MIDTERMS

PLASMODIUM SPECIES

Stage of development

1. Ring Forms

– Early Trophozoites

– as the name implies, refers to a ring like appearance of the malarial parasite following
invasion into a previously healthy RBC
– space inside the ring is known as a vacuole

2. Developing/Growing Trophozoites

– remnants of the cytoplasmic circle and chromatin dot are still intact until late development
– the parasite is actively growing during this stage, the amount of RBC space invaded is
significantly more than that of the ring form

3. Immature/Presegmenting Schizonts
– active chromatin replication is seen
– expands and occupies more space within the RBC

4. Mature Schizonts
– Merozoites: emergence of the fully developed stage of the asexual sporozoa
trophozoite

5. Microgametocytes
– typical microgametocyte is roundish in shape (except P. falciparum, which is
crescent-shaped)
– large diffuse chromatin mass that stains pink to purple and is surrounded by a
colorless to pale halo
– pigment is usually visible

6. Macrogametocytes
– round to oval (except P. falciparum, which is crescentshaped)
– pigment is also present, and its color and distribution in this morphologic form vary by
individual Plasmodium species
Plasmodium falciparum

■ Disease: malignant malaria, aestivo-autumnal, falciparum malaria, subtertian malaria,

pernicious malaria, Black water fever malaria
■ It is most prevalent in the tropics and subtropics
– It causes the most severe form of malaria
– It still remains almost unchallenged as the greatest killer of the human race over most
parts of Africa and elsewhere in the tropics.

■ Size of Erythrocytes: normal, multiple-infected RBC are common

■ Maurer’s dots occasionally seen
■ Young rings are small, delicate, often with double chromatin dots, accole, applique

🌛
■ > 1 ring form can be found in 1 RBC (multiple infection)
■ Gametocytes are crescent or elongated
■ Pigment: black, coarse and conspicuous in parasite
■ Number of merozoites: 6-32, average is 20-24
■ Schizonts: bad prognosis
■ Stages found in Circulating Blood: Young, growing trophozoites (ring forms) and
gametocytes

▪ numerous rings without mature forms

▪ slightly smaller
▪ marginal forms
▪ trophozoites and schizonts
▪ not normally seen in peripheral circulation
▪ severe disease
▪ compact parasite
▪ 6-32 merozoites

▪ crescentshaped gametocytes
Plasmodium vivax

■ Disease: vivax malaria or benign tertian malaria

■ Most widespread, found in most endemic areas including some temperate zones
■ It is more common in temperate than in tropical region.
■ It is the second common Malaria in the Philippines.

■ Size of Erythrocytes: enlarged, maximum size may be 1 ½ - 2 times normal (attained

with mature trophozoites and schizonts)
■ Ring forms occupies 1/3 diameter of RBC
■ Schuffner’s dots present in all stages except early young forms
■ Irregular, ameboid trophozoites, has spread-out appearance
■ Pigment: Golden brown, inconspicuous
■ Number of merozoites: 12-24, average is 16
■ Stages found in circulating blood: all stages

•enlarged erythrocyte
•Schüffner’s dots
•‘ameboid’ trophozoite
•12-24 merozoites

Plasmodium malariae

■ Disease: malariae or quartan malaria

■ Similar range as P. falciparum, but less common and patchy distribution
■ Common in tropical Africa, Burma, Sri lanka, India, Malaysia and Indonesia.
■ It is occasionally seen in the Philippines.
■ Size of erythrocytes: normal
■ Ziemann’s dots rarely seen
■ Rounded, compact trophozoites with dense cytoplasm.
■ Band form trophozoites occasionally seen
■ Pigment: dark brown, conspicuous
■ Rosette schizonts occasionally seen
■ No. of merozoites: 6-12, average is 8
■ Stages found in circulating blood: all stages
▪ compact trophozoite
▪ 'band' form

🌺
▪ 6-12 merozoites in mature schizont
▪ ‘rosette’
Plasmodium ovale
■ Disease: ovale malaria, Benign tertian malaria
■ It is the least common Plasmodium infecting man.
■ It occurs mostly in tropical Africa, principally on the west coast and is endemic in
Ethiopia.

■ Size of erythrocytes: enlarged, maximum size may be 1 ¼ - 1 ½ times normal,

approximately 20% or more infected RBC are oval and fimbriated (border has irregular
projections)
■ Schuffner’s dots present in all stages except early ring forms
■ Rounded, compact trophozoites, occasionally slightly ameboid
■ Growing trophozoites have large chromatin mass
■ Pigment: dark brown, conspicuous
■ No. of merozoites: 6-14, average is 8
■ Stages found in circulating blood: all stages
▪ similar to P. vivax

▪ enlarged erythrocyte
▪ Schüffner’s dots

▪ subtle differences

▪ ‘compact’ trophozoite
▪ fewer merozoites (8)
▪elongated erythrocyte

Plasmodium knowlesi

🐵
■ a primate malaria parasite commonly found in Southeast Asia.
■ It causes malaria in long-tailed macaques (Macaca fascicularis), but it may also
infect humans, either naturally or artificially.
■ The fifth major human malaria parasite
■ This is an emerging infection that was reported for the first time in humans in 1965.
■ It accounts for up to 70% of malaria cases in South East Asia where it is mostly found
Plasmodium knowlesi (Trophozoite)

■ In developing trophozoites of P. knowlesi, band forms may appear that are similar in
appearance to P. malariae.
■ As the vacuole is lost during maturation of the trophozoite stage, the parasite becomes
smaller and more compact.
■ The pigment appears as dark grains and the red nucleus increases in size.
■ Stippling appears, often referred to as 'Sinton and Mulligan's' stippling

Plasmodium knowlesi (Schizont)

■ In developing schizonts of P. knowlesi, Sinton and Mulligan's stippling may be

observed.
■ The nucleus continues to divide until there are up to 16 (average 10) merozoites.
■ As the schizont matures, it fills the host RBC and the pigment collects into one or a few
masses.
■ In the mature schizont, the merozoites may appear 'segmented' and the pigment has
collected into a single mass.

■ It may cause severe malaria as indicated by its asexual erythrocytic cycle of about 24
hours.
■ The typical fever becomes quotidian
Invertebrate Phase
■ 4-15 days after ingestion of gametocyte
■ Female Anopheles mosquito takes a blood meal containing gametocytes from infected person
o Microgametocytes – male
o Nuclear division and exflagellation
o Macrogametocytes – female
o Shifting of nucleus to the surface to form a projection
o Microgamete penetrates macrogametes producing an ookinete

Vertebrate Phase
■ Mosquito injects sporozoites to man
■ Sporozoites disappear from the blood
– Some are destroyed by the host immune system
– Enters liver parenchymal cells (hypnozoites in P. vivax and P. ovale)

Insect Vectors in the Philippines

■ Anopheles flavirostris – primary vector in the Philippines, night biter, breeds in slow-flowing
clean water mountain streams
■ Anopheles balabacensis - rest either indoors or outdoors, in puddles, pools, ponds, and in
shades.
■ Anopheles lesteri - rest either indoors or outdoors, in pools, ponds, lakes, and in ricefields.
■ Anopheles philippinensis - rest either indoors or outdoors, in pools ponds or lakes.
■ Anopheles umbrosus - rest out of doors, in pools, ponds, lakes, running streams and canals in
shades.
■ Anopheles leucosphyrus – vector of Plasmodium knowlesi, typically found in forest areas in
South East Asia but with a greater clearing of forest areas for farmland
■ Anopheles litoralis, Anopheles maculates, Anopheles mangyanus

Malaria Transmission

🦇 natural (sporozoites/Anopheles)
💉 blood transfusions
▪
▪
▪ shorter incubation period
▪ fatality risk (P. falciparum)

💉
▪ relapses possible (P. vivax/ovale)

👶
▪ syringe sharing
▪ congenital
▪relatively rare although placenta is heavily infected

Clinical features

▪ characterized by acute febrile attacks (malaria paroxysms)

▪ periodic episodes of fever alternating with symptom-free periods
▪ manifestations and severity depend on species and host status
▪ immunity, general health, nutritional state, genetics
▪ recrudescences and relapses can occur over months or years
▪ can develop severe complications (especially P. falciparum)
Malarial paroxysms

