CLINICAL PARASITOLOGY  Vittaforma cornea

WEEK 8  Pleistophora spp.

SPOROZOA  Brachiola vesicularum
 Microsporidium spp.
(PLASMODIUM SPP. AND BABESIA SPP.)
 The protozoan parasites characterized by the Plasmodium spp.
production of spore like oocyts containing  Plasmodium falciparum- responsible for 90% of
sporozoites where known as sporozoa all human malaria cases
 They live intracellularly at least during their life  Plasmodium vivax- responsible for 90% of all
cycle and some stage in their life cycle they human malaria cases
possess a structured called as apical complex by  Plasmodium malariae
means of which they attached to and penetrate  Plasmodium ovale
to the host cells
 Plasmodium knowlesi
 The other name of sporozoa would be apical
complexa Babesia spp.

Classification of Protozoan Parasites  Babesia microti

 Babesia divergens
 Babesia bovis

MALARIA
 The name Malaria was given in the 18th
Century in Italy.
 Malaria from Italian word "mal'aria" which
means "bad air"
 Believed to be caused by emanation from the
marshy soil.
 Considered to be the most important parasitic
disease affecting man (Belizario, 2015)
Phylum Apicomplexa  Leading parasitic disease that causes mortality
 Babesia spp. worldwide
 Cryptosporidium hominis  Identified by WHO as one of the major
infectious disease threats along with HIV, AIDS
 Cyclospora cayetanesis
and tuberculosis
 Isospora belli
 Peak transmission of Malaria – beginning and
 Plasmodium spp.
end of rainy season.
 Toxoplasma gondii
 Primarily, Malaria is vector borne or arthropod
SPOROZOA borne.
 The protozoan parasite characterized by the
VECTOR
production of the spore-like oocyst containing
 female Anopheles mosquito
the sporozoites is known as the Sporozoa.
 female mosquitoes – bite/suck blood while
 They live intracellularly
male mosquitoes –acquire nutrients from fruits
 At some stage in their life cycle, they possess a
and flowers
structure called apical complex (important for
 Vector of Malaria: Anopheles minimus var.
attachment and penetration in cells).
flavirostris
Phylum Microspora  Other spp. under Anopheles family:
Anopheles litoralis
 Enterocytozon bineusi Anopheles maculates
 Encephalitozoon spp. Anopheles mangyamus

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 Mostly, the children and pregnant women are  Congenital malaria – natural form of
affected with malaria. merozoites induced malaria where the parasite
Children- chronic malaria may lead is transmitted transplacentally from the mother
to anemia, impaired physical and to the fetus.
mental growth and development.
LIFE CYCLE OF MALARIA PARASITE
Pregnant women- anemia is the
leading contributor of maternal
morbidity and mortality.
 Vector Biology: Anopheles flavirostris
 Aquatic Habitat: slow flowing streams; shaded
streams
 Adult biting: Night biting (indoor and outdoor)
 Adult resting: inside walls

a. Sporongony
 Sporogonic Cycle (sporogony)
 The sexual phase takes place in the female
Anopheles mosquito even though the sexual
HOST
forms of the parasite or the gametocytes are
 Final host: female Anopheles mosquito
originating in the human red blood cells.
The sexual cycle occurs in Anopheles
 Microgamete and macrogamete- they are
mosquito (invertebrate and definitive
produced in human body and those serve
host)
infective stage to the vector
 Intermediate host: Man
 The sexual phase it takes phase to the female
The asexual stage occurs in humans
anopheles mosquito making it as definitive host
(vertebrate and intermediate host)
of the parasite
INFECTIVE STAGES  It is the sexual cycle in the mosquito which
 sporozoites (man) leads to the formation of sporozoites
 gametocytes (mosquito)  Sporozoites- infective stage to humans
 bakit females lang ang kumakagat at hindi ang Union between the microgamete and
mga males it depends on the biological macrogamete (sex cells of Plasmodium
morphology of mosquito spp. developed in the RBC of humans).
 female mosquito- they are the ones who are Zygote -> ookinete -> oocyst
thriving with human blood Ruptured Oocyst -> release Sporozoites
 male mosquito- they prefer nutrition from  The maturation and fertilization takes place in
fruits or nectar of flowers mosquito giving rise to a large number of
sporozoites (sporos = seed)
SOURCE OF EXPOSURE TO INFECTION
 Hence, this phase of sexual multiplication is
 Vector borne (Arthropod borne) – also known
called sporogony
as introduced malaria
 Sporogony- sexual cycle in the mosquito which
OTHER MODES OF TRANSMISSION lead to the formation of the sporozoites which
 Imported malaria – acquired by visitors or is the infective stage of the parasite
residents of country with endemic disease. End product the sporozoites
 Transfusion malaria – associated with blood Sporozoites- infective stage to humans
transfusion from infected donors.  Also called as invertebrate, extrinsic and
 Mainline malaria – sharing of needles and exogenous phase (because it occurs outside the
syringes among drug users. human body)

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  In humans, Schizogony occurs in two locations:
RBC (erythrocytic schizogony) and in the liver
(exo-erythrocytic schizogony or tissue phase).
 Schizogony in liver is essential step before the
parasite can invade the erythrocyte it is called
as Pre-erythrocytic Schizogony.
 Products are merozoites
Sporozoite infect liver parenchymal
cells (since the detoxifying organ is the
liver, the sporozoites infect it)
->Schizont ->Rupture liver cells >
merozoites
The Mosquito Cycle (Sporogony)

 Exflagellating male gametocytes: the nuclear

material and cytoplasm of the male
gametocytes divides to produce 8
microgametes with long, actively motile, whip-
like filaments.
 The female gametocyte does not divide but
undergoes a process of maturation to become
the female gamete or macrogamete. It is
fertilized by one of the microgametes (male) to
produce the zygote.
 Ookinete: the zygote, which is initially a
motionless, round body, gradually elongates
becomes a vermicular motile (traveling Pre-erythrocytic (Tissue) Stage or Exoerythrocytic
vermicule) form with an apical complex
anteriorly.  The hepatocyte is distended by the enlarging
 Oocyst: rounded into a sphere with an elastic schizont and the liver cell nucleus is pushed to
membrane within which numerous sporozoites the periphery.
are formed.  These normally rupture in 6-15 days and
 Sporozoites: when the oocysts ruptures, the release thousands of merozoites into the blood
sporozoites enter into the hemocele or body stream.
cavity, from where some find their way to the  In the latent stage of Plasmodium vivax and
mosquito's salivary glands. Plasmodium ovale two kinds of sporozoites are
 The mosquito is now infective and when it feeds seen.
on humans, the sporozoites are injected into  Some multiply inside the hepatic cell to form
skin capillaries to initiate human infection. schizonts while others persist and remain
b. Schizogony (Pre-erythrocytic Cycle) dormant/resting stage
 Inside the human body  Hypnozoites (hypnos: sleep): resting forms in
 Asexual phase Plasmodium vivax and Plasmodium ovale
 In this stage, the malaria parasite multiplies by Dormant, exo-erthyrocytic forms and
division or splitting process – Schizogony may remain for quiet years.
 Schizo (split) gony (generation) Merozoites can go back into liver and
 Occurs in humans (it is vertebrate, intrinsic and rest and these are the dormant/resting
endogenous phase) making humans as the forms.
intermediate host. Some are activated to become
schizonts and release merozoites, which

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 will infect RBC producing clinical Merozoites are pear-shaped bodies,
relapse. about 1.5 um in length, possessing an
Clinical relapse is associated with apical complex (rhoptery). They attach
resting/dormant forms of parasite to the erythrocytes by their apex.
called Hypnozoites. Ring forms or young trophozoites: the
 In the case of P. falciparum and P. malariae, merozoite loses its internal organelles
initial tissue phase disappear completely and and appears as a rounded body having a
no hypnozoites are found. vacuole in the center with the
cytoplasm pushed to the periphery and
Schigony (asexual cycle)
the nucleus at one pole.
Malaria pigment or haemozoin
pigment: parasite feeds on the
hemoglobin of the erythrocyte but it
does not metabolize hemoglobin
completely and therefore, leaves
behind a hematinglobin pigment as
c. Schizogony (Erythrocytic Cycle)
residue.
 The merozoites will invade the RBCs while
some merozoites of Plasmodium vivax and Ring forms (early trophozoites)
Plasmodium ovale reinvades the liver cells
forming the hypnozoites.
Inside the RBCs they will develop to
become young trophozoites (ring
formations)
Mature trophozoites > Schizonts
>Ruptured schizonts > merozoites
Size 1/3 RBC Up to 1/3 1/3 RBC 1/3 RBC
Some proceed to the development as RBC
gametocyte. Shape Delicate Compact Very delicate Dense
ring ring ring ring

Chromatin Fine dot One Fine dots Dense,

mass frequently well-
often two defined
ring mass
Accole Sometimes None Frequently None
forms
Pigment None at Maybe None at this None at
this stage present stage this
stage
Multiple Sometimes Rare Frequently rare
parasitized with high
cells parasitaemia
Erythrocytic Stage
 The appearance of malaria pigments varies in
 The merozoites released by pre-erythrocytic different species as follows:
schizonts invade the red blood cell: P vivax: numerous fine golden-brown
The receptor for merozoites is dust-like particle
glycophorin, which is a major P. falciparum: few 1-3 solid blocks of
glycoprotein on the red cells. black pigment

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 P. malariae: numerous coarse dark - Scattered Scattered Aggregated Scattere
brown particles distributi fine dumps and in one or d coarse
P ovale: numerous blackish brown on particle rods two dumps particle
particles. Immature schizonts
 Amoeboid form or late trophozoite form: as
the ring form develops, it enlarges in size
becoming irregular in shape and shows
amoeboid motility.
 When the amoeboid form reaches a certain
stage of development, its nucleus starts dividing
by mitosis followed by a division of cytoplasm Size Almost Almost Almost Almost
to become mature schizonts or meronts. fills RBC fills RBC fills RBC fills RBC
 The merozoites invade fresh erythrocytes Shape Somewhat Compact Compact Compact
within which they go through the same process amoeboid
of development. Chromatin Numerous Few Irregular Few
 The rupture of the mature schizont releases irregular irregular masses irregular
large quantities of pyrogens. This is responsible masses masses masses
for the febrile paroxysms characterizing Pigment Scattered Scattered Single Scattered
malaria. (Erythrocytic Stage) dump
Febrile paroxysms- one of the Mature schizonts
distinguishing features of malaria. (on
and off fever)

