoid in freshwater fish


infection

Lab. Diagnosis eggs in stool

GROUPS
● Pseudophyllidean (aka FAKE TAPEWORM)
Scolex Almond shape/ spoon/
spatula shape with sucking
grooves

Proglottids Anapolytic (they contain Eggs of D. latum: oval or ellipsoidal, with at one end
uterine pore: secrete eggs) an operculum that can be inconspicuous. At the
opposite (abopercular) end is a small knob that can be
Gravid Proglottids All reproductive organs are barely discernible.
intact (MOST MATURE)

Egg/Ova Ovoidal shape; OPERCULATED

Intermediate Host 2

● Cyclophyllidean (aka TRUE TAPEWORM)


Scolex Quadrate shape; possess 4 D. latum scolex(LEFT) and gravid proglottids (RIGHT)
cup like suckers

Proglottids Apolytic (no uterine pore)

Gravid Proglottids Only uterus

Egg/Ova Spherical in shape; NON


OPERCULATED Proglottids of D. latum: broader than it is long; size 2
to 4 mm long by 10 to 12 mm wide; uterus coiled in
Intermediate Host 1 rosette appearance; genital pore at the center of the
proglottid.
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ARAULLO, BAIS, BALATBAT, BALUYUT, BRIONES, BUNDALIAN, DE CASTRO, DE LEON, DELOS TRINOS, DURAN, MAGDALERA, MENDOZA, RASING, RODRIQUEZ, TOLENTINO
CLINICAL PARASITOLOGY
CESTODES ( LEC & LAB)
1st SEM, 2021
Clinical Manifestations Taenia Saginata
● Diphyllobothriasis can be a long-lasting
Disease Solitario Disease
infection (decades).
● Most infections are asymptomatic. Common Name Beef tapeworm
● Manifestations may include abdominal
discomfort, diarrhea, vomiting, and weight Habitat duodenum
loss.
● Vitamin B12 deficiency with pernicious Infective Stage Cysticercus bovis larva
anemia may occur.
● Massive infections may result in intestinal Diagnostic Ova in stool, gravid segment
obstruction. Stage

Diagnostic Findings MOT oral fecal route


● Microscopic examination of stool
Final Host man
Treatment Intermediate Cow, cattle or carabao
● Praziquantel: is the drug of choice. Host
Alternatively, Niclosamide can also be used to
treat diphyllobothriasis.
LIFE CYCLE
Sparganum mansoni
Disease Sparganosis

Accidental Host man

Final Host Frogs, snakes

1st IH Cyclops

2nd IH freshwater fish

Habitat Skin, subcutaneous tissue,


Muscle

Infective Stage Procercoid/ Plerocercoid larva

Diagnostic Plerocercoid larva


Stage

MOT ingestion of cyclops

Clinical Manifestations
● Localized inflammation
● Cerebral/Ocular sparganosis
● Nodule formation in vital organs
● Toxemia

Diagnosis Taeniid eggs: rounded or subspherical, diameter 31 to


● Muscle/ tissue biopsy 43 µm, with a thick radially striated brown shell. Inside
● X-ray, CT Scan, MRI each shell is an embryonated oncosphere with 6
hooks (hexacanth embryo)

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ARAULLO, BAIS, BALATBAT, BALUYUT, BRIONES, BUNDALIAN, DE CASTRO, DE LEON, DELOS TRINOS, DURAN, MAGDALERA, MENDOZA, RASING, RODRIQUEZ, TOLENTINO
CLINICAL PARASITOLOGY
CESTODES ( LEC & LAB)
1st SEM, 2021

Taenia egg: Note the thick, "striated" shell and several


of the larval hooks; approximate size = 40 µm.

T. solium: scolex (LEFT) gravid proglottid (RIGHT)

T. Saginata gravid proglottid: has 15 to 30 main


uterine branches on each side of central stem;
proglottids are much longer than wide
Symptoms and Pathology
Scoleces of Taenia saginata and Taenia solium: Scolex
● Patient exhibit voracious appetite
of T. saginata has 4 suckers and no hooks. T. solium
● Vague abdominal pain
has 4 suckers in addition to a double row of hooks.
● Peptic ulcer like symptoms
● Intestinal obstruction
Symptoms and Pathology
● Intoxication
● Patient exhibit voracious appetite
● Anal pruritus
● Vague abdominal pain
● Obstruction of bile duct
● Muscle pain and atrophy
Diagnosis
● Hysteria
● Ova in stool
● Blurring and loss of vision
● Gravid segment using Rapid Slide Test
● Tachycardia
● Scotch Tape swab
CYSTICERCOSIS
Taenia Solium
● Degree of infection and severity depends on:
Disease pork tapeworm infection ○ Organ invaded
○ Number of cysticercoid larva
Site of Host small intestines ● Cysticercoid larva can cause necrosis and
fibrosis
Portal of Entry mouth ● There could be 4-7 adult T. solium in one
patient
Definitive Host human