■ Periodicity varies according to species

■ Depends on the length of the asexual cycle
■ Plasmodium falciparum
– Malignant tertian malaria (36 hours or less)
■ Plasmodium vivax and P. ovale
– Benign tertian malaria (48 hours)
■ Plasmodium malariae
– Quartan malaria (72 hours)

Pathogenicity of Malaria
■ In P. falciparum infections, as the parasite begins to grow, the red cell membrane becomes
sticky and cells adhere to the endothelial lining of the capillaries of the internal organs
■ thus, only ring forms and gametocytes appear in the peripheral blood

Anemia
■ More pronounced in P. falciparum
■ Hemolytic, normochromic, normocytic anemia
■ Decrease Oxygen carrying capacity leading to anoxia

Splenomegaly
■ Caused by an increase in splenic activity
■ Parasitized red cells pass through the spleen, loss their deformability, thus destroyed in the
process
■ Normal RBC’s are destroyed due to increase activity of macrophages

Nephrotic Syndrome
■ Seen in Plasmodium malariae infection
■ Deposition of antigen – antibody complexes causes thickening of the capillary walls of the
basement membrane
■ Presence of focal hyalinizing lesions of the tuft of the glomerulus and segmental endothelial
cell proliferation progressing to glomerular sclerosis

Blackwater Fever
■ Sydrome of acute intravascular hemolysis, accompanied by hemoglobinemia and
hemoglobinuria
■ Abrupt onset, passage of dark red or almost black urine, vomiting of bile stained fluid, jaundice
■ High mortality
■ Rapid and severe hemolysis of both parasitized and non – parasitized red cells
■ Presence of the parasite changes the antigenic structure of individual erythrocytes and
stimulates the production of antibodies

Disseminated Intravascular Coagulation (DIC)

■ Most serious hematologic complication
■ Activation of the clotting system resulting to thrombin generation and intravascular coagulation

Severe Falciparum Malaria

■ Prostration: first probable symptom, a condition characterized by confusion or drowsiness with
extreme weakness
■ Unarousable coma (Cerebral malaria)
■ Generalized convulsions
■ Severe normocytic anemia
■ Hypoglycemia
■ Metabolic acidosis with respiratory distress
■ Fluid and electrolyte disturbances
■ Acute renal failure
■ Acute pulmonary edema and Adult Respiratory Distress Syndrome (ARDS)
■ Circulatory collapse, shock, septicemia (algid malaria)
■ Abnormal bleeding
■ Jaundice
■ Hemoglobinuria
■ High fever
■ Hyperparasitemia
Relapse
■ Present in P. ovale and P. vivax
■ Activation of hypnozoites (liver stages) resulting to renewal of malarial infection.

Recrudescence
■ Renewal of parasitemia or clinical features arising from persistent undetectable asexual
parasitemia in the absence of an exoerythrocytic cycle
■ P. falciparum: Due to infected RBC sequestered by the spleen

Diagnosis
■ Prompt and adequate diagnosis is necessary
■ Clinical diagnosis: symptoms
■ History of being in endemic area

🔬
Diagnosis

💉
■ Microscopic identification of the malarial parasites
■ Thick and thin blood smear
•thick film: screening for positivity and parasite count
•thin film: species identification easier
■ Stained with Giemsa or Wright’s stain
■ Gold standard for malarial diagnosis
■ Taken at the before height of the fever (schizogony) and before antibiotic administration,
highest number of parasite in the blood
■ repeat smears every 12 hours for 48 hours if negative

🔬
Diagnosis
■ Quantitative Buffy Coat (QBC)
– Usually prepared capillary tube coated with acridine orange
– Malaria parasites take up the stain and appear bright green and yellow under a fluorescent
microscope

🖥
Diagnosis
■ Rapid Diagnostic Tests (RDT)
– Detects parasitic antigens:
o Pan malaria: p-LDH (Diamed Optimal IT)
 o Falciparum malaria: HRP-II (Paracheck Pf Test, ParaHIT f Test)
– Makes use of immunochromatographic methods in order to detect Plasmodium-specific
antigens in a finger-prick blood sample
– Advantages: Can be performed in 15-30 mins, 90% specific
– Disadvantages: lack of sensitivity at low levels of parasitemia, inability to quantify, more costly

🖥
Diagnosis
▪ Serological Tests
– Cannot differentiate current and past infections
– Most helpful in epidemiological studies o Indirect Hemagglutination (IHA)
o Indirect Fluorescent Antibody Test (IFAT)

🖥
o Enzyme-linked Immunosorbent Assay (ELISA)
■ Polymerase chain reaction (PCR)
– To significantly enhance the microscopic diagnosis of malaria especially in cases of low
parasitemia and in cases of mixed infection

Malaria Control

💁Reduce Human-Mosquito Contact

•Insecticide treated bed nets (ITN)
•repellants, protective clothing
•screens, house spraying

🦇Reduce Vector
•environmental modification
•larvacides/insecticides
•biological control

🦍Reduce Parasite Reservoir

•diagnosis and treatment
•chemoprophylaxis

💊
Treatment
■ Most drugs used in the treatment are active against the parasite forms in the blood
– Chloroquine: drug resistance with P. falciparum
– sulfadoxine-pyrimethamine (Fansidar®)
– mefloquine (Lariam®)
– atovaquone-proguanil (Malarone®)
– quinine – doxycycline
– artemisin derivatives
■ In addition, primaquine is active against the dormant parasite liver forms (hypnozoites) and
prevents relapses

Babesia Species

Babesia Taxonomy

■ Phylum Apicomplexa
■ Class Sporozoea
■ Subclass Coccidia
■ Subclass Piroplasmia – no oocyst
■ Order Piroplasmida
■ Genus Babesia

▪ Common tick-borne parasite of domestic and wild animals

▪ Parasites of red blood cells, causes malaria-like infections
▪ No intracellular pigment in developmental stages
▪ Rare zoonotic human infection, natural host are the rodents and deers
▪ white-footed mouse (Peromyscus leucops)
Geographic Range

■ Worldwide, especially in:

– Europe (although, mostly Babesia divergens)
– Asia
– United States
■ Particularly in the Northeast: Especially New England, New York & other coastal regions
■ Has been spotted in other parts of the U.S., such as the mid-west

Human Babesiosis

Mode of Transmission

🐞 Tick-bite
👶 Transplacental
■

💉 Blood transfusion
■
■
Babesia microti

▪ Common species diagnosed in human.

▪ Small rings within the red blood cell, very much like Plasmodium falciparum with a darkly
staining nucleus and very little cytoplasm.
▪ It do not have associated pigment in the red blood cell.
▪ Asexual multiplication by binary fission in the RBC with production of merozoite that invade
other RBC.
▪ When taken up by the ticks, there is complex cycle of multiplication that includes a sexual
stage, resulting ultimately in the presence of the parasites in the salivary gland of the tick.
Definitive Hos

■ A tick is the definitive host

■ Transmission occurs from an animal to a human, normally using the northern deer tick or
black-legged tick (Ixodes scapularis) as the vector.
Babesia divergens

■ transmitted by the tick Ixodes ricinus

■ main agent of bovine babesiosis, or redwater fever in Europe
■ it can also infect immunocompromised humans, causing medical emergencies characterized
by rapid fulmination and parasitemias that may exceed 70%

Life cycle
Human Babesiosis

▪ Clinical disease
▪ asymptomatic to fatal
▪ more severe in splenectomized persons, elderly, or immunocompromised
▪ characterized by fever, chills, sweating, myalgia, fatigue, nausea, loss of appetite
▪ moderate to severe hemolytic anemia ▪ Renal failure, jaundice and hepatosplenomegaly

💉
Diagnosis
▪ parasite in thin or thick blood smear

🗺
▪ Tetrad-forms or Maltese-cross arrangement of merozoites

🖥
▪ no travel history
▪ Serology
▪ IFA
▪ lack of response to anti-malarials

Treatment

▪ no generally effective drugs

▪ Clindamycin (DOC) + quinine is recommended
▪ reduces duration of parasitemia
▪ high level of adverse side affects
▪ atovaquone + azithromycin
▪ as effective as clindamycin + quinine
▪ fewer adverse affects
▪ blood transfusions for severe anemia