Developing trophozoite

Size Fills RBC Nearly Nearly fills Fills ¾ RBC

fills RBC RBC
Shape Segmente Segment Segmented Segmented
d ed daisy
Size Large Small, but Small Small
head
appears
large Merozoi
relative to tes
size of rbc -range 14-24 6-12 8-32 6-12
Shape Very Compact, Compact compac -mean 16 8 24 8
irregular, often band with t -size Medium Large Small Large
amoeboi form cytoplasmi Pigment Aggregate Aggregat Aggregated Aggregated
d c d in ed in in centre in centre
vacuolatio centre centre (black) (dark
n (yellow (dark yellow
Chromati Doths or Prominent, Dots and Large brown) brown) brown)
n threads often as a threads irregula
band r dumps
GAMETOGONY
Pigment
 Sexually differentiated form
-texture Fine Coarse Coarse Coarse
 Development of gametocytes generally takes
-color Yellow Dark Black Dark
place within the internal organs and only the
brown brown yellow
brown mature forms appear in circulation.
-quantity Medium Abundant Medium Medium

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  The mature gametocytes are round in shape, Macrogametocytes (female)
except in P. falciparum, in which they are
crescent-shaped.
 In all species, the female gametocyte is larger
(macrogametocyte) than the male gametocyte
(microgametocyte).
 The gametocytes do not cause any clinical
illness in the host, but are essential for Time of 3-5 days 7-14 7-12 days 12-14
transmission of the infection. appearance days days
 Gametocyte- Infective stage to mosquito Number in Many Scantly Many Scantly
 A gametocyte concentration of 12 or more per bloodstream
cumm of blood in the human host is necessary Size ¾ fills RBC ½ to 2/3 Larger ½ to 2/3
for mosquitoes to become infected. fills RBC than RBC fills RBC
Shape Round or Round Crescentic- Round
Microgametocytes (male) oval compact sharply compact
compact rounded
or pointed
ends
Cytoplasm Dark blue Dark Dark blue Dark
blue blue
Chromatin Compact As for P. Compact As for P.
peripheral vivax masses vivax
Time of 3-5 days 7-14 7-12 days 12-14
mass near
appearance days days
centre
Number in Many Scantly Many Scantly
Pigment Small As for P. Black, rod- As for P.
bloodstream
masses vivax like vivax
Size ¾ fills RBC ½ to 2/3 Larger than Round
round granules
fills RBC RBC compact
periphery round
nucleus
Shape Round or Round Kidney- Round
oval compact shaped compact
compact bluntly COMPONENTS OF THE MALARIA LIFE CYCLE
round ends

Sausage
shape or
banana
shape
Cytoplasm Pale blue Pale Reddish Pale
blue blue blue
Chromatin Single As for P. Fine As for P.  The mosquito bite a gametocytemic person
choromatin vivax granules vivax they will go to sporogonic cycle. In sporogonic
mass scattered cycle there is the union between the
throughout macrogamete and the microgamete producing
Pigment Abundant As for P. Dark As for P. zygote, oocynite and eventually producing
brown vivax granules vivax sporozoite which is the infective stage of the
granules throughout parasite.
throughout  gametocyte- infective stage to vector
 The pre-patent and incubation period depends
on the parasite strain, dose of sporozites

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 inoculated, immune status and
chemoprophylaxis therapy.
Classical Malaria Paroxysms
 Pre-patent period- interval from the sporozoite
injection to the detection of the parasite in the 1. Cold stage
blood  sudden coldness and apprehension
 Incubation period- it is the time between the  mild shivering turns to teeth chattering and
sporozoite injection and the appearance of the shaking of the whole body
clinical symptoms  may last for 15 to 60 minutes
2. Hot stage/ flush phase : best stage to collect
INTERVALS AND PERIODICITY/FEBRILE CYCLE
blood sample
Intervals of Plasmodium spp.
 High temperature (40-41 C), headache,
Species Prepatent Incubation palpitations, epigastric discomfort, thirst,
period period nausea and vomiting. May lead to convulsion
P. falciparum 11-14 days 8-15 days  patient is confused and delirious
P. vivax 11-15 days 12-20 days  may last for 2 to 6 hours
P. malariae 3-4 weeks 18-40 days 3. Sweating stage (Defervescence or Diaphoresis)
P. ovale 14-26 days 11-16 days  profuse sweating, temperature lowers and
Periodicity/Febrile Cycle of Plasmodium spp. symptoms diminishes
Species Febrile cycle Interval Age of Infected  may last for 2 to 4 hours
(hours) Erythrocytes b. Malignant Tertian Malaria
P. falciparum * Malignant 36-48 RBC of all stages  The most serious and fatal type of malaria is
tertian malignant tertian malaria caused by P.
P. vivax Benign 48 Young RBC falciparum.
tertian  Pernicious malaria
P. malariae Quartan 72 Aging RBC Has been applied to a complex of life-
P. ovale Ovale 48 Young RBC threatening complications that
tertian sometimes supervene in acute
 The interval between the attacks is determined falciparum malaria.
by the length of erythrocytic cycle.  Cerebral Malaria
 P. falciparum, P. vivax, P. ovale – paroxysm Is the most common cause of death in
occurs in alternate days or every second day. malignant malaria, capillary plugging of
(tertian) cerebral microvasculature, which
 Quartan malaria- paroxysm occurs on day 1 and results in anoxia, ischemia, and
day 4 or every third day. 72 hours hemorrhage in brain.
Late stage schizonts of P. falciparum
*Aestivoautumnal malaria - associated to P. falciparum
secretes protein on the surface of RBC
(it occurs commonly in late summer and autumn)
to form knob-like deformities. This
CLINICAL FEATURE knob produces specific adhesive
 No absolute clinical feature of malaria except proteins, which promote aggregation of
for regular paroxysms (sudden attack or violent infected RBC to other non-infected RBC
expression of fever with asympyomatic interval) and capillary endothelial cells.
a. Benign Malaria Most common death
 The typical picture of malaria consists of  Blackwater fever
periodic bouts of fever with rigor, followed by Malarial hemoglobinuria is sometimes
anemia and splenomegaly. Severe headache, seen in falciparum malaria. Clinical
nausea, and vomiting are common. manifestation include bilious vomiting
- Anemia- decrease RBC count and prostration, with passage of dark
- Splenomegaly- enlargement of spleen red or blackish urine (black water).

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 There is a massive intravascular RECRUDESCENCE AND RELAPSE
hemolysis caused by anti-erythrocyte Recrudescence
antibodies, leading to massive
 New malarial attacks that appear after a period
absorption of hemoglobin by the renal
of latency usually within 8 weeks after the
tubules (hemoglobinuric nephrosis).
primary attack and resulting from persistence
of the erythrocytic cycle of the parasites.
 Renewed outbreak of the disease. The disease
is reduced to the point that it is undetectable
but still persist in the body and will reoccur
after some days or weeks.
 May persist inside the body but they are not
active to cause signs and symptoms.
 Algid Malaria  Reduced/light infectivity – undetectable in
Peripheral circulatory failure, rapid blood smear.
thready pulse with low blood pressure,  Stopping of the treatment early.
and cold clammy skin. There may be
severe abdominal pain, vomiting, Relapse
diarrhea, and profound shock.
 Common to P. vivax and P. ovale infections, as
 Septicemic malaria
result from the reactivation of hypnozoite
High continuous fever with
forms of the parasite in the liver
dissemination of the parasite to various
 Suffering deterioration after a period of
organs, leading to multiorgan failure.
improvement.
Death occurs in 80% of the cases.
 Pre mature stage of organism resides in the
c. Merozoite-induced Malaria
body that are in dormant stage and will cause
 Injection of merozoites can lead to direct
disease after recovering completely from the
infection of red cells and erythrocytic
previous occurrence of the disease.
schizogony with clinical illness. Such merozoite
induced malaria may occur in transfusion Recrudescence Relapse
malaria, congenital malaria, renal Seen in P. falciparum and P. Seen in P. vivax and P. ovale
transplantation and mainline malaria. malariae
d. Tropical Splenomegaly Syndrome Due to persistence of the Due to reactivation of
 Also known as hyper-reactive malarial parasite at a subclinical level hypnozoites present in liver
splenomegaly (HMS) is a chronic benign in circulation cells
condition seen in some adults in endemic areas, Occurs within a few weeks Occurs usually 24 weeks to 5
mainly tropical Africa, New Guinea, and and or months of a previous years after the primary
attack attack
Vietnam.
Can be prevented by Can be prevented by giving
 Abnormal immunological response to malaria
adequate drug theraphy or primaquine to eradicate
causing splenomegaly, high titers of circulating
use of newer antimalarial hypnozoites
anti-malaria antibodies and absence of malaria drugs in case of drug
parasites in peripheral blood smears, resistance
hypergammaglobulinemia (lgM),
cryoglobulinemia reduced C3, and presence of
rheumatoid factor without arthritis PATHOLOGICAL PROCESS OF THE RBC
 Body produces immune analytes causing 1. Pathological Process of the RBC
splenomegaly to the infected host Poikilocytosis – alteration in shape
Anisocytosis – alteration in size
2. Altered RBC membrane transport
3. RBC stiffness and cytoplasmic viscosity

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 MORPHOLOGY
Morphology of Plasmodium spp.

Paramete P. P. vivax P. P. ovale

r falciparum malariae
Size of Normal Enlarged Normal Normal-
RBC or sl. sl.
Smaller Enlarged
Trophozoi Usually not Ameboid Band Fimbriate
te present form d
No. of 8-36 12-24 6-12 in 8
merozoite rosette
in form IMMUNITY
schizont Duffy negative RBCs
Stipplings Maurer’s Schuffne Zeimman Schuffne
Stephen’s r’s ’s r’s  It has been found that persons, who lack the
Christophe (James) Duffy blood group (Fya and Fyb alleles) antigen,
r’s are refractory to infection by P. vivax. These
Ring Single, Single Single Single genetically determined blood group antigen
forms double appears to be the specific receptor for P. vivax
Chromati Single, Single, Single Single  Receptor of P. vivax on the erythrocyte surface
n dot double dense, is the Duffy protein
big
Applique Present Nature of hemoglobin
or accole  Since malaria infects RBC, any alterations to the
Gametocy Macro- Large, Large, Large, hemoglobin, which is essential to RBC function,
te crescent round, round, round,
generally protects the RBC from the invasion of
micro- oval oval oval
Plasmodium parasites or replication within the
banana,
sausage RBC.
shape  Problem with hemoglobin – it will not sustain
Stages in Ring forms all all all the life cycle of malaria (resistance to the
peripheral and disease).
blood gametocyt  Hemoglobin E provides natural protection
es against P. vivax. P. falciparum does not multiply
properly in sickled red cells containing HbS.
Sickle cell anemia trait is very common in Africa,
where falciparum malaria is hyperendemic and
offers a survival advantage. HbF present in
neonates protects them against all Plasmodium
species.