Intermediate Host pig Diagnosis


● Ova in stool
Infective Stage Cysticercus cellulosae ● Gravid segment using Rapid Slide Test
● Radiological examination
Sources of Infection cysts in pork; autoinfection ● Muscle biopsy
● ELISA
Lab. Diagnosis segments and eggs in stool;
Scotch tape swab

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ARAULLO, BAIS, BALATBAT, BALUYUT, BRIONES, BUNDALIAN, DE CASTRO, DE LEON, DELOS TRINOS, DURAN, MAGDALERA, MENDOZA, RASING, RODRIQUEZ, TOLENTINO
CLINICAL PARASITOLOGY
CESTODES ( LEC & LAB)
1st SEM, 2021
Infective Stage cysticercus larva
Hymenolepis nana
Common Name Dwarf tapeworm Sources of Infection cysts from insects
Smallest tapeworm of man
Lab. Diagnosis eggs in stool
Habitat upper ileum

Infective Stage Embryonated ova, cysticercoid


larva

Diagnostic Stage Ova in stool

MOT Ingestion of ova or larva Egg of Hymenolepis diminuta: round or slightly oval,
size 70 - 86 µm X 60 - 80 µm, with a striated outer
Final Host man, rats membrane and a thin inner membrane. The space
between the membranes is smooth or faintly granular.
Intermediate Fleas (Ctenocephalides sp.) or The oncosphere has six hooks.
Host Flour beetles (Tenebrio sp.)

2 LIFE CYCLE
● Indirect
○ Infective stage is cysticercoid larva
○ Involvement of Intermediate host
● Direct Mature proglottids of Hymenolepis diminuta
○ Infective stage is ova Causal Agents
○ No involvement of Intermediate host ● Hymenolepiasis is caused by two cestodes
Symptoms and Pathology (tapeworm) species, Hymenolepis nana (the
● Asymptomatic in light infection dwarf tapeworm,) and Hymenolepis diminuta
● Diarrhea (rat tapeworm). Hymenolepis diminuta is a
● Eosinophilia cestode of rodents infrequently seen in
● Headache/ Dizziness humans and frequently found in rodents.
● Patient exhibit voracious appetite Geographic Distribution
● Hymenolepis nana is the most common cause
Diagnosis of all cestode infections, and is encountered
● Ova in stool worldwide. In temperate areas its incidence is
higher in children and institutionalized groups.
Treatment Hymenolepis diminuta, while less frequent,
● Praziquantel has been reported from various areas of the
world.
Hymenolepis diminuta Life Cycle
Disease Hymenolepiasis;
rat tapeworm infection

Site of Host small intestines

Portal of Entry mouth

Definitive Host human, mice and rats

Intermediate Host insects (rat and mouse flea,


the flour moth and flour
beetle)

____________________________________________________________________________________ 4
ARAULLO, BAIS, BALATBAT, BALUYUT, BRIONES, BUNDALIAN, DE CASTRO, DE LEON, DELOS TRINOS, DURAN, MAGDALERA, MENDOZA, RASING, RODRIQUEZ, TOLENTINO
CLINICAL PARASITOLOGY
CESTODES ( LEC & LAB)
1st SEM, 2021
Clinical Features
● Hymenolepis nana and H. diminuta infections
are most often asymptomatic. Heavy
infections with H. nana can cause weakness,
headaches, anorexia, abdominal pain, and
diarrhea.
Diagnostic Findings Adult tapeworm of Dipylidium caninum. The scolex of
● Microscopic examination of stool the worm is very narrow and the proglottids, as they
mature, get larger.
Treatment
● Praziquantel: drug of choice Life Cycle
Dipylidium caninum
Disease Dipylidiasis
dog tapeworm infection

Site of Host small intestines

Portal of Entry mouth

Definitive Host dog & cat (or humans)