Prevention
 🙌
🐞
■ Skin checks for ticks after being in wooded areas

🕺
■ Check animals for ticks
■ Wear long clothing
■ Find a good tick repellant

WEEK 8 (COCCIDIANS)

PHYLUM APICOMPLEXA

Review:
-Toxonomy review of Species under Phylum Apicomplexa
-Under Phylum Apicomplexa are the parasites that don’t have locomotory organelle
-Under Phylum Apicomplexa we have the Class Sporozae
Class Sporozae- Parasite that don’ts have locomotory organelle that produces Spores
-Under the Class Sporozea we have the Subclass Coccidia
-Under the Subclass Coccidia we have the Sub-Order Haemosporina
-Under the Sub-Order Haemosporina we have the Plasmodium Species
-Under the Subclass Coccidia we also have another Sub-Order which is the Sub-Order
Eimeriina
-Under the Sub-Order Eimeriina we have the Toxoplasma gondii, Cryptosporidium
parvum, Cyclospora cayetanensis, Cytoisospora belli, & Sarcocystis Species

Coccidians
Coccidia

■ Class Sporozoea.
-Under Sub-Order Eimeriina
■ Coccidian parasites infect the intestinal tracts of animals
■ The largest group of apicomplexan protozoa.
■ obligate, intracellular parasites, which means that they must live and reproduce within an
animal cell.
■ with no definite organ of locomotion
■ It may have body flexion, gliding or undulating of longitudinal ridges(NOT ALL OF
THEM).

- These Coccidian Parasites tends to Infect Intestinal Tract of Animal or Any kinds or Any
specific Host
- We can call the Coccidians as Intestinal Coccidians because they tend to infect the
Gastro-Intestinal Tract of their Host
- Only discussing the only coccidians that concerns the Human
- This Coccidians are Obligate Intracellular Parasites that mean it requires that this
parasites specific Stage (Merozoite) of these parasites should invade the cells of their
Host and to continue its life cycle they must live and reproduce within the animals cells
- For them (Coccidians) to continues their life cycle and inorder to live they must invade
and infect a cell. Within that cell they (Coccidians) will reproduce, differentiate, &
replicate
- They don’t have an definite organ for locomotion. Generally they are Emotile
Coccidia
- In Coccidian parasites we will describe & Characterize a specific developmental stage in
the life cycle of the parasite which is the OOCYST

▪ characterized by thick-walled oocysts excreted in feces

OOCYST- is a cyst structure that contains Sporozoites inside
- In the same way in the malarial parasites and Plasmodium species yung Oocyst ng
coccidians ay may Sporozoites sa loob
- As for the morphology of the Coccidians magkakaiba sila ng morphology ng oocyst
- Generally the Oocyst of the Coccidians have a Thick Outer Wall ( Ang Outer walls ng
Coccidians ay makakapal) that means na may prinoprotektahan doon sa loob. The Thick
Wall of the Oocyst will serve as a protection for the developing Sporozoites inside
- The Oocyst is usually Secreted on the FECES of its Definitive Host

In Humans

•Cryptosporidium
•Isospora
•Cyclospora
•Toxoplasma
•Sarcocystis

Coccidia

■ In Isospora, Cyclospora and Cryptosporidium (*ICC) only a single direct cycle of

transmission occurs, both the asexual and sexual stages of multiplication occurs in a single
host and that is to man.
- The MAN harbors both Asexual & Sexual stages of the Parasite Isospora,
Cyclospor & Cryptosporidun (ICC)
- The Man can also called as the Definitive Host or the Final Host
- Isospora, Cyclospora and Cryptosporidium (*ICC) are part of the Coccidains that
shows both Asexual & Sexual Reproduction on its host which is the MAN
 - MAN is the only host for the Isospora, Cyclospora and Cryptosporidium (*ICC)

■ In Sarcocystis and Toxoplasma, the sexual stages are usually in the intestinal mucosa of a
carnivorous host (the predator). The result in an oocyst or sporocyst that passes out in the
feces to infect an intermediate host (the prey) in which asexual multiplication of the parasite
occur.
- The Sarcocystis & Toxoplasma are only seen at the Intestinal Mucosa of a Carnivorous
Host (PREDATOR)
- When we say sexual Stages that means it is seen at it’s definitive host
- Definitive Host means that it harbors the Sexual Stages of the parasite
- The sexual spores like the Gametocytes (Doon nagyayari yung cartilization of the
gametocytes
- Oocyst or Sporocyst will passes out the feces of its Definitive Host and will infect the
Intermediate Host
- Within the Intermediate Host the multiplication, replication & differentiation of the
Asexual stages of the parasite will happen
- Pag Intermediate ang host it harbors the Asexual stage of the parasite
- Basta ang tatandaan lang on the species ng Sarcocystis & Toxoplasma is yung
Definitive host ang nangyayari sa kanya is yung Sexual stage ng parasite anf sa
intermedite host naman is yung Asexual stage ng parasite
- For example is yung Cat as a definitive Host ng toxoplasma gondi and makaka infect sa
kanya is yung Sexual stage ng parasite tapos dudumi sya, within doon sa dumi nya
nadoon ang asexual stege ng parasite na yun ang makaka infect naman sa rats yung
asexual stage ng parasite na yun kaya maiinfect si rat, kasi si rat yung intermediate hot.
Tapos si cat kakainin nya si rat na infected ng Asexual stage ng parasite tapos magiging
sexual nanaman ang stage within the cat

Life Cycle

▪ Merogony (Only Happens on Intermediate Host because it is a Asexual reproduction of the

parasite)
▪ schizogony other Name for the Merogony (Asexual Stage occuring in the various Nucleated
Cells of it’s Intermediate Host)
▪ produce merozoites (End product of the Merogony is the Production of the Merozoites)

▪ Gametogony (Happens also within the cells)

▪ gamogony or gametocytogenesis (Other name for the Gametogony)
▪ produce micro- and macrogametes (End product of the Gametogony)

▪ Sporogony (Sexual stage reproduction of the parasite that happens in Definitive host)
▪ produce sporozoites
▪ completed on host cell
 ▪ thin (autoinfection) or thick walled oocysts (Final Product of the Sporogony is the
production of Thin-walled Oocyst or commonly the production of Thick-walled Oocyst)
- The Thin-walled Oocyst is responsible for Autoinfection and usually the Thick-walled
Oocyst is past through the environment to find a new Intermediate host

-If the Sporozoites is the infective stage for the intermediate host
-The Sporozoites that is ingested by the intermediate host, and this sporozoites that is ingested
will migrate to the cells of the Intermediate host

Toxoplasma gondii
● One of the most important coccidian parasite
● Causes toxoplasmosis
● Most acute infections are asymptomatic
● Immunosuppressed: infections with T. gondii usually presents with CNS involvement
● Toxoplasma gondii is a protozoan parasite that has affinity to infect tissues of human
CNS

● cosmopolitan distribution
● seropositive prevalence rates vary
● generally 20-75%
● generally causes very benign disease in immunocompetent adults
● tissue cyst forming coccidia
○ predator-prey life cycle
■ Predator - definitive host
■ Prey - intermediate host
○ felines are definitive host
○ Infects wide range of birds and mammals (intermediate hosts)
 ● Sexual/Enteric (Definitive Host)
○ Intestine of cat
● Asexual (Intermediate Host)
○ Outside the intestine of cat, animals, man

Typical Life Cycle in Felines

● Cats will serve as the definitive hosts

● All stages of the parasite can occur inside the body of the cat
● It is the cat which is the primary host of T. gondii, other animals are considered as
reservoir host and humans are considered as accidental host
● Life cycle will revolve around the cats
○ Rats and birds can be included because they are reservoir host