G6PD deficiency

 RBC - Bite cells (there is an abnormality on the

morphology of RBC)
 Innate immunity to malaria has also been
related to G6PD deficiency found in
Mediterranean coast, Africa, Middle East, and
India

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HLA-B53 Plasmodium LDH - produced by both
sexual and asexual stages. Can
 HLA-B53 is associated with protection from
distinguish between P. falciparum and
malaria. There is some evidence that severe
non-P. falciparum (DiaMed OptiMAL IT)
malnutrition and iron deficiency may confer
some protection against malaria

DIAGNOSIS
a. Microscopy
 (Gold Standard) - "Thick and Thin Blood
Smear"
 stained with Giemsa or Wright's stain
 perform multiple sets of blood films (blood
collected every 6 to 12 hours for up to 48  Anti-malaria antibody and control: Non-
hours) falciparum or it is caused by other spp.
 Thin smear- absence or presence of parasite  Anti-falciparum and anti-malaria antibody:
Pure or mixed infection with P. falciparum
Manner of Reporting d. Serologic Tests (IHA, FAT, ELISA)
 Qualitative  (IHA, FAT, ELISA)
+= 1-10 parasite/100 thick field e. Molecular Methods
++= 11-100 parasite/100 thick field  through PCR (low cases and mixed infection)
+++= 1-10 parasite/thick field TREATMENT
++++ = more than 10/thick field  Anti-malaria drugs are used with various
 Quantitative objectives like clinical cure, prevention of
no.of parasites
Malaria parasite/uL = 𝑊𝐵𝐶
x 8.000 relapse, prevention of transmission and
Tally the parasite against WBC until you prophylaxis.
have counted 500 parasites or 1000 a. Protective
WBC whichever comes first.  Chemoprophylaxis: Objective is to prevent
Express the result as parasites/uL of infections in non-immune person visiting
blood endemic areas (Mefloquine and Doxycycline)
b. Quantitative Buffy Coat (QBC) b. Curative
 uses a special capillary tube with acridine  Action on established infection
orange  Therapeutic: Objective is to eradicate the
 (+) bright green and yellow under fluorescent erythocytic cycle and clinical cure
microscope  Radical cure: Objective is to eradicate the
exoerythrocytic cycle in liver to prevent relapse
 Artemether-Lumefantrine (Coartemtm ) - first
line drug for confirmed P. falciparum cases. Not
recommended in pregnancy, lactation and
infants.
c. Rapid Diagnostic Test (RDT)  Quinine (plus Tetracycline or Doxycycline) -
 Use test kits if (-) with microscopy and you are second line drug for confirmed P. falciparum
suspecting a malaria cases which AL fail or not available.
 detects Plasmodium-specific antigens in finger  Quinine IV drip - drug of choice for
prick sample complicated or severe P. falciparum malaria.
Histidine-rich protein Il (HRP Il) - water  Chloroquine- anti-malarial drug used in P.
soluble CHON produced by trophozoites falciparum before but it is resistant now.
and young gametocytes (e.g., Paracheck Sensitive with P. vivax
Pf test, ParaHlT f test)

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c. Preventive  Parasites divide through binary fission or
 Gametocidal: Objective is to destroy budding
gametocytes to prevent mosquito transmission  cycle in the tick is still uncertain
and thereby reducing human reservoir
VECTOR
In addition to AL and Q+T,D,
 Ticks (Ixodes scapularis)
Primaquine is given on the 4 th day as
Hard ticks
single dose to prevent transmission
Scapularis - capable of carrying Borrelia
PREVENTION burgdorferi (CA of Lyme disease)
 Use of mosquito repellant
 Use of insecticide treated nets (lTN)
 Take prophylactic medication
 Wearing of light-colored clothing which cover
most of the body

CONTROL
 Environmental cleanliness (stream cleaning to DEFINITIVE HOST
speed up water flow and exposing to sunlight)  Ixodid ticks
 Indoor residual spraying
INTERMEDIATE HOST
 Zooprophylaxis - use of carabao to deviate
 Man or other mammals
mosquitoes
 Use of biologic control methods INFECTIVE FORM
Bacillus thuringiensis- larvicidal  Sporozoites
Larviparous fishes- oreochromis
MODE OF TRANSMISSION
niloticus
 bite of the nymphal stage of Ixodid ticks
Plasmodium knowlesi  Other modes of transmission:
 A primate malarial parasite common in South Blood transfusion
East Asia Organ transplantation
 Causes malaria in long tailed macaques Transplacental route
(Macaca fascicularis)
DIAGNOSTIC STAGE
 May also infect humans
 "Maltese cross" arrangement of the merozoites
 The appearance of P. knowlesi is similar to that
and ring-form trophozoite
of P. malariae
 PCR assay and molecular characterization are Maltese cross merozoite of babesia spp.
the most reliable methods for detecting and
diagnosing P. knowlesi infection
 However, P. vivax appears to interfere PCR
testing (cross reactivity)

Babesia spp.
 Babesia microti (Rodent strain)
 Babesia divergens and Babesia bovis (cattle
strain) Life Cycle of Babesia spp.
 First described to cause "Texas cattle fever or  Sporogony occurs in final host or definitive host
red water fever” (tick)
 Blood parasites that cause malaria-like  Humans are dead end host. (Merozoite form
infections only). Trophozoites are not developing into
 "Babesiosis" - pathology due to Babesia spp. gametocytes.
(tick, splenic, nan tucket fever)

| SERRANO, RAE ALISON D.

 But may develop in other animals like mouse.
(Merozoite > gametocyte)
TREATMENT
 Clindamycin - Drug of choice
 Drug combination: Clindamycin and Quinine or
Azithromycin and Atovaquone
 Chloroquine - former drug of choice (it only
improve the symptoms but not the degree of
the parasitemia)
 In the Philippines: human babesiosis is not yet
reported however, it could be present in dogs
(Babesia canis).

PREVENTION AND CONTROL

 avoidance of places where ticks are usually
found
 wearing of light-colored pants tucked into one's
socks
PATHOLOGY  tick check (especially for children)
 Associated with excessive pro-inflammatory  Rodent population should be controlled –
cytokines such as the tumor necrosis factor rodents are the major carriers and reservoir of
(TNF) the parasite.
 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
 Microscopy of the Giemsa-stained peripheral
blood smear
Merozoites in Maltese cross
arrangement
Ring form most frequent
intraerthrocytic form found
 Polymerace chain reaction (PCR) (gold
standard)
 Immunofluorescent assays (IFA)
 Immunochromatographic test (OCT)

| SERRANO, RAE ALISON D.

 CLINICAL PARASITOLOGY
WEEK 9
COCCIDIANS PARASITES
COCCIDIAN PARASITES
 Unicellular protozoans
 Live intracellularly. At some stage in their life INFECTIVE STAGE
cycle, they possess a structure called apical  Sporulated oocyst containing 8 sporozoites of
complex (important for attachment and the parasite.
penetration in cells).
 Some do not have intermediate host MODE OF TRANSMISSION
 Under class Sporozoa (Phylum Apicomplexa)  ingestion of food and water contaminated with
 Microscopic spore forming single cell obligate sporulated oocyst
intracellular protozoans LIFE CYCLE OF CYSTOISOSPORA BELLI
 In class Sporozoa, the life cycle is characterized  When a sporulated oocyst is swallowed, 8
by an alternations of generation: sporozoites were released from the 2 sporocyst
Sexual: Sporogony phase (Oocyst as the in the small intestine and will invade the
products) (formation of the sporozoite) intestinal epithelial cells.
Asexual: Schizogony phase (Merozoites  The primary invasion is occurring in the
> gametocytes are produced) intestine
 Cystoisospora belli (Isospora belli)  In the epithelium, the sporozoites will transform
 Cryptosporidium hominis to become trophozoites, which will multiply
 Cyclospora cayetanensis asexually by schizogony.
 Toxoplasma gondii  In the process of schizogony, a number of
 Sarcocystis hominis and Sarcocystis suihominis merozoites will be produced.
 The merozoites will invade the adjacent
CYSTOISOSPORA BELLI
 The name belli came from the word bellum epithelial cells to repeat the asexual cycle.
“war”. Several cases of the infection with this  Some of the trophozoites will undergo sexual
parasite were seen among troops stationed in cycle or gametogony in the cytoplasm of
the Middle East during the First World War. enterocytes. Eventually, they will transform to
become microgamete and macrogamete
MORPHOLOGY (capable of fertilization).
 Oocysts of Cystoisospora belli are elongated  After fertilization a zygote is formed which
ovoid and measure 25 um x 15 um. secretes a cyst wall and develop into an
 Each oocyst is surrounded by a thin smooth 2 immature oocyst.
layered cyst wall.  The immature oocysts will be excreted in the
 Immature oocyst seen in the feces of patients feces and will mature outside.
contain two sporoblasts.  Diagnostic Stage: immature oocyst (in the
They are being pass out immature and feces)
they mature outside the body
 The oocysts mature outside the body. On
maturation, the sporoblast convert into
sporocysts. Each sporocyst contain 4 crescent
shaped sporozoites.
 There is a need of environmental contamination
for the cyst to develop and become mature

| SERRANO, RAE ALISON D.