Intermediate Host larval flea

Infective Stage cysticercoid larva

Sources of Infection flea and louse

Lab. Diagnosis eggs in stool or egg packets Clinical Features


in stool, proglottid ● Most infections with Dipylidium caninum are
asymptomatic. Pets may exhibit behavior to
relieve anal pruritis (such as scraping anal
region across grass or carpeting). Mild
gastrointestinal disturbances may occur. The
most striking feature in animals and children
consists of the passage of proglottids. These
Egg packets of Dipylidium caninum: Proglottids of can be found in the perianal region, in the
Dipylidium caninum contain characteristic egg packets feces, on diapers, and occasionally on floor
that are round to ovoid and contain 5 to 15 covering and furniture. The proglottids are
(sometimes more) eggs each. motile when freshly passed and may be
mistaken for maggots or fly larvae.
Diagnostic Findings
● Microscopic examination

Treatment
● Treatment for both animals and humans is
Proglottids of D. caninum: barrel-shaped proglottids simple and very effective. Praziquantel is
(average mature size 12 mm × 3 mm) have two genital given either orally or by injection (pets only).
pores, one in the middle of each lateral margin.
Proglottids may be passed singly or in chains, and
occasionally may be seen dangling from the anus.
Proglottids are much longer than broad.

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ARAULLO, BAIS, BALATBAT, BALUYUT, BRIONES, BUNDALIAN, DE CASTRO, DE LEON, DELOS TRINOS, DURAN, MAGDALERA, MENDOZA, RASING, RODRIQUEZ, TOLENTINO
CLINICAL PARASITOLOGY
CESTODES ( LEC & LAB)
1st SEM, 2021
Echinococcus granulosus ADDED NOTES:
Disease Echinococcosis, Differences between CESTODES, TREMATODES &
hydatid disease NEMATODES
Shortest of all tapeworms Cestodes Trematodes Nematodes

Habitat small intestine of dogs Shape Tape like Leaf like Elongated,
segmented unsegmented cylindrical,
Intermediate Host Sheep,goat, cat unsegmented

Infective Stage to Hydatid cyst Sexes Sexes NOT Sexes NOT Sexes are
dogs separate separate separate
Monoecious Monoecious Diecious
Infective Stage to ova Hermaphrod Schistosoma
ite
man
Head end Suckers, Suckers, No No suckers, no
Diagnostic Stage Hydatid cyst containing often with hooks hooks, well
hydatid sand hooks developed

Alimentary Absent Present, Present,


canal incomplete, no complete, anus
anus present

Body cavity Absent Absent Present

Classification of Cestodes Infecting Man


● Pseudophyllidean cestodes: possessing false
slit like grooves (bothria)
○ Adult worms in intestine:
Symptoms and Pathology
■ Diphyllobothrium latum (fish
● Enlarged abdomen
worm)
● Pressure on the organ leads to organ
○ Larval stages (Plerocercoid) in man:
malfunction Osseous cyst if found in bound
■ Sparganum mansoni
● Anaphylactic shock
■ Sparganum proliferum
Differences between Pseudophyllidean VS.
Diagnosis
Cyclophyllidean Cestodes
● Radiological examination
● Hydatid drill Pseudophyllidean Cyclophyllidean
● Exploratory puncture
● Casoni’s test Head Bears 2 slit like Bears 4 cup like
● Serological tests (IHA, IFA, EIA) grooves suckers

Uterus No branching, Branching may or


Treatment rosette shaped may not be
● Surgical removal of the cyst Type of cyst: convoluted tubule present
Unilocular, Osseus, Alveolar
● PAIR Treatment (Hibitane, 95% EtOH) Uterine pore Present Absent

Common Ventral, in the Lateral


genital pore midline

Eggs Operculated giving Not operculated,


rise to ciliated larvae do not give rise to
ciliated larvae

____________________________________________________________________________________ 6
ARAULLO, BAIS, BALATBAT, BALUYUT, BRIONES, BUNDALIAN, DE CASTRO, DE LEON, DELOS TRINOS, DURAN, MAGDALERA, MENDOZA, RASING, RODRIQUEZ, TOLENTINO
CLINICAL PARASITOLOGY
CESTODES ( LEC & LAB)
1st SEM, 2021

____________________________________________________________________________________ 7
ARAULLO, BAIS, BALATBAT, BALUYUT, BRIONES, BUNDALIAN, DE CASTRO, DE LEON, DELOS TRINOS, DURAN, MAGDALERA, MENDOZA, RASING, RODRIQUEZ, TOLENTINO

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