1. Cats are infected by ingestion of T. gondii cyst (it is composed of bradyzoites simply
merozoites)
2. Upon ingestion, bradyzoites will become trophozoites inside the small intestine of the
parasite
3. The trophozoites will invade intestinal epithelial cells and will undergo merogony
4. Merozoites will multiply and differentiate into the cell
5. Male gametes will fertilize the female gametes that will produce a zygote
6. Zygote will become oocyst
7. Oocyst will be passed out in the feces of the cat
8. Immature oocyst needs to undergo sporogony or sporulation outside the environment
and it is considered as immature cyst when sporoblast is only seen
9. Mature oocyst that is seen in soil will be considered mature if there is a presence of 2
sporocyst (each sporocyst contains 4 sporozoites)
a. Mature oocyst - infective stage to the intermediate host

● Fertilization within infected host cells

● Immature oocysts in feces
● Sporulation in environment (1-4 days)
Merozoites: Tachyzoites vs. Bradyzoites

● Tachyzoites has been coined for the first, actively multiplying merozoites that develop
within the intermediate host, irrespective of whether infection is from oocysts or
tissue cysts
○ Diagnostic stage that is found in the tissue of humans

Tachyzoites in peritoneal macrophage

● Metrocytes (noninfectious) and

● bradyzoites (infectious) are merozoites that develop within tissue cysts
○ slower
 Pseudocyst: filled with bradyzoites

Tachyzoite Stage
● Ingestion of oocysts
● Sporozoites penetrate intestinal epithelium
● Rapid intracellular replication (any cell)
● Dissemination via macrophages

2 sporocyst and 4 sporozoite

Tachyzoite Stage
● merogony → 'merozoites'
● typical apicomplexan
○ motile invasive stages
○ intracellular replication
● 'binary fission' = endodyogony

▪ repeated rounds of merogony

▪ acute stage infection
▪ primarily in reticulo-endothelial cells
Bradyzoite Stage
● Dormant, slowly replicating
● Due to host immune response
● Chronic or latent infection
● Tissue cysts primarily in brain and muscle
● Tough cyst wall - Zoitocyst

😿
Human Transmission

🍗
● ingestion of sporulated oocysts (cat feces + incubation)

👼
● ingestion of zoites (tachyzoite & bradyzoites (undercooked meat)

😰
● congenital infection (only during acute stage)
● organ transplants
○ chronic infection in donor

💉
○ Immunosuppression
● blood transfusions (only during acute stage)
LIFE CYCLE
● Main host: cat and rat
● Definitive host: Cat
● Intermediate host: Rat

1. Cat acquires the infection by ingesting tissue cysts that contain bradyzoites that will
develop into trophozoite in the intestine of the cat
2. Trophozoite will become merozoites and merozoites will multiply and eventually will
become gametocytes
3. Male will fertilize the female producing a zygote called oocyst
4. Oocyst that is passed out from the stool of the definitive host is immature. It will mature
in the soil and will become a mature oocyst.
5. The mature oocyst will become the infective stage to the intermediate host which is the
rat. Within the rat, sporozoites will be liberated inside the oocyst.
6. Sporozoites will be released and will directly infect the intestinal epithelial cell of the
intermediate host. Within the cell, 2 merozoites will develop.
a. Tachyzoites
b. Bradyzoites

How are humans infected?

1. Humans are infected through the ingestion of oocyst (primarily the mature oocyst) from
contaminated water and food
2. Mature oocyst will release its sporozoites inside the intestine and the sporozoites will
invade the intestinal epithelial cells
3. Sporozoites will become tachyzoites
4. Parasites from tissue cyst most likely in the skeletal muscle, myocardium, brain, and
eyes
5. Another way to be infected is by ingestion of undercooked cattles, pigs, and sheeps
6. Another way is blood transfusion from the infected host
7. Man is the final host

Pathogenesis
● The organisms can grow in any organs or tissues, developing in the brain, eyes and
skeletal muscles
● There is localized proliferation of the organisms and immunologic hypersensitivity
reactions.
● Multiplication of the organisms within the infected cell leads to death and rupture of the
cell.

Clinical Manifestations
● Most of the cases are asymptomatic.
● Congenital toxoplasmosis is often severe and even fatal.
 ● Sabin syndrome (tetrad of signs)
○ Chorioretinitis
○ Cerebral calcification
○ Convulsion or psychomotor disturbances
○ Hydrocephalus or microcephalus

Other Forms of Toxoplasmosis

● Typhus-like exanthematous form
○ may produce myocarditis, meningoencephalitis and atypical pneumonia
● Cerebrospinal form
○ There is involvement of the CNS and the CSF is xanthochromic.
○ Normal color: crystal clear
● Non-congenital retinochoroiditis infection
○ The ocular lesion originates in the retina and spread to the choroids.

Ocular Toxoplasmosis
● retinochoroiditis: likely due to both active parasite proliferation and immune
hypersensitivity
● generally a recrudescence--rarely from primary infection
● congenital infection
○ 20% exhibit ocular symptoms at birth
○ 82% by adolescence
● most lesions are focal and self-limiting
● rapidly destructive in AIDS patient
 🔬
Diagnosis
● Identification of the organism in smears of lymph nodes, bone marrow, spleen or

🐭
brain or other materials.

🔬
● Inoculation into mice or cell culture (only acute stage)
● Sabin-Feldman methylene blue dye test: very sensitive and specific but requires
maintenance of live organism

🖥
○ Gold standard for T. gondii
● Serological test: to detect antibodies
○ Polymerase chain reaction (PCR) : detection of the parasites DNA
○ ELISA
○ IFA
○ EIA
○ Latex agglutination

Treatment
● Pyrimethamine and sulfadiazine
○ controls Toxoplasma but does not kill it.
○ Leucovorin (folic acid): pyrimethamine can cause lower blood counts
○ Sulfadiazine: causes allergic reaction but can be substituted by clindamycin
○ Corticosteroids: prevent occurrence of hypersensitivity
● Trimethoprim-sulfamethoxazole: prophylaxis for immunocompromised
 🍖
Prevention and Control
■ Proper cooking of meat (66oC, 150oF)
– wear gloves when handling

⛺
– wash hands after

🙀
■ Environmental sanitation
■ Careful attention to cat feces
– clean litter box promptly (<24 hr)
– wear gloves
– keep cat in house
– cover sand box
– no cats in home
– control strays

🌍
Isospora belli
● Though rare, it has a wide geographical distribution (higher prevalence in warmer
climates)
● The least common of the intestinal coccidia that infect humans
● Can cause severe disease with fever, malaise, persistent diarrhea and even death in
AIDS patients
● Monoxenous (required one host) , probably not zoonosis: Asexual and sexual
multiplication occurs in man

● Mode of Transmission: Human are probably infected by accidental hand-to-mouth

ingestion of mature oocyst in food and water.
● Habitat: Distal duodenum and proximal jejunum
Pathology
● invades intestinal epithelial cells
● often asymptomatic (seldom reported)
● symptoms range from mild gastro-intestinal distress to severe dysentery
● often self-limiting, but can become chronic (wasting, anorexia)
● symptoms more severe in AIDS patients

● 30 x 12 mm oocyst
● 2 sporocysts
● 4 sporozoites each

Pathogenesis
● Infection is confined to intestinal epithelial cells.
● Destruction of the surface layer of the intestine.
 ● There is malabsorption markedly abnormal intestinal mucosa with short villi,
hypertrophied crypts and infiltration of the lamina propia with eosinophilia,
neutrophils and round cells.

Clinical Manifestations
■ Infections are often asymptomatic and self -limiting.
■ It may be from mild gastrointestinal distress to severe dysentery.
■ The loose, pale yellow and foul-smelling stools are suggestive of malabsorption process.
■ There may be chronic diarrhea, vague or crampy abdominal pain, weight loss, weakness,
malaise and anorexia.
■ There may be diarrhea over a period of several months to 15 years.

🔬
Diagnosis
■ Stool examination to demonstrate the immature oocyst from the feces

🔬
– Iodine stain which facilitates identification.
■ Modified acid fast stain (Kinyoun’s stain/Auraminerhodamine) wherein oocyst wall

🎈
does not stain and sporoblast is deep red stained.

🛢
■ Enterotest™
■ Concentration technique
– zinc sulfate flotation method
– Formalin-ether sedimentation method
– Sheather’s sugar flotation

Treatment and Prevention

■ For mild or asymptomatic infection, non specific measures such as rest and bland diet mat be
sufficient.
■ AIDS patients: trimethoprim-sulfamethoxazole
■ Prevention: same as Entamoeba histolytica
Sarcocystis spp.