 PATHOLOGY  Both thin walled and thick walled oocyst
 Infection is usually asymptomatic among the contain 4 crescent-shaped sporozoites
immunocompetent. May present a self-limiting
gastroenteritis.
 Symptomatic: diarrhea, fever, malaise,
abdominal pain and flatulence
 Disease is common to children and male
homosexuals with AIDS
 In AIDS patients, reports on dissemination of
parasite to other organs are present.
INFECTIVE STAGE
(Opportunistic pathogens)
 Oocys
 The stool may contain fatty acid crystals and
charcot-leyden cystals. There is a flattened LIFE CYCLE OF Cryptosporidium hominis
mucosa and damaged villi causing high fecal fat  Thick-walled oocyst is infective stage when
content in the stool (steatorrhea). These ingested. Sporozoites will attach to the surface
findings are not specific of epithelial cells of the GIT.
 Sporozoites will develop to become small
DIAGNOSIS
trophozoites, and the trophozoites will divide
 Direct microscopy (routine stool examination)
(schizogony) producing merozoites.
 Concentration techniques (FECT, ZnS04 and
Gametocytes are produced
sugar floatation)
 Gametocytes > zygote > oocyst (both
 Staining techniques (Iodine, Kinyoun,
sporulated)
Auramine-Rhodamine, Ziehl Neelsen)
 Thin walled oocyst will infect other enterocytes
Coccidians are acid fast organisms
resulting to autoinfection
 Enterotest and duodenal aspirate
 Can also infect animals like cows
 Molecular testing
 There is a granular red color against in green
background

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

PREVENTION AND CONTROL

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

CRYPTOSPORIDIUM HOMINIS

MORPHOLOGY
 The oocyst is spherical or oval and measures
PATHOLOGY
about 5 um in diameter
 Immunocompetent: self-limiting diarrhea
 Oocysts does not stain with iodine and is acid
within 2-3 weeks
fast.
 Immunocompromised: severe diarrhea, bile
 Thin walled oocysts are responsible for
duct and gallbladder maybe heavily infected,
autoinfection
blunted intestinal villi, varying degrees of
 Thick walled oocyst (passed out with feces).
malabsorption and excessive fluid loss

| SERRANO, RAE ALISON D.

 AIDS patient: severe form of diarrhea,  It contains 2 sporocysts
progressively worse and life-threatening  Each sporocyst contains 2 sporozoites. Hence,
each sporulated oocyst contains 4 sporozoites.
SOURCES OF INFECTION
 Faulty water purification system
 Swimming in contaminated recreation water
 One person to another: infected food handlers
 Nosocomial infection (infections that are
acquired inside the hospital)

DIAGNOSIS
 Sheather's sugar floatation, Zinc sulfate
floatation technique and Formalin ether/ethyl
acetate concentration technique.
 Kinyoun's modified acid-fast stain (method of
choice in diagnosing. Oocyst appear as red-pink
doughnut-shaped circular organisms): cheapest
and simplest method of diagnosis
 IFA
 DNA probe
INFECTIVE STAGE
 Oocys

LIFE CYCLE OF CYCLOSPORA CAYETANENSIS

 The oocyst is shed in the feces and it
unsporulates outside the host. (requires
environmental contamination before it
develops)
TREATMENT  The sporulated oocyst are infectious to humans
 No acceptable treatment yet and humans acquired the infection by ingestion
 Supportive therapy with fluid, electrolytes, and of food and water contaminated with the feces
nutrient replacement containing the oocyst
 Nitazoxanide is said to be effective in  Excystation of the sporocyst releases cyrentic
preliminary studies sporozites and the sporozoites infect interosite
 Bovine colostrum (milky fluid that comes from in the small intestine and then further
the breast of cows), paromomycin and producing microgametocyte and
clarithromycin: treatment of severe diarrhea macrogametocyte and the zygote

PREVENTION AND CONTROL

 Chlorination is NOT effective (infective stage
has thick wall)
 Use of multiple disinfectant and combined
water treatment
 Proper disposal of human and animal excreta

CYCLOSPORA CAYETANENSIS

MORPHOLOGY
 The oocyst is a non-refractile sphere, measuring
8-10um in diameter.

| SERRANO, RAE ALISON D.

 MODE OF TRANSMISSION
 Ingestion
 Disease is usually self-limiting

PATHOLOGY
 Chronic and intermittent watery diarrhea occurs
in early infection and may alternate with
constipation.
 Fatigue, anorexia, weight loss, nausea,
abdominal pain, flatulence, bloating and
dyspnea may develop. Infections are usually
self-limiting.
 No death is associated.

DIAGNOSIS
 DFS
 Concentration techniques
 Kinyoun stain
 Fluorescent microscopy INFECTIVE STAGE
 Safranin staining  Trophozoite (tachyzoite), tissue cyst
 PCR (bradyzoite) and the oocyst
 Only the asexual forms (trophozoites and tissue
cyst) are present in other animals including
humans and birds.

HOST
 Definitive Host: Cats (complete life cycle occurs
in cats)
 Clinical manifestation is apparent if immune
system is suppressed
TREATMENT  Intermediate Host: Humans
 No treatment needed
LIFE CYCLE OF TOXOPLASMA GONDII
 If pharmacologic treatment is warranted,
 Enteric Cycle
cotrimoxazole is given.
Occur in cats and other definitive host
 If diarrheal symptoms are prominent, either
Asexual and sexual reproduction occurs
metronidazole or iodoquinol can be used.
in the mucosal epithelial cells of the
PREVENTION AND CONTROL small intestine of cats. (gametogony,
 Good sanitary practices schizogony)
 Access to safe and clean drinking water Cats acquire the infection by ingestion
 Proper food preparation of the tissue cyst from the meat of the
rats or by ingestion of the oocyst that
CRYPTOSPORIDIUM HOMINIS are pass in the feces. The bradyzoite
released in the small intestine and they
MORPHOLOGY undergo asexual multiplication leading
 Crescentic tachyzoites- extracellular and to the formation of merozoite
intracellular form within a macrophage. Tachy A mature oocyst containing 8
means fast (fast multiplying). sporozoite is the infective form which
 Tissue cyst- bradyzoite (slow multiplying) may be ingested by the rats or in other
mammals to repeat the cycle (infective)

| SERRANO, RAE ALISON D.

 Exoenteric Cycle 1. Congenital Toxoplasmosis
Humans acquire the infection by eating  Results when T. gondii is transmitted
undercooked or uncooked infected transplacentally from mother to fetus.
meat particularly lamb or pork  Most infected newborns are asymptomatic at
containing tissue cyst. birth and may remain so throughout. Some
May be passed from mother to fetus develop clinical manifestations of toxoplasmosis
(congenital toxoplasmosis during weeks, months, and even years after birth.
pregnancy), blood transfusion or organ  Manifestations: chorioretinitis, cerebral
transplantation. calcifications, convulsions, strabismus,
The sporozoites from the oocyst and deafness, blindness, mental retardation,
bradyzoites from the tissue cyst will microcephaly, and hydrocephalus.
enter into the intestinal mucosa > 2. Acquired Toxoplasmosis
multiply asexually > tachyzoites are  Infection acquired postnatally is mostly
formed. asymptomatic (if immunocompetent).
Tachyzoites (fast multiplying) will  The most common manifestation of acute
continue to multiply and spread locally acquired toxoplasmosis is lymphadenopathy.
through the blood or lymphatic system. The cervical lymph nodes being most
(some spread in distant extra intestinal frequently affected.
organs like brain, eyes, liver, spleen,
lungs and skeletal system then it will
form a tissue cyst)
The slow multiplying forms
(bradyzoites) may remain viable for
years. Dormant and may reactivate (in
immune suppression) causing renewed
infection in the host. 3. Ocular Toxoplasmosis
Human infection is a dead end for the  It may present as uveitis (eye inflammation
parasite occurring in the cats affects the middle layer of the tissue in the
eyewall called uvea), choroiditis, or
choriorentinitis (inflammation of the retina and
the choroid)

PATHOLOGY 4. Toxoplasmosis in Immunocompromised

 Toxoplasmosis commonly asymptomatic, if Patients
immune system is good.  Most serious and often fatal in
 Active progression of infection is more likely in immunocompromised patients, particularly in
immunocompromised individuals. AIDS, whether it may be due to reactivation of
 Encephalitis is the most common manifestation latent infection or new acquisition of infections.
 Clinical manifestation is apparent if immune
system is suppressed

| SERRANO, RAE ALISON D.

 ANTIGEN DETECTION

 Detection of antigen by ELISA indicates recent

Toxoplasma infection
 Useful in AIDS and other immunocompromised
patients
 Detection in amniotic fluid is helpful to diagnose
congenital toxoplasmosis.
DIAGNOSIS
MICROSCOPY SKIN TEST OF FRENKEL

 Tachyzoites and tissue cysts can be detected in  Diluted toxoplasmin is injected intradermally
various specimens like blood, sputum, bone and delayed positive reaction appears after 48
marrow aspirate, cerebrospinal fluid (CSF), hours. This test is not very reliable for diagnosis
amniotic fluid, and biopsy material from lymph of toxoplasma.
node, spleen, and brain.  Wheal-and-flare reaction indicates a positive
 Smear made from above specimens is stained test
by Giemsa, PAS, or Gomori methenamine silver
MOLECULAR METHODS
(GMS) stain. Tachyzoites appear as crescent
shaped structures with blue cytoplasm and dark  DNA hybridization techniques and polymerase
nucleus. chain reaction (PCR) are increasingly used to
 Gomori methenamine silver (GMS) stain- detect Toxoplasma from different tissues and
special stain used in histopathology particularly body fluids
in CNS.
IMAGING

 Magnetic resonance imaging (MRI) and

computed tomography (CT) scan are used to
diagnose toxoplasmosis with central nervous
system involvement.
 Ultrasonography (USG) of the fetus in utero at
20—24 weeks of pregnancy is useful for
diagnosis of congenital toxoplasmosis

TREATMENT
 Congenital toxoplasmosis: pyrimethamine (can
lower blood count it is given with folic acid) and
ANTIBODY DETECTION sulfadiazine
 Ocular toxoplasmosis: pyrimethamine plus
 Acute infection with T. gondii can be made by
either sulfadiazine or clindamycin.
detection of the simultaneous presence of lgM
 Immunocompromised patients: Trimethoprim
and lgG antibodies.
sulfamethoxazole is the drug of choice,
 Tests for detecting lgG antibody include:
dapsone-pyrimethamine is the recommended
Enzyme linked immunosorbent assay (ELISA),
alternative drug of choice.
Indirect fluorescent antibody test (IFAT), Latex
Adverse effect of pyrimethamine-
agglutination test and Sabin Feldman dye test.
lowers the blood count. It should be
 Sabin Feldman dye test- special test
taken together with leucovorin or folic
incorporated to diagnose T. gondii. (usually
acid.
used to confirm Toxoplasmosis infection)
 Serodiagnosis. (Serology is the mainstay for the
diagnosis of toxoplasmosis)

| SERRANO, RAE ALISON D.

 PREVENTION AND CONTROL MODE OF TRANSMISSION
 Good sanitation and hygiene  acquired by eating raw or undercooked
 Proper food preparation beef/pork
 Pregnant women should avoid contact with cats
PATHOLOGY
CRYPTOSPORIDIUM HOMINIS  Sarcosporidiosis and sarcocystosis
 Sarcocystis species produce cyst in the muscle  Gastroenteritis, diarrhea, myalgia, weakness,
of the intermediate hosts. These cysts are called fever
Sarcocysts, contain numerous bradyzoites  For intermediate host, brain, muscle and kidney
 Sarcocystis hominis from cattle tissues may be damaged.
 Sarcocystis suihominis from pigs  May cause abortion to cows
 Definitive host: Humans
DIAGNOSIS
 Fecal floatation methods: sporocysts will be
seen
Fecal floatation wet mount using Bright
Field Microscopy
Floatation methods- based on high-
density solutions incorporating sodium
chloride, cesium chloride, zinc sulfate,
sucrose, percoll, Ficoll-Hypaque and
LIFE CYCLE OF TOXOPLASMA GONDII
 When the sarcocysts is eaten by the definitive other density gradient media.
host the merozoites are released in the  Demonstration of sarcocysts in the skeletal
intestine where they develop into male and muscle and cardiac muscle by biopsy or during
female gametes autopsy
 After fertilization the zygotes develops into an  Western blot
oocyst containing 2 sporocysts each having 4  Serologic tests (IFA, ELISA)
sporozoites  PCR
 In the intermediate host the sporozoite invade TREATMENT
the bowel and enrich the vascular epithelial  No specific treatment is available for
cells where they undergo schizogony producing sarcocystosis
the tachyzoite  Corticosteroids were found to be useful in
 This spread to muscle fibers and develop to muscular inflammation
sarcocysts  Trimethoprim-sulfamethoxazole is seen as
 Infective and diagnosis stage it can be the cyst potentially effective in treating intestinal
with bradyzoite indested in under cooked meat infections
 Diagnosis and infective stage sporocyst and the
thin wall oocyst that are pass in the feces PREVENTION AND CONTROL
 Uncooked animal carcass should not be fed to
other animals
 Avoiding eating raw or undercooked beef or
pork
 Thoroughly cooking and freezing meat to kill
bradyzoites (Freeze: -5C for several days)

| SERRANO, RAE ALISON D.

 CLINICAL PARASITOLOGY  Male is generally smaller than female in size
WEEK 10 and its posterior end is curved or coiled
INTRODUCTION TO NEMATODES ventrally.
 Female nematodes may be oviparous
PHYLUM NEMATHELMINTHES (NEMATODA) (producing eggs), viviparous (producing larvae)
 Nematodes are the most worm-like of all the
or ovoviviparous (producing eggs that will
helminths because they resemble the common
hatch out to become larvae).
earthworm appearance, which is considered as
the prototype of the worms.

GENERAL CHARACTERISTICS
 The name nematode came from “nema” which
means thread. They are thread-like
helminths/worms.
 Free-living forms found in soil and water
 Shape: elongated, cylindrical or filariform in
shape, unsegmented worms with tapering ends.
 Sensory organs (with exception): amphids
LIFE CYCLE
(anterior portion) and phasmids (posterior part)
 Consists typically of 4 larval stages and the adult
Amphids- these are cuticular
form
depressions present on the lips
 The cuticle is shed while passing from one stage
surrounding the mouth of the
to the other
nematode and it serves as
 Man is the optimum host for all the
chemoreceptors.
nematodes. (humans are the definitive/final
Phasmids- useful in grouping the
host)
nematodes and it is found at posterior
 They pass their life cycle in one host, except for
part or at the caudal portion of the
the Filarial worms and Dracunculus medinensis
parasite.
where two hosts are required.
 Those are neurons that where  Nematodes localize in the intestinal tract (small
recently shown to function in and large intestine) and their eggs pass out with
modulation of the the feces of the host.
chemopulsion behavior of the Most commonly encountered
parasite nematodes in the laboratory are
 Locomotion: move by contraction of the intestinal in nature.
longitudinal muscles
 Body wall: covered with a tough outer cuticle
(smooth, striated, bossed, or spiny), middle
layer is hypodermis and the inner layer is the
somatic muscular layer
 Sexes: Diecious (separate sexes)
Have male and female parasite
Some of the nematodes they are
parthenogenic (female worm is capable
of fertilizing her own eggs without the
benefit of the male)
Parthenogenic- there is asexual
reproduction in which the offspring
develops from unfertilized egg

| SERRANO, RAE ALISON D.

 CLASSIFICATION OF NEMATODES  Somatic Human Nematodes- extrainstestinal
A. Presence of Absence of Chemoreceptors nematodes
 Phasmid nematode- with caudal
chemoreceptors FILARIAL WORMS
The chemoreceptors at the posterior FILARIAL WORMS
end of the parasite  Came from the Latin word filum (thread)
 Aphasmid nematode- without caudal
chemoreceptors GENERAL CHARACTERISTICS
Ex. of aphasmid nematode: Trichuris  Slender thread-like worms
trichiura, Trichinella spiralis, Capillaria  Female worms are viviparous and give birth to
philippinensis (they do not contain the larvae known as microfilariae.
posterior sensory organ or posterior The mode of reproduction is viviparous
caudal chemoreceptor) meaning those female adult parasites
B. Infective stages and Mode of Transmission they are producing larva and those larva
 Ingestion of embryonated eggs- Ascaris, they are seen as microfilariae in the
Trichuris, Enterobius peripheral blood.
 Ingestion of infective larva- Capillaria,  Microfilariae- infective stage
Trichinella, Angiostrongylus They can have covering or the sheaths
 Ingestion of encysted larvae in muscle- and they exhibit periodicity
Trichinella
 Skin penetration of L3- Hookworms and
Strongyloides
Predominantly found if you are walking
barefoot on the soil
 Vector-borne- Wuchereria and Brugia
MODE OF TRANSMISSION
 Autoinfection- Strongyloides and Enterobius
 By the bite of blood-sucking insects
 Transmission through inhalation- Enterobius
Vector borne in nature
and Ascaris
vectors are mosquitoes
C. Habitat
PERIODICITY
Intestinal Human Somatic Human
 Rhythmical appearance of the microfilaria in the
Nematodes Nematodes
peripheral blood smear
Small intestine Lymphatics
Nocturnal periodicity: when the largest
 Ascaris lumbricoides  Wuchereria bancrofti
number of microfilariae occur in blood
 Ancylostoma duodenale  Brugia malayi
 Necator americanus  Brugia timori at night
 Strongyloides stercoralis There is a high chance na mas makuha
 Trichinella spiralis or mas ma isolate yung microfilaria if
 Capillaria philippinensis you collect blood small during the night
Large intestine Skin/subcutaneous  Wuchereria bancrofti
 Trichuris trichiura tissue Diurnal periodicity: when the largest
 Enterobius vermicularis  Loa loa number of microfilariae occur in blood
 Onchocerca volvulus during day.
 Dracunculus  Loa loa
medinensis Nonperiodic: when the microfilariae
Mesentery circulate at constant levels during the
 Mansonella ozzardi day and night.
 Mansonella perstans  Onchocerca volvulus
Conjunctiva
 Loa loa

| SERRANO, RAE ALISON D.

 Subperiodic or nocturnally subperiodic: lymphangitis and elephantiasis in
when the microfilariae can be detected chronic cases
in the blood throughout the day but are  Has its social and economic impact
detected in higher numbers during the Hindi mo na magagawa ang mga day to
late afternoon or at night. day activities mo
 Brugia malayi  Habitat: Lymphatic vessels (lymph nodes)
 Microfilaria they may contain sheaths and that
MODE OF TRANSMISSION
sheaths those are egg membranes
 Skin penetration through a vector
 The microfilariae are found in the capillaries
and blood vessels of the lungs during the period VECTOR
when they are not present in the peripheral  mosquito
blood.  Aedes spp., Culex spp. and Anopheles spp. (W.
bancrofti)
COVERING AND HABITAT
 Mansonia spp. eg. M. bonnae and M. uniformis
 Sheathed microfilaria (retain their egg
(B. malayi)
membrane)
 Unsheathed microfilaria (during fertilization, INFECTIVE STAGES
their egg membrane ruptures > unsheathed)  L3 larva or filariform larva (man)
Ininject ng mosquito pag kumagat siya
Covering of filarial worms
ng humas
Sheathed microfilaria Unsheathed microfilaria  Microfilariae (mosquito)
Wuchereria bancrofti Onchocerca volvulus Since microfilariae can be seen in the
Brugia malayi Mansonella perstans peripheral blood
Loa loa Mansonella ozzardI
DIAGNOSTIC STAGE
 Microfilariae in the peripheral blood
Habitat of filarial worms
DEFINITIVE HOST
Lymphatic Subcutaneous Serous cavity  Man
filariasis filariasis filariasis
Wuchereria Loa loa Mansonella Differentiation of Wuchereria bancrofti and Brugia
bancrofti perstans malay
Brugia malayi Onchocerca Mansonella
Parameter Wuchereria Brugia malayi
volvulus ozzardi
bancrofti
Brugia timori Mansonella
Common name Bancroft's Malayan filarial
streptocerca
filarial worm worm
 Considered as somatic nematodes
Vector Culex spp. Mansonia spp.
LYMPHATIC FILARIAL PARASITES Anopheles spp.
 Wuchereria bancrofti and Brugia malayi Aedes spp
 One of the "most debilitating disease" in Area affected Lower Upper
lymphatics lymphatics
tropical countries
(they prefer
 Filariasis- parasitic infection caused by
lymph node)
microscopic threadlike worms acquired through
Periodicity Nocturnal Subperiodic
a mosquito bite (vector borne) (8PM-2AM)
If the threadlike worms (microfilaria)
are acquired, it will develop to become
adult worms, with the adult worms BANCROFTIAN FILARIASIS
being lodge in the lymphatic system,  Vector Biology:
these worms will cause lymph edema, Anopheles flavirostris
Aedes poecillus

| SERRANO, RAE ALISON D.