Sarcocystis

▪ The name is dervived from Greek: sarx = flesh and cystis = bladder
▪ rare human infection
▪ heteroxenous parasite
▪ predator-prey life cycle
▪ humans support both stages
▪ originally identified as 2 species
▪ intestine ~ Isospora
▪ tissue ~ Sarcocystis
▪ taxonomic confusion
▪ generally named after host species
▪ Sarcocystis hominis
▪ Sarcocystis suihominis

Intestinal Disease

▪ ingest undercooked meat

▪ transient mild to severe diarrhea
▪ excrete sporulated sporocysts
▪ 13x10 mm
▪ 4 sporozoites
Muscle Disease

▪ ingest sporocysts
▪ develop sarcocysts
▪ several 100 mm
▪ compartments
▪ sometimes thick striated wall
▪ muscle tenderness
▪ episodic inflammation

Pathology and Clinical Manifestation

■ Human sarcocystosis/sarcosporidiosis
– gastroenteritis with diarrhea
– eosinophilic enteritis
– myalgia and weakness
– mild increase of creatine kinase
■ Intermediate host
– gait abnormalities
– muscle wasting
– head tilt
– animals observed to move in circles
– abortion in pregnant animals

Diagnosis

🐮 bradyzoites
■ Fecal floatation methods
■ Brain tissue biopsy in animals:
■ Serological methods:
 – IFA
– ELISA
– PCR
– Western blot

Treatment

■ No effective treatment known

■ Corticosteroids: treating muscular inflammation

Cryptosporium spp.

Cryptosporidium
▪ fecal-oral transmission (monoxenous)
▪ wide range of animal hosts (C. parvum)
▪ several host-adapted species
▪ C. hominis for human species
▪first human case reported in 1976
▪ self-limiting diarrhea in immunocompetent persons
▪ profuse, watery diarrhea associated with AIDS (life threatening)

Cryptosporidium

■ C. baileyi (birds)
■ C. felis (cat)
■ C. meleagridis (turkeys)
■ C. muris (mouse)
■ C. nasorum (fish)
■ C. serpentis (snakes)
■ C. wrairi (guinea pigs)
■ C. parvum (mammals)
■ C. hominis (humans)

Cryptosporidium hominis

■ Disease: Cryptosporidiosis
■ World wide in distribution
■ Common cause of diarrhea among travelers and in day care centers.
■ Can occur as water-borne outbreaks
■ Zoonosis from domestic animals.
■ More common in children than adult.

Cryptosporidium hominis

▪ 4-5 mm oocysts
▪ 4 sporozoites
▪ no sporocysts

Cryptosporidium hominis
■ Habitat:
– Brush border of the mucosal epithelium of the stomach or intestine.
– May involved the gallbladder and pancreatic duct.

■ Pathogenesis:
– Destruction of the host cells
– villi of intestine: infiltration of inflammatory cells into the lamina propia and elongated
crypts

Clinical Manifestations

■ Self-limiting in person with sound immune function

■ Nausea and vomiting, abdominal cramps, weight loss and fever
■ Diarrhea
■ Severe fluid loss from diarrhea and vomiting can lead to fatal outcome in children

Diagnosis

🔬
🎈
■ Stool examination to identify the oocyst.

🔬
■ Enterotest™: to recover oocyst.
■ Kinyoun’s modified acid fast stain: red-pink doughnut shaped circular organism in a

🛢
blue background
■ Concentration test

🖥
– Sheather’s sugar flotation
■ Serological test:
– EIA
– DNA probes specific for C. hominis

Treatment and Prevention

■ 💊Treatment:
– Spiramycin
– Pyrimethamine and sulphadiazine

🛀
– Somatostatin
■ Preventive Measures:
– Environmental sanitation
– Personal hygiene
Cyclospora cayetanensis
● Inhabits in small intestine
○ Cryptosporidium
○ Cyclospora
○ Cytoisospora
● Sarcocystis
○ Small intestine - definitive host
○ Muscle - intermediate host

Cyclospora cayetanensis
● First human case in 1979
● Named in 1993
● Initially called ‘cyano-bacteria like body’ (CLB) or large Cryptosporidium
● No known animal reservoir
● More common in tropical and sub-tropical areas
● Infection most common in HIV/AIDS patients.

● In freshly passed stools, the oocyst is not infective (direct fecal-oral transmission
cannot occur; this differentiates from Cryptosporidium).
● Immature oocyst
○ Crumpled cellophane
○ Red against the blue background
○ Diagnostic stage
○ Not readily infective
● In the environment, sporulation occurs after days or weeks at temperatures between
22°C to 32°C, resulting in division of the sporoblast into two sporocysts, each containing
two elongate sporozoites.
 ○ 8-10 mm oocytes
■ Mature
■ Infective stage
○ 2 sporocysts
○ 2 sporozoites each

● Fresh produce and water can serve as vehicles for transmission

○ water-borne

Pathogenesis
● Onset of symptoms may occur 12-24 hrs after exposure
● Chronic and intermittent diarrhea alternating with constipation
● Fatigue, anorexia, weight loss, nausea, vomiting, abdominal pain, flatulence, bloating,
dyspnea
● Mature oocyst → sporozoites → invade the intestinal epithelial cell → within the small
intestine, merozoites will develop inside the cell and can either re-infect another cell
when liberated and can transform into gametes → merozoites → gametes → fertilization
→ zygote will become immature oocyst → sporozoites

Pathology
● Cyclospora infects enterocytes of the small bowel where various stages, sexual and
asexual stages have been observed.
 ● Villous blunting, mild crypt hyperplasia and variable increased chronic inflammatory
cells in the lamina propria.

● In the immunocompromised patient, severe diarrhea can last up to 4 months or longer

even if treated thus producing a disease syndrome that is debilitating and life
threatening
● Extra-intestinal infection appears to be more common in AIDS patients

🍽
Transmission
● associated with food-borne outbreaks
● luncheons, social events, weddings, etc.

🍒
● possible source always involved foreign country and fresh fruit or vegetables

🥗
● raspberries from Guatemala

🥗
● leafy vegetables from Peru and Nepal
● lettuce and basil pesto in US
● presumed source: contaminated water or human waste as fertilizer

🔬
Diagnosis
● demonstration of oocysts in feces
○ acid-fast stain (kinyoun’s stain) - COLD METHOD
○ safranin staining and microwave heating
○ Autofluorescence: blue or green circles

🖥
■ Uses ultraviolet light
● Serologic methods:
○ PCR: to differentiate with closely related Eimeria species

💊 Treatment
● Self-limiting, immunity may result with repeated infection
 ● Trimethoprim-sulfamethoxazole: only effective drug
○ Oocyst should disappear after few days if the treatment is said to be effective

Comparison: Oocysts of Different Genera

Pneumocystic jiroveci
● Now considered as fungus
● Classified as protozoan parasite
WEEK 9 (BLOOD AND TISSUE NEMATODES)

BLOOD AND TISSUE NEMATODE/FILARIAE

-BLOOD AND TISSUE NEMATODES & INTESTINAL TISSUE NEMATODES

-TALK ABOUT NEMATODES

NEMATODES- Common name Round Worms (Bulate na Cylindrical ang shape)

- Round Worms (Cylindrical in nature)
- Like Earth worms
- Nematodes are under subkingdom Metazoa

Protozoa- Unicellular
Metazoa- Multicellular

Nematodes(Metazoa)- Some of the nematodes are can be seen by the naked eye but still there
are life stages such as the larvae, adult worms, eggs and other stage that still needed aid by the
microscope

-Discussing Subkingdom Metazoa specifically the Phylum Nemathelminthes or Phylum

Nematoda
-The discussion will be divided in Tissue Nematodes & Intestinal Nematodes

What kind of tissue is the parasite targeting

- Depends on the specific Specie
- If talking about blood and tissue nematodes, it can be disseminated throughout the body
because when we say blood it pertains to the circulation throughout the body, so that the
worms can lodge to the different sites inside the body

Under the Phylum Nemahelmintes we are going to discuss the Order Spirurida that is under the
Class of Rhabditea, Subclass Secernentia