 Aquatic habitat: axils of abaca and banana plant LIFE CYCLE OF BRUGIA MALAYI
(watery)  Same life cycle with Wuchereria bancrofti but it
 Adult biting: day and night biting, indoor and prefers the upper lymphatic.
outdoor  Intermediate host of Brugia- genera of
 Adult resting: base of abaca plants (cool, shady Mansonia
area)  L3 larvae- infective stage
 The microfilaria that are isolated in the
peripheral blood- diagnostic stage

LIFE CYCLE OF WUCHERERIA BANCROFTI

 Definitive host is man. No animal host or
reservoir host is known for Wuchereria
bancrofti
 Intermediate host or the vector is female
mosquitoes. Different species acts as vectors in
different geographic area.
The major vector in India and most
other parts of Asia is Culex. PATHOLOGY
 If fertilization occurs the adults will produced CLASSICAL FILARIASIS
sheathed or covering microfilariae that may  Due to blockage of lymph vessels and lymph
migrate to lymphatic and peripheral blood nodes by the adult worms.
circulation  Prefers lymph because it is less aggressive than
 If another mosquito takes a blood meal blood. No platelets, complement system,
makukuha niya yung mga microfilariae in the incomplete coagulation system, no granulocytes
blood and the microfilariae they will shed their and the flow is less violent than in blood.
sheaths penetrate the mosquito’s midjut and  The blockage could be due to mechanical
migrate to thoracic muscle. They become to factors or allergic inflammatory reaction to
develop L1 larvae, L3 larvae and there is worm antigens and secretions
migration to head and proboscis.
 The adult worms are usually localized in the Infiltration: lymph nodes and vessels are infiltrated with
lymph vessels of lower extremities, inguinal macrophages, eosinophils, lymphocytes, and plasma
lymph nodes, epididymis of male and the labia cells. First react WBC
of female. Lymph stasis and dilatation of lymph vessels: vessel
walls get thickened, and the lumen narrowed or
occuled.

Granuloma formation, with subsequent scarring and

even calcification.

Hard pitting or brawny edema of filariasis: increased

permeability of lymph vessel walls lead to leakage of
protein-rich lymph into the tissue.

| SERRANO, RAE ALISON D.

 ACUTE FILARIAL DISEASE tissues causing swelling of the arms,
 Adenolymphagitis (ADL) or legs, genitalia
Dermatolymphangioadenitis (DLA) The lymphangitis and the lymphadenitis
 Characterized by sudden onset high-grade fever can involve the upper and lower
with rigors and last for 2 or 3 days, lymphatic extremities in both Bancroftian and
inflammation (lymphangitis and lymphadenitis), Bruigian filariasis
and transient local edema The involvement of genital lymphatics
Lymphangitis- inflamed lymph vessels occurs exclusively with Wuchereria
seen as red streaks underneath the bancrofti.
skin. Genital involvement can be in the form
Acute lymphangitis- usually caused by of funiculitis, epididymitis and
allergic or inflammatory reaction to hydrocoele formation
filarial infection. May be often  Lymphoangiovarix
associated with Streptococcal infection Dilatation of lymph vessels commonly
as well. occurs in the inguinal, scrotal, testicular,
Lymphadenitis- inflammation of lymph and abdominal sites.
nodes.  The lymphangitis and lymphadenitis can involve
 Most commonly affected lymph nodes: both the upper and the lower extremities in
inguinal nodes followed by axillary nodes. both filariasis but the involvement of the genital
 Lymphatics of the testes and spermatic cord are lymphatics occurs exclusively in wuchereria
frequently involved, with epididymo-orchitis bancrofti infection.
and funiculitis
ELEPHANTIASIS
 Disabling and disfiguring of lymph edema of the
limbs, breast and genitals accompanied by a
mark thickening of the skin.
 Delayed sequel to repeated lymphangitis,
obstruction and lymphedema.
 There is non-pitting brawny edema with growth
CHRONIC FILARIAL DISEASE of the new adventitious tissue and thickened
 more commonly encountered than its acute skin, cracks, and fissures with secondary
form bacterial and fungal infections.
 Lymphedema  Lower limbs are commonly affected but upper
Follows successive attacks of limb and male genitalia may be involved. Breast
lymphangitis and usually starts as and genitalia of females may be affected but
swelling around the ankle, spreading to relatively uncommon.
the back of the foot and leg.
It may also affect the arms, breast,
scrotum, vulva, or any other parts of
body. The edema is pitting in nature but
in the course of time, it becomes hard
and non-pitting.
Edema forms because there is fibrosis
and cellular hyperplasia in and around HYDROCOELE
the lymphatic walls, postulated to  Accumulation of fluid occurs due to obstruction
render the lymphatic endothelial cells of lymph vessel of the spermatic cord and also
less effective in transporting the by exudation from the inflamed test and
interstitial fluid and forming abnormal epididymis.
accumulation of the lymph and the

| SERRANO, RAE ALISON D.

  The fluid is usually clear and straw colored but  Hypersensitivity reaction to microfilarial
may sometimes be cloudy, milky, or antigens, not directly due to lymphatic
hemorrhagic. involvement.
 Microfilariae are not found in blood, as they are
destroyed by the tissues.
 Clinical manifestations: massive eosinophilia
(30-80%), hepatosplenomegaly, pulmonary
symptoms (dry nocturnal cough, dyspnea, and
asthmatic wheezing)
 Has also been reported to cause arthritis,
LYMPHORRHAGIA glomerulonephritis, thrombophlebitis,
 Chylocele, milky appearance caused by the tenosynovitis, etc.
presence of lymph, rupture of lymph varices
leading to release of lymph or chyle and TROPICAL PULMONARY EOSINOPHILIA
resulting in chyluria (kidney damage: “milky  Manifestation: low-grade fever, loss of weight,
urine”), chylous diarrhea, chylous ascites, and and pulmonary symptoms
chycothorax, depending on the involved site.  Children and young adults are more commonly
affected in areas of endemic filariasis including
the Indian subcontinent.
 There is a marked increase in eosinophil count
(>3000 um which may go up to 50,000 or more)
 Chest X-ray shows mottled shadows similar to
miliary tuberculosis.
 It is associated with a high level of serum lgE
EXPATRIATE SYNDROME and filarial antibodies.
 Occurs to migrants who were infected from  Serological tests with filarial antigen are usually
endemic regions. It is characterized by clinical strongly positive.
and immunologic hyperresponsiveness to  The condition responds to treatment with
maturing worms. Exhibits acute manifestations diethylcarbamazine (DEC).
and allergic reactions (hives, rashes and blood
eosinophilia). Difference between Classical and Occult Filariasis

Classical Occult Filariasis

Filariasis
Cause Due to adult Hypersensitivity
and developing to microfilaria
worms antigen
Basic lesion lymphangitis, Eosinophilic
lymphadenitis granuloma
OCCULT FILARIASIS formation
 Microfilariae cannot seen in the blood but they Organs ymphatic lymphatic
involved vessels and system, lung,
can be isolated somehow in the tissues
lymph node liver, spleen,
 Synonyms: Weingartner's syndrome, Meyer's-
joints
Kouwenaar syndrome, Pseudotuberculosis of
Microfilaria Present in Present in
the lung, Eosinophilic pseudo-leukemia, Tropical blood tissues but not
eosinophilic asthma and Frimödt-Möller and in blood
Barton syndrome. Serological test Complement Complement
fixation test not fixation test
so sensitive highly sensitive

| SERRANO, RAE ALISON D.

 Therapeutic No response Prompt
response response to
DEC
 diethylcarbamazine (DEC)- drug of choice for
lymphatic filarial diseases

STAGING SYSTEM FOR CHRONIC LYMPHEDEMA

(DREYER ET. AL 2002)
 Stage 1: swelling increases during day but
reversible once the patient lies flat in bed
 Stage 2: irreversible swelling
 Stage 3: presence of shallow skinfolds
 Stage 4: knobs, lumps and protrusions
 Stage 5: deep skin folds
 Stage 6: mossy lesions with leaking of
translucent fluid
 Stage 7: foul-smelling infected area, patient is
unable to adequately or independently perform
activities of daily living.

DIAGNOSIS
1. Microscopy
 “wet smears”- demonstrate motile microfilariae
 "thick blood smears" 2. Knott's concentration technique
Giemsa stain  Anticoagulated blood (1 ml) is placed in 9 ml of
demonstration of the microfilaria 2% formalin and centrifuged 500 x g for 1
most practical diagnostic procedure minute. The sediment is spread on a slide to dry
Differences in Microfilariae thoroughly. The slide is stained with Wright or
Giemsa stain and examined microscopically for
Parameter Wuchereria Brugia malayi microfilariae.
bancrofti 3. Nucleopore filtration
Mean length 290 222  In the filtration methods used at present, larger
(um) volumes of blood, up to 5 ml, can be filtered
Cephalic space/ 1:1 2:1 through millipore or nucleopore membranes (3
breadth
um diameter). The membranes may be
Sheath affinity Unstained Pink
examined as such or after staining, for
to Giemsa
microfilariae. More sensitive
Body nuclei regularly spaced irregular and
overlapping 4. DEC provocation test
Terminal nuclei none 2 nuclei  A small dose of diethylcarbamazine (2 mg per kg
Appearance in smoothly or kinky body weight) induces microfilariae to appear in
blood film gracely curved peripheral blood even during daytime.

| SERRANO, RAE ALISON D.

 5. Other specimens
 Microfilaria may be demonstrated in
centrifuged deposits of lymph, hydrocele fluid,
chylous urine or other appropriate specimens.
6. Ultrasonography
 High frequency ultrasonography (USG) of
scrotum and female breast coupled with
Doppler imaging may result in identification of
motile adult worm (filaria dance sign) within LIFE CYCLE OF LOA LOA
 The infective L3 larvae enters the subcutaneous
the dilated lymphatics
tissue and will develop into adult worm over 6-
7. Radiology
12 months.
 Dead and calcified worms can be detected
 The female worms’ produces sheathed, which
occasionally by X-ray. In tropical pulmonary
have diurnal periodicity.
eosinophilia (TPE), chest X-ray shows mottled
 The microfilariae ingested by the Chrysops
appearance resembling miliary tuberculosis
(during its blood meal to an infected host) will
8. Demonstration of Antibody
cast off their sheaths, penetrate the stomach
 Complement fixation, indirect hemagglutination
wall of fly and will reach the thoracic muscles
(IHA), indirect fluorescent anti- body (IFA),
wherein they develop into infective larvae (L3
immunodiffusion, and immunoenzyme tests
larvae).
have been described.
9. Demonstration of Circulating Antigen
 Highly sensitive and specific test for detection
of specific circulating filarial antigen (CFA) have
been developed for detection of recent
bancroftian filariasis.
10. Molecular Diagnostic Technique
 Polymerase chain reaction (PCR) can detect
filarial DNA from patient's blood, only when
circulating microfilaria are present in peripheral
blood but not in chronic carrier state.

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

| SERRANO, RAE ALISON D.

 MANSONELLA PERSTANS Lakshadweep Island, after an initial
 Old name: Acathocheilonema perstans reduction in prevalence had been
 Culicoides species are the vectors  Infection achieved by mass or selective treatment
may cause dermatitis with pruritus and of microfilaria carriers
hypopigmented macules  Ivermectin: In doses of 200 ug/kg
 rare parasite of man can kill the microfilariae but has no
effect on adults.
MANSONELLA OZZARDI
 Tetracyclines: Also have an effect in
 rare parasite of man, infections does not cause
the treatment of filariasis by
any illness
inhibiting endosymbiotic bacteria
Differentiation of O. volvulus, M. perstans and M. (Wohlbachia species) that are
ozzardi Parameter O. volvulus M. perstans M. ozzar essential for the fertility of the
worm
Parameter O. volvulus M. perstans M. ozzardi  Supportive therapy: elevation of the affected
Vector Black flies Small flies Small flies
limb, use of elastic bandage, and local foot care
Simulium (gnats) (gnats)
reduce some of the symptoms of elephantiasis.
damnosum Culicoides Culicoides
Medical management of chyluria includes bed
austeni furens
Habitat Subcutaneous Body cavities Body rest, high protein diet with exclusion of fat, drug
tissue cavities therapy with DEC, and use of abdominal
Pathology Onchocerciasis Non- Non- binders. Surgery is required for hydrocele.
, River pathogenic pathogenic
PREVENTION AND CONTROL
blindness
 Detection and treatment of carriers.
Specimen Skin snips - -
 Eradication of Vector Mosquito
Antilarval measures: The ideal method
of vector control would be elimination
of breeding places by providing
adequate sanitation and underground
waste water disposal system
Chemical control: Using antilarval
chemicals (Mosquito larvicidal oil,
TREATMENT Pyrosene oil-E, Organophosphorous
 Diethylcarbamazine citrate (DEC) is the drug of larvicides like temephos and enthion)
choice. Following treatment with DEC severe  Removal of Pistia plant: mainly restricted to
allergic reaction (Mazzotti reaction) may occur control of Mansonia mosquitoes leading to
due to death of microfilariae. brugian filariasis.
 Administration:  Personal prophylaxis: using mosquito nets and
Mass therapy: In this approach, DEC is mosquito repellants is the best method.
given to almost everyone in community
DRACUNCULUS MEDINENSIS
irrespective of whether they have
 "Guinea worm", "Worm of Medina", "Dragon
microfilaremia disease manifestation or
worm" or "Fiery serpent"
no signs of infection except those under
 Longest nematode to man (1 meter)
2 years of age, pregnant women, and
 Causes "Dracunculiasis" or "Guinea worm
seriously-ill patients.
disease" (GWD)
Selective treatment: DEC is given only
 Mature female worms migrate along the
to those who are microfilaria-positive.
subcutaneous tissue to reach the skin below the
DEC medicated salts: Common salt
knee, forming a painful ulcerating blister
medicated with 1-4 g of DEC per kg has
been used for filariasis control in

| SERRANO, RAE ALISON D.

 Can also emerge to the head, torso, upper
extremities, buttocks and genitalia
 Common symptoms: rashes, fever, nausea,
vomiting, diarrhea, dizziness
 Until there is formation of blister and causes a
burning sensation
 those blister can be secondary infected by
bacteria
 Complications: cellulitis, abscess, sepsis, lock
jaw (tetanus)
 It has been suggested that the Rod of Asclepius
HOST (which represents the medical practice since
 Definitive Host: man ancient times) once represented a worm
 Intermediate host: Cyclops wrapped around a rod; parasitic forms such as
Dracunculus medinensis were common in
INFECTIVE FORM
ancient times, and were extracted from
 third-stage larva present in the hemocele of
beneath the skin by winding it slowly around
infected Cyclops
the stick.
MODE OF TRANSMISSION  According to this theory, physicians might have
 drinking unfiltered water containing infected advertised this common service by posting a
Cyclops sign depicting a worm on a rod.
 The technique of extracting the worm by
INCUBATION PERIOD
twisting it on the stick, still practiced by patients
 about 1 year
in endemic areas, is devised by Moses.
LIFE CYCLE OF DRACUNCULUS MEDINENSIS  The picture of “serpent worm” on a stick may
 humans can get it by drinking the unfiltered have given rise to the physician’s symbol, the
water containing the coke pods or Cyclops with Caduceus.
L3 larvae
TREATMENT AND MANAGEMENT
 after that the larvae release when the coke
 Immersion of affected body part to water
pods is die and the larvae penetrate the host’s
 Wound is cleaned
stomach and intestinal wall when their mature
 Worm extraction
and reproduce
 Topical antibiotics are given to prevent infection
 after the fertilization the fertilized female they
 Aspirin and Ibuprofen are given to ease the pain
will migrate to the surface of the skin and they
Antihistamines and steroids are of help in the
can cause blisters and discharge the larvae
initial stage of allergic reaction
 the female worm begins to emerge from the
 Metronidazole, niridazole, and thiabendazole
skin 1 year after the infection and the L1 larvae
are useful in treatment.
are release to the water from the emerging
female worm PREVENTION AND CONTROL
 Surveillance and case containment
 Provision of protected piped water supply is the
best method of prevention or else boiling of
filtering water through a cloth and then
consuming water.
 Destroying cyclops in water by chemical
treatment with Abate (temephos).
 Not allowing infected persons to bathe or wade
in sources of drinking water.

| SERRANO, RAE ALISON D.

 CLINICAL PARASITOLOGY MORPHOLOGY
WEEK 11 A. Worm
NEMATODES 1
Adult Worm
 has a ova as their infective stage most of this
 Large cylindrical worms, with tapering ends, the
parasite they have their embrayonated eggs or
anterior end being more pointed than the
the ova.
posterior
ASCARIS LUMBRICOIDES  Pale pink or flesh colored when freshly passed
 Common name: Giant intestinal/round worm in stools but become white outside the body.
 Final Host: man  The mouth at the anterior end has 3 finely
 Habitat: small intestine toothed lips, 1 dorsal and 2 ventrolateral
 Diagnostic stage: fertilized and unfertilized egg (trilobate lips)
 Infective stage: embryonated egg
Male Worm
 Source of exposure to inf.: soil-transmitted
helminth  Smaller than female, measures 10-31 cm in
 MOT: Ingestion of emnroyonated egg length
 Pathology: Ascariasis  Posterior end is curved ventrally to form a
 Diagnosis: Stool Exam, Concentration technique hook and carries 2 copulatory spicules.
 Drug of choice: Albendazole (Mebendazole and  copulatory spicules- used for mating
Pyrantel Pamoate)
Female
*Ascaris suum - Ascaris of Pigs
 Larger than male, measuring 22-35 cm in length
Most common intestinal nematode of  Posterior extremity is straight and conical
man (occurs most frequently in tropics)  Vulva is situated mid-ventrally
Its specific name “lumbricoides” is  A distinct groove is often seen surrounding the
derived from its resemblance with the worm at the level of the vulvar opening (genital
earthworm. girdle or vulvar waist)
Lumbricus – means earthworm in Latin.
Soil-transmitted helminth (along with T.
trichiura and hookworms)
The soil plays a major role in the
development and transmission of the
parasite.
The children are particularly vulnerable
since they are at risk in ingesting the
embryonated Ascaris eggs while playing
in soil contaminated with human feces.
Soil-transmitted helminth - considered Ascaris lumbricoides. A. adult female and male
as disease of the poverty and may worms; B. anterior end of worm, head-onview,
contribute to malnutrition and showing 1 dorsal and 2 ventral lips with
impairment of cognitive performance papillae; C. posterior end of female, showing
anal opening, a little above the conical tip; D.
posterior end of male, showing 2 protruding
copulatory spicules

| SERRANO, RAE ALISON D.

 mammillary coat; B. fertilized egg, median
focus, showing unsegmented ovum surrounded
by 3 layers of coats; C. decorticated fertilized
egg, the mammillary coat is absent; D.
unfertilized egg, elongated, with atrophic ovum

Has been shown to produced pepsin inhibitor 3

that protects the worm from digestion and
phosphoryl choline that suppresses the
lymphocyte proliferation
B. Egg

Fertilized eggs

 aid by females, inseminated by mating with a

male
 embryonated and develop into the infective
eggs
 round or oval Corticated, unfertilized egg- longer and
 always bile-stained, golden brown in color narrower than fertile egg. They have thin shells
 surrounded by thick smooth translucent shell and irregular mammillated coating that filled
with an outer coarsely mamillated albuminous with retractile granules. They may be difficult to
coat, a thick transparent middle layer and the identify because they resemble some fecal
inner lipoidal vitelline membrane (covering- debris
corticated egg, no covering-decorticated egg) Corticated fertilized egg- having a coarsely
mammilated albuminous covering. The
Unfertilized eggs surrounding of the ova has a rough edges
 laid by uninseminated female Decorticated, fertilized egg- smooth covering
 non-embryonated and cannot become infective without the mammilated albuminous covering
 Elliptical in shape, narrower and longer Embrayonatd egg- infective stage of the
 has a thinner shell with an irregular coating of parasite and evident larva inside
albumin The fertilized and fertilized egg is not infective
some of the eggs that are found in the feces LIFE CYCLE
they have their outer mammillated covering  Does not need intermediate host.
there are consider as corticated eggs  When embryonated eggs are ingested > it will
corticated- have alter covering hatch in the lumen of small intestine releasing
the larvae > larvae will migrate to the cecum or
proximal colon where they penetrate the
intestinal wall > they enter the venules and will
go to the liver through portal vein, to the heart
or to pulmonary vessels.
 Female A. lumbricoides produces about 200,000
eggs per day. The eggs are deposited into the
soil, and it takes about 2-3 weeks for the eggs to
develop under favorable condition with suitable
Types of ascaris eggs found in stools. A. temperature, moisture and humidity.
fertilized egg surface focus, showing outer

| SERRANO, RAE ALISON D.

 Can survive the acidity of the stomach because clumped together into a mass, filling the lumen,
of pepsin inhibitor 3 (protein). leading to worm bolus, intestinal obstruction
 You have to ingest embrayonated egg to and intestinal perforation.
indicate the infection  Ectopic ascariasis (Wanderlust): worms may
wander causing acute biliary obstruction or
pancreatitis, liver abscesses, respiratory
obstruction or lung abscesses and obstructive
appendicitis. The wandering is enhanced when
the host is ill (If the temperature is above 39C it
may provoke the worms to wander around).
The male worm they are more responsive to
the illness of the host
 Erraticity: if worm migrates to ectopic sites
(gallbladder, hepatobiliary tree, appendix and
pancreas), maybe regurgitated and vomited,
may escape through the nostrils or inhaled to
the trachea maybe due to medication, spicy-
diet and fever. *Usually observed in male
worms.