Under the Order Spirurida we will going to discuss Wuchereria bancrofti, Brugia malayi, Loa loa,
Onchocerca volvulus, Mansonella perstans, Mansonella ozzardi, Mansonella streptocerca,
Dirofilaria immitis, & Dracunculus medinensis

- Wuchereria bancrofti, Brugia malayi, Loa loa, Onchocerca volvulus, Mansonella

perstans, Mansonella ozzardi, & Mansonella streptocerca are Filarial Worms (They are
the Blood Tissue Nematodes)
- While the Trichinella spiralis (Class Adenophorea, Order Trichurida) & Dracunculus
medinensis are considered Intestinal Tissue Nematodes
Additionally we are going to discuss the Angiostrongylus species (Angiostrongylus cantonensis
& Angiostrongylus costaricersis that is under the Order Strongylida

FILARIAL WORMS

▪Blood and tissue inhabiting nematodes

▪Female larviparous or viviparous and insect vector are needed for the transmission of the
infection
✓Oviparous: lays eggs in unsegmented stage (unembryonated)
✓Ovoviviparous/oviviparous: lays eggs in segmented stage (embryonated)
✓Viviparous/larviparous: larva
▪The time and day whereby blood contains abundant number of micrifilariae, as compared to
other hours is called periodicity
✓nocturnal:occurring at night
✓diurnal: occurring during the day
✓subperiodic: timing of occurrences not clear-cut
✓non-periodic

PHYLUM NEMAHELMINTHES/NEMATODA (ROUND WORMS)

-General characteristics of Nematodes whether intestinal or whether tissue
nematodes

1. Hemoxenous/Heteroxenous
- Depending to the number of host requirment they can be also be a
parasitic or a free living type of parasite
- When we say parasitic it means that they need to reside inside a
host
- And when we say Free living the parasite are able to live outside
the environment without a need for a host
2. Unsegmented, bilaterally symmetrical helmets with elongated
cylindrical bodies
- Unsegmented that means that we will cannot view segments inside
the parasite unlike earthworms that are segmental. Roundworms are
non segmental.
- Common to Roundworms and Earthworms they are both Cylindrical
- Roundworms are Bilaterally Symmetrical Helminths with Elongated
Cylindrical bodies
 3. Bodies are covered with a thick hyaline covering called Cuticula
- Bodies of Roundworms are covered with a Thick Hyaline Covering
called Cuticula
- On some species or most of the roundworms have modifications of
this Thick Hyaline Covering (Cuticula)
4. Complete set of digestive system
- Roundworms have a Complete Set of Digestive System
- When we say complete they have a structure of a Mouth,
Esophagus, Intestines, and lastly they also have Anus
5. Sexes are separate
- Common to all roundworms that there sexes are separate
- That means that there are Male Roundworms and a separate sex of
Female Roundworms
- For them to reproduce the male worms should mate with the female
roundworms for them to produce eggs or larvae
- Or for the female to become Gravid (Para mabuntis)
-When we say Gravid this is a term for parasites like worms that
refers to the female being pregnant or those worms that are capable
of producing either eggs or larvae

There are classifications of roundworms that we have to mention:

- Firstly we have to classify the Female Roundworms according to the Type
of Offspring that they are capable of reproducing. Female Roundworms
have 3 classification which are:

a. Oviparous- when we say oviparous, the female roundworm is

capable of producing eggs that is not containing a fully developed
larvae or simplified as the egg of this female roundworm is producing
a Unembryonated eggs
- It means that when a oviparous female roundworm lays eggs,
the eggs must embryonate on the environment or eggs should
be mature outside the environment inorder for the larvae to
develop inside the egg (Larvae inside the egg is not fully
develop and the egg needs the environment for its
development)
 b. Ovoviparous/Oviviparous- when we say ovoviparous or
oviviparous, female roundworms are capable of producing fully
developed larvae which means that the eggs of it is already
embryonated (Embryonated Eggs)
- It means that when a ovoviparous/oviviparous female
roundworms lays an egg, eggs are embryonated that means
larvae inside the eggs are matured or fully developed (Eggs of
the ovoviparous/oviviparous female roundworms has a fully
developed larvae)
- Hatching of the eggs are fast because it doesn't need to be
embryonated

c. Viviparous/Larviparous- when we say larviparous or viviparous,

the female roundworms is capable of reproducing a Fully developed
Larvae, This type of female roundworms do not produce eggs but
rather capable of giving birth to a fully developed larvae
- It means that when viviparous/larviparous female roundworms
lays an direct fully developed larvae and not an egg that
contains mature larvae
- It will not reproduce an egg but it will directly produces an
Larvae (Parang Fetus na agad rekta-rekta walng nang
itlog-itlog)

BLOOD AND TISSUE NEMATODES OR FILARIAL WORMS

- We can also classified the roundworms according to their habitats
- They can be at Intestinals or Extraintestinals
- We are talking about Extraintestinals that are Blood & Tissue Nematodes
and the Intestinal Tissue Nematodes
FILARIAL WORMS

● Blood and Tissue inhabiting nematodes

● Female larviparous or viviparous and insect vector are needed for the transmission
of the infection
- Oviparous: lays eggs in unsegmented stage (Unembryonated)
- Ovoviviparous/Oviviparous: lays eggs in segmented stage (Embryonated)
- Viviparous/Larviparous: Larva

● The time and day whereby blood contains abundant number of microfilariae, as
compared to other hours is called Periodicity
- Nocturnal: Occurring at night
- Diurnal: Occurring during day
- Subperiodic: Timing of occurrences not clear-cut
- Non-periodic

-Filarial Worms are Blood & Tissue Nematodes or they inhabits the blood and tissue
-Specific stages for example are those that are found in the “Blood” are the Larvae and those
are found in the “Tissue” are the Adult Worms
-Female Filarial Worms are considered Larviparous or Viviparous
-Meaning larviparous, parasites of Female Filarial Worms does not produce eggs but rather
they deliver a fully developed larvae (So the Filarial Worms specifically do not lay eggs but it just
rather produce fully developed Larvaes)
- Usually the first description on the first developmental stage of larva was L1 (Maliit na
bulate or a young larvae)

-On Filarial Worms we also have to consider the time and day where by blood contains an
abundant number on microfilariae, as compared to others this is called PERIODICITY

Periodicity- The periodic intervals or the specific time that the microfilariae (Larvae forms) of
the parasite can be seen at Abundant Numbers. Or the specific time where we can see
Abundant number of microfilariae
- We consider that the filarial worms have Nocturnal periodicity if the microfilaria is seen in
abundant numbers during Night
- We can also mention that filarial worms has a Diurnal periodicity if the microfilaria is
seen in abundant number during the Day

- Subperiodic pertains to the periodicity of microfilaria wherein the timing of occurrence is

Not Clear-Cut
- Non-Periodic pertains if there are No Specific time or sure that there is no specific time
that the microfilaria is can be seen in abundant number, it either can be seen at day or
night
FILARIAL WORMS

● Presence or absence of a delicate transparent covering known as a sheath

- Sheathed
- Unsheathed

-We can classify or differentiate the filarial worms according to the presence or absence of
delicate transparent covering known as the SHEATH
-The Sheath pertains or referred to the covering
-The Sheathed or Unsheathed are described at Microfilaria Larvae Form stage

We will describe here 2 basic and major morphological forms in the life cycle of Filarial Worms

2 MORPHOLOGICAL FORMS

1. Adult Worms
- appear creamy white and assume a threadlike appearance
- males may measure from 20 to 500 mm in length, which is often half that of
typical adult females. (Females are larger or longer in length)
- Generally the females are bigger than the males because they need more body
mass to support & nurture their larvae (Opspring)
- The adult female would lay a fully developed larvae thats why its called a
larviparous

2. Larvae/Microfilarae
- First stage larvae (L1)
- Second stage larvae (L2)
- Third stage larvae (L3) “INFECTIVE STAGE”

- slender and may range in size from just under 150 μm to 350 μm in length
- distribution of nuclei within the tip of the tail
- presence or absence of a sheath

- Larvae that is coming from the female larva (Larvae or Microfilariae)