PATHOLOGY
a. Due to larva
 Ascaris pneumonitis or Loeffler's Syndrome:
occurs during lung migration resulting in allergic
reactions such as lung infiltration, asthmatic
attacks and edema of the lips, similar symptoms
of pneumonia, vague abdominal pain.
DIAGNOSIS
Eosinophilia is present
 The clinical diagnosis should be confirmed or
 Sputum- often blood-tinged and may contain
established by microscopic examination of stool
Charcot-Leyden crystals.
sample.
 The larvae may occasionally be found in the
 Direct fecal smear is less sensitive compare to
sputum but are seen more often in gastric
Kato-thick and Kato-katz.
washing
 Stool Examination
 If the larvae is penetrating the lungs
 Direct Fecal Smear
b. Due to adult worm
 Kato-thick (qualitative)
 Spoliative or nutritional effects: enormous
 Kato-katz (provides a quantitative
numbers occupying a large part of the intestinal
diagnosis in terms of intensity of the
tract interferes with proper digestion and
helminth infection in eggs/gram of the
absorption of food. Ascariasis may contribute to
stool. Usefull in monitoring the efficacy
protein-energy malnutrition and vitamin A
of the treatment in the clinical trials)
deficiency.
 Concentration Technique
 Toxic effects: due to hypersensitivity to the
 Formalin Ether/Ethyl Acetate
worm antigens and may be manifested as fever,
Concentration Technique (FECT)
urticaria, angioneurotic edema, wheezing, and
 Merthiolate Iodine Formaldehyde
conjunctivitis.
Concentration technique (MIFCT)
 Mechanical effects: most important
 Brine floatation
manifestations of ascariasis, worms may be
 Zinc sulfate floatation technique

| SERRANO, RAE ALISON D.

  X-ray (extra-intestinal ascariasis: lungs) 4. Special groups, e.g., food handlers and
 CBC (demonstrate eosinophilia) operators, soldiers, farmers and indigenous
people
PREVENTION AND CONTROL
 Selective deworming is the giving of
 Sanitary disposal of human feces
anthelminthic drug to an individual based on
 Health education
the diagnosis of current infection. However,
 Mass chemotherapy
certain groups of people should be given
 Avoid using night soil
deworming drugs regardless of their status once
 Proper food preparation
they consult the health center.
INTEGRATED HELMINTH CONTROL PROGRAM (DOH)  Special groups like soldiers, farmers, food
1. Target and Doses handlers and operators, and indigenous people
are at risk of morbidity because of their
Children aged 1 year to 12 years old exposure to different intestinal parasites in
 For children 12 —24 months old relation to their occupation or cultural
 Albendazole - 200 mg, single dose every practices.
6 months. Since the preparation is  For the clients who will be dewormed
400mg, the tablet is halve and can be selectively, treatment shall be given anytime at
chewed by the child or taken with a the health centers
glass of water or TRICHURIS TRICHIURA
 Mebendazole - 500 mg, single dose  Common name: Whipworm
every 6 months  Final Host: man
 For children 24 months old and above  Habitat: large intestine
 Albendazole - 400 mg, single dose every  Diagnostic stage: egg
6 months or  Infective stage: Embryonated egg
 Mebendazole -500 mg, single dose  Source of ex. to inf.: soil-transmitted helminth
every 6 months  MOT: Ingestion
 Note: If Vitamin A and deworming drug  Pathology: Rectal prolapse, IDA, diarrhea
are given simultaneously during the GP  Diagnosis: Stool exam, Concentration technique
activity, either drug can be given first  Drug of choice: Mebendazole (Albendazole as
2. Adolescent females alternative drug)
 It is recommended that all adolescent females
who consult the health be given anthelminthic *Usually observed occurring together with Ascaris
drug lumbricoides
 Albendazole -400 mg once a year or
MORPHOLOGY
 Mebendazole -500 mg once a year
A. Worm
3. Pregnant women
 It is recommended that all pregnant women Adult Worms
who consult the health be given anthelminthic
 Flesh-colored
drug once in the 2nd trimester of pregnancy.
 Resembles a whip with the anterior three-fifth
 In areas where hookworm is endemic: Where
thin and thread-like and the posterior two-fifth
hookworm prevalence is 20 — 30%
is thick and fleshy, appearing like the handle of
 Albendazole - 400 mg once in the 2nd
a whip.
trimester Or
 Attenuated anterior portion, which contains the
 Mebendazole - 500 mg once in the 2nd
capillary esophagus is embedded in the mucosa
trimester

Where hookworm prevalence is > 50%, repeat

treatment in the 3rd trimester

| SERRANO, RAE ALISON D.

 lemon shaped/barrel-shaped/football shaped/
Japanese lantern with plug-like translucent
polar prominences a.k.a “mucoid bipolar plugs”

LIFE CYCLE
 the embrynated eggs are passed in the stool in
the soil the eggs develop into a two cells stage
an advance cleavage stage and then they
embryonate and the eggs become infective in
15-30 days
 after the ingestion the egg hatch in the small
intestine and release the larvae that mature
and establish themselves as adults in the colon
 The worms inhabit the cecum and colon. It
secrets pore-forming protein called TT47 which
allows them to embed their entire whip-like
portion into the intestinal wall.
Comparison of Male and Female worm of T. trichiura  The female worms lay eggs, which are passed
out with the feces and deposited in the soil,
MALE FEMALE
under favorable conditions the eggs will
30-45 mm 35-50 mm
develop and become embryonated. If
Coiled posterior with a Rounded/blunt posterior
single spicule and 3,000-20,000 eggs/day swallowed, the infective embryonated eggs will
rectractile sheath go to the intestine and undergo four larva
 Attenuated anterior 3/5 - slender, hair-like, stages to become adult. No heart-lung
transversed by a narrow esophagus resembling migration.
"string of beads" - used for attachment
 Robust posterior 2/5 - contains the intestines
and single set of reproductive organs
B. Egg
 brown in color being bile-stained
 triple shell, the outermost layer of which is
stained brown
 barrel-shaped with a projecting mucus plug at
each pole containing an unsegmented ovum
 resembles Capillaria philippinensis- peanut
shape ova with flattened bipolar plug

PATHOLOGY
1. Rectal prolapse
 Condition in which the rectum (the lower end of
the colon, located just above the anus) becomes
stretched out and protrudes out of the anus.
Weakness of the anal sphincter muscle is often
associated with rectal prolapse at this stage,
resulting in leakage of stool or mucus.

| SERRANO, RAE ALISON D.

 *Familial disease-extremely contagious and can easily
spread among the members of the family or
institution.

Can cause autoinfection and retroinfection

Autoinfection- you on yourself is the source of
infection
Retroinfection- migration of newly hatched
2. Appendicitis and granulomas
larvae from the anus back to the rectum.
 Due to irritation and inflammation brought by
the worms MORPHOLOGY
3. Blood streaked diarrheal stools, abdominal A. Worm
pain, tenderness, anemia (associated with IDA)
and weight loss Adult Worms

DIAGNOSIS  short, white, fusiform worms with pointedalae

 Flotac technique- more sensitive in diagnosing ends, looking like bits of white thread
 Stool Examination  they can be microscopic pero maliliit lang sila
 Direct Fecal Smear  mouth is surrounded by 3 wing-like cuticular
 Kato-thick (highly recommended) expansions, which are transversely striated
 Kato-katz esophagus has a double-bulb structure, a
 Concentration Technique feature unique to this worm
 FECT Male Worm
 MIFCT
 Brine floatation  posterior end is tightly curved ventrally, sharply
 Zinc sulfate floatation technique truncated and carries a prominent copulatory
spicule
PREVENTION AND CONTROL
 Treatment of infected individuals Female Worm
 Sanitary disposal of human feces, construction  posterior third is drawn into a thin pointed pin-
of toilets like tailand straight
 Washing of hands  vulva is located just in front of the middle third
 Health education (sanitation and hygiene) of the body
 Proper food preparation practices

ENTEROBIUS VERMICULARIS
 Common name: Pinworm, Seatworm, Society
worm* (because it has familial disease)
 Final Host: man
 Habitat: (cecum) large intestine
 Diagnostic stage: ova
 Infective stage: embryonated egg
 Source of ex. to inf.: contact-borne
 MOT: Ingestion, inhalation
 Pathology: Enterobiasis or oxyuriasis
 Diagnosis: Scotch tape swab
 Drug of choice: Pyrantel pamoate
(Mebendazole and Albendazole as alternative)

| SERRANO, RAE ALISON D.

  The gravid females will migrate nocturnally
outside the anus and oviposit while crawling on
the skin of perianal area. > migrate down to the
intestinal tract and they exit through the anus
to deposit the eggs on the perianal skin.
 After egg deposition, the female usually dies.
 Eggs are resistant to disinfectants.
 Best time to collect sample: morning

Comparison of Male and Female E. vermicularis

MALE FEMALE
2 to 5 mm 8-13 mm
Curved tail and has a long pointed tail
single spicule 5,000-17,000 eggs/day
*rarely seen because
they die after copulation
B. egg

PATHOLOGY
 Mild catarrhal inflammation of the intestinal
mucosa
 Nocturnal pruritus ani- "perianal itching" which
may lead to secondary bacterial infection and
lack of sleep
 Other complications: appendicitis, vaginitis,
endometritis and peritonitis.
 Poor appetite, weight loss and abdominal pain.

D-shaped eggs of E. vermicularis.

Asymmetrical, with one side flattened and the
other side is convex. Translucent shell: triple
albuminous outer layer for mechanical
DIAGNOSIS
protection and inner embryonic lipoidal layer  Graham’s scotch adhesive tape swab (Perianal
for chemical protection. Ovum develops into cellulose tape swab)
“tadpole-like embryo”  Provides the highest percentage of (+)
LIFE CYCLE results
 Infection occurs via self-inoculation or through
exposure to the eggs in the environment.
 Following the ingestion of infective eggs, the
larvae will hatch in the small intestine and the
adults will establish themselves in the colon
usually at cecum.

| SERRANO, RAE ALISON D.

 PREVENTION AND CONTROL
 Personal cleanliness and hygiene are essential
 Hand washing
 Boiling of linen and clothing

| SERRANO, RAE ALISON D.