- The larvae has 3 stages which is its developmental process (Ex. Preschool-College)
- As this larvae goes to one stage to another it can change its appearance or it can “Molt”
(Molting process)
- Molting- refers to a change on lavae’s structure (Maturing). This molting process
completes the parts of the larva (Digestive organs, Organs for population, etc.). This
molting process helps the larva to mature and helps them to reproduce
- The L3 is the “Infective Stage” for the Filarial Worms because the Mode of Transmission
(MOT) is by “L3 Injected by a Vector (Mosquito Bite)” to a man
 - The Vector is not just mosquito but is is dependent of a specific specie
- Larvae are smaller than the typical adult. It is Slender (Mas Payat) because it didn't eat
much

2 MORPHOLOGICAL FORMS

Two helpful characteristic speciating the microfilariae

1. Distribution of nuclei in tip of tail

2. Presence or absence of sheath

WUCHERERIA BANCROFTI

COMMON NAME: BANCROFT’S FILARIA

DISEASE ASSOCIATED: BANCROFT’S FILARIASIS or BANCROFTIAN FILARIASIS,
FILARIASIS BANCROFTI, ELEPHANTIASIS & HYDROCOELE

ADULTS
• White and assume a threadlike appearance.
• Females are typically larger than male measuring 40-100 mm and 20-40 mm, respectively

Wuchereria bancrofti (Microfilaria)

Parameter Description

Size range 240-300 um long

 Sheath Present

Arrangement of Nuclei in tail Tip of tail free of nuclei

- The diagnostic stage is the “Microfilariae of the Filarial Worms or the Larvae”
- This Microfilariae are found in the “Blood”. The blood is easily obtained or easily
collected and therefore microfilariae are the stages that is demonstrated
- Adult Forms are not usually demonstrated on the laboratory settings because they reside
inside the “Tissues or Deep Tissues” of the body

ADULT Wuchereria bancrofti

- “Wuchereria bancrofti Adults” has a “White Color” and assumes “Treadlike Appearance”
- “Females are typically larger than Males” (Females: 40-100mm & Males: 20-40mm)

MICROFILARIA (LARVAE) Wuchereria bancrofti

- The microfilaria of the Wuchereria bancrofti has “240-300um size range”
- Since it has a 240-300mm size long it need the aid of the microscope for us to view the
description or morphology of this type of microfilaria
- The sheath in the Wuchereria bancrofti is “Present” (Sheathed)
- The Nuclei are absent on the tip of the tail of the Wuchereria bancrofti (Nuclei is Absent
at the tip of the tail), Free from nuclei, or no nuclei found at the tip of the tail
-
LABORATORY DIAGNOSIS

● 🌛 Nocturnal periodicity: peak hour of specimen collection are between 9:00 pm to

4:00 am

🔬
- Diethylcarbamizine: stimulates microfilariae to come out even during daytime

🔬
● Examination of fresh Giemsa-stained blood

🔬
● Nuclepore filter: heparinized blood
● Knott Technique
- Using 10ml of 2% Formalin and 1ml blood

● 🖥 Serologic Test
- PCR
- detection of Circulating Filarial Antigen (CFA)

- Wuchereria bancrofti has a “Nocturnal periodicity” (Obtaining high number of Wuchereria

bancrofti during the night. Larvae is active or seen in high amounts during the night)
- During “9pm-4am” is the peak for us to collect blood, so that we could obtain high
amounts of larvae
- When we use “Diethylcarbamizine” it stimulates microfilariae to come out even during
day time
 - This “Diethylcarbamizine” drug is use only on “Small amounts or Low Amounts” (kikiliit
no lang kasi gusto lang natin makita yung filarial worm or larvae even this Wuchereria
bancrofti is nocturnal and not active during day time)
- If we use standard amount of Diethylcarbamizine is is now calle the “Treatment or
recommended treatment for Filarial Infection”
- It is recommended to Examine & Routine examination of Filarial worms is the
“Examination of Fresh Blood” either preferred using “Wet Smear or Thick Smear”
(Giemsa-Stained Blood)
- The “Nuclepore Filter & Knott Technique” is also used on examination
- Nuclepore Filtration is recommended for “Membrane Filtration”. Nuclepore Filter is the
main filter that we have
- This Nuclepore Filter is a “Polycarbonate Membrane Filter” & an additional equipment
which is the “Holder or Swinney Filter Holder”
- This Wuchereria bancrofti is will be filtered by the Nuclepore filter and the blood that is
hemolyzed by the “Heparin” will just pass through on the filter, which the microfilariae will
remain intact and be filtered. The filtrated substance or blood will be placed on the slide
(Thin Smear) and examined using the microscope
- When using Knott Technique we employ “10ml of 2% Formalin + 1ml Blood”. After
adding we proceed to “Centrifugation” to obtain the sediment and the supernatant is
discarded. The obtained sediment will be examined under the microscope
- Serologic test is also can be employed such detecting the particular antigen using
specific antibody (Circulating Filarial Antigen or CFA)
- We can also use a More Specific test using a “Molecular Technique known as
”Polymerase Chain Reaction”
LIFE CYCLE

- Discussing not only the life cycle of Wuchereria bancrofti but the common life cycle of all
filarial worms (That means all Filarial Worms have same Life Cycle)
- On different species there are different on Life Cycle if:
 1. “Location of the Adult Worm” (Iba-ibang species may kanya kanyang
pinupuntahan na common location of the adult form or may specific na location
sa katawan ng tao kung saan pumupunta yung adult worm)
2. “Vector or Intermediate Host”. Difference on the vectors or the Intermediate
Host. Difference on the specific species of vectors/Intermediate host that causes
filarial worms
3. Difference on the “Time it takes for the Larvae to develop” within the
vectors/Intermediate Hosts
4. Difference on the “Incubation Period”
5. Difference on “Periodicity” wherein the Filarial Worms will would be active

LIFE CYCLE OF Wuchereria bancrofti

Start:
- Mode Of Transmission (MOT): L3 is Injected to Man (Injection of L3)
- L3 is injected to man through a vector bite or “Skin Inoculation” (Skin Inoculation by a
vector)

- No. 1: Mosquito take a blood meal (L3 Larvae enter Skin)

- During Blood meal the mosquito will bite us by his Proboscis (Mouth). Within his
Proboscis it has a larvae
- The larvae will enter and penetrate the skin through that bite pool
- This larvae will reach the lymphatic vessels, lymph nodes, specific tissues
(Ex. Wuchereria bancrofti larvae will reach the “Lower Lymphatics, Lower Lymph nodes,
or Lower Vessels” will be the habitat of the worm)
From a larvae it will develop into a adult worm in the Lower Lymphatics

- No. 2: The adults will develop in the Lymphatics

- Adults have separate sexes (Male & Female)
- For them to reproduce, they should mate (the male will impregnate the female)

- No. 3: Adults produce a sheathed microfilariae that enter peripheral circulation

- Adult Female & male will produce microfilariae since they are larviparous (Larvae
production)
- This microfilariae will go and enter the peripheral circulation (will go to the different
sites of the body by the blood flow) or it can be picked up by a mosquito that bites you

- No. 4: Mosquito takes a blood meal

- If the mosquito had been ingested the microfilariae
- “Microfilariae”- Infective stage for the mosquito

- No. 5: Microfilariae inside the mosquito shed sheaths, penetrate mosquito’s mudgut, and
migrate to thoracic muscles
 - The microfilariae inside the mosquito will be unsheathed for its penetration on the
midgut of the mosquito
- After penetrating the midgut of the mosquito it will go to its thoracic muscle
- When the unsheathed larvae reaches the Thoracic muscle of the mosquito it will now
start to develop. (Unsheathed larvae will developed in Thoracic muscle of the mosquito)
- In thoracic muscle of the mosquito the larvae will develop (L1-L3)
- About “1-2 weeks” after the maturation of the larvae from thoracic muscle of the
mosquito the L3 will migrate to its proboscis

- No. 8: L3 Migration from Thoracic Muscle to the Proboscis & Head of the mosquito
- When the L3 is in the Head & Proboscis of the mosquito it will be an infective mosquito
- The mosquito that has the infection will now transmit the L3 to another host one it take
a blood meal again
● Man- Definitive Host. Because man harbors the sexual stages (Sa man nakikita yung
male and female na worms that is capable on reproducing that lays larvae )
● Vector (Mosquito)- Intermediate Host. Vector is considered intermediate host because
it only harbors the asexual stages which is the larvae stages
● L3- Infective stage to Humans
● Diagnostic Stage- Microfilariae (Either L1-L2). Larval form found on blood of humans
● The Adult form is not diagnostic (Adult forms are not seen in the blood). Because
adult form is too difficult to describe
● Halos magkakamukha ang adult forms ng filarial worms kaya microfilarae ang diagnostic
stage

TRANSMISSION
- Vectors that is responsible for the transmission of the Wuchereria bancrofti or Bancroft's Filaria
● Vector:
- Aedes
- Culex
- Anopheles
- Mansonis (Sometimes)

- These are all mosquitos

- These species are arthropod vectors that is commonly known as “mosquitos”

● W. bancrofti may be found in the subtropical and tropical areas of the world
including the philippines.
● Wuchereria bancrofti is common in the philippines. Which there are so many places
in the philippines that this kind of parasite is endemic
● Wuchereria bancrofti is common or endemic in Visayas & Mindanao Region
CLINICAL SYMPTOMS

- The patient can undergo Asymptomatic Stages then Acute Stages and then Chronic
Stages
- But some patients will only have the asymptomatic stage

● Asymptomatic : Infection of this type are self-limiting because the adult worms
eventually die and there are no signs of microfilariae being present. A patient may
undergo the entire process and not even know it.
- On Asymptomatic Stage infection of this type are “Self-limiting”, it can be
self-limiting because the adult worms will eventually die and there is no signs of
microfilariae being present. Specially in low loads or the number of added worms
that has developed in the tissues is low in number
- The adult worms will eventually die ones there are done with there jobs in terms
of reproduction (Ex. If the worms are all female or all male or even if the worm is
only one in the tissue the reproduction will not continue), this are the times where
the adult worms will die and will not be replaced or no new generations will be
produced
- Microfilariae will not be present that means the reproduction has not taken place
or it is very low in numbers

- The patient may undergo the entire process of the development of filarial worms
inside the body without even knowing it (Maaring nagkaroon lang ng slight fever
but di nya napansin na filarial worm na pala ang naka pasok sa kanyang
katawan). It’s not been diagnosed because microfilarial’s is not present in the
blood and there are no considerable clinical manifestations
- Asymptomatic patients specially if the loads of filarial worms can progress to
acute stages and chronic stages (Kung saan nakakakita na tayo ng sign and
symptoms)

- There are cases of asymptomatic patients that are considered to be a “Carrier”.

When we say carrier it can transfer the infection to a vector
If ever a vector taken up a blood meal, vectors will be capable of transmitting the
infection

- They are considered asymptomatic because the patients do not develop any signs and
symptoms. This can be attributed to the ability of the filarial worms to escape
immunologic responses or mechanisms. In that case the patient remains asymptomatic
but can still transmit the infection
Symptomatic

● They develop a fever, chills, and eosinophilia (Common Symptoms)

- All of the parasite is acted upon WBC’s which is the Eosinophils
- Eosinophils is a type of major WBC that acts against parasites
- If there is a parasitemia there is also a eosinophilia
● Adenolymphangitis/Dermatolymphagio Adenitis: formation of granulomatous lesions
following microfilarial invasion into lymphatics, chills, lymphadenopathy, lymphangitis,
and eosinophilia.
- Adenolymphangitis/Dermatolymphagio Adenitis or this is also known as the
“ADLA”, The first A pertains to “Acute”, because

- ADLA is a type of acute manifestation of the infection. This disease is a

“Cellulitis type of Infection or Erysipelas like Infection”, because the signs
and symptoms of lesions are similar to the “Bacterial Group A” or the
“Streptococcus pyogenes”
- It is described that the lesions are “Granulomatous”. These Granulomatous
lesions are formed following the microfilarial invasion in to the lymphatics (The
Presence of Microfilarials are “Very Antigenic or Immunologic” on the
lymphatics)
- We can have “Chills, Inflammation (Lymphadenopathy or Lymphangitis), or
Eosinophilia” because of the migration of the microfilaria
● Bacterial infection with streptococcus may occur
- Secondary Bacterial Infection can happen or the Inflammation describe is the
“Bacterial Etiology”
● Elephantiasis or swelling of the lower extremities especially the legs develop due to
obstruction of the lymphatics
- We can have “Lower Lymphatic Blockage” (Lymphatic Vessels or Lymph Nodes
are blocked)
- It is not a simple adenopathy, It is a “Swelling” because of the “Severe Edema
(Accumulation of Fluid or Lymph Fluid)”
- It is called Elephantiasis because you will have an Elephant like Lower
extremities (Yung pa’a mo is like elephant or lumaki ng sobra yung pa’a mo)
● Tropical pulmonary eosinophilia (TPE)
- There is an observation of “Paroxysmal Nocturnal Cough” (Sa gabi ubo ng ubo
si patient)
- There is also a presents of Eosinophilia (Increase amount of Eosinophil in the
blood)
- The Symptoms of Tropical Pulmonary Eosinophilia is “Impaired Lung Function”
- There is a findings os Impaired Lung Function because of “Microfilariae Lodge
the deep Tissues” (Ex. Lungs)
 - This type of Infection was miss diagnosed as “Asthma or Pulmonary
Tuberculosis (PTB)”
- This Tropical Pulmonary Eosinophilia mimics the signs and symptoms of asthma
and pulmonary tuberculosis
● Hydrocoele/Chylocoele: obstruction of lymphatics of the tunica vaginalis(Scrotum)
- If the Accumulation of Fluid happens in “Tunica Vaginalis (Found at Scrotum)”
it will cause “Hydrocoele or Chylocele”
- When we say “Hydrocoele” it is “Accumulation of a Clear Fluid”
- While when we say “Chylocele” is is the “Accumulation of the Lymph Fluid”.
Because our “Lymph Fluid” is also known as the “Chyl” (Milky or Chylous Fluid).
It is like a Creamy White that’s why it is called a Milky Fluid
- The “Hydrocoele or Chylocele” was also known as “Scrotal Elephantiasis”,
because the accumulated fluid here had been accumulated in “Scrotal
Lymphatics”

● Milky urine: rupture of lymphatics

- The “Scrotal Elephantiasis or Hydrocoele or Chylocele” is responsible for
producing “Milky Urine”
- Rupture of Lymphatics that is near to the Kidney can produce Milky Urine
- Rupture of Lymphatics in the Scrotum & Rupture of Lymphatics near the Kidney’s
can be the responsible for the production of Milky Urine
- In the Urinalysis we call it “Chyluria” which means that the Chyl or Lymph Fluid
was poured/excreted out in the urine because of the rupture of the lymph fluid.
Why it is ruptured?, Because at first there's an “Obstruction” due to the presence
of the filarial worm, when the filarial worms are plenty on the area there will be a
“lack of lymph flow on the area” and eventually leads to the “rupture of the
lymphatics”
- The Hydrocoele is common at cases of Wuchereria bancrofti but not at the cases
of Brugia malayi

- Tropical Pulmonary Eosinophilia (TPE)- a classical example of “Occult

Filariasis”. Occult Filariasis is a general term one of its example is the Tropical
Pulmonary Eosinophilia
- Occult Filariasis- Microfilariae’s may be found on “Deep Tissues”.
- Occult Filariasis are not found in the blood or there is a possibility that they are
not demonstrated in the peripheral blood
- Case of Occult Filariasis can lead to a “False Negative Infection Result”
(There are some cases the are report ni doctor is negative even though positive
naman sya sa filarial (microfilariae) infection and it is due to Occult Filariasis.
Because of the case ng Occult Filariasis si Filarial (microfilariae) worms is
nagtatago sa deep tissues)
 ● On the death of the adult worms, calcification or formation of abscess may occur
- Possible dead adult worms that lodge on the tissues will “calcify” (Dead adult
worms will not clear out by the blood flow or lymph flow and it will be stocked or
calcify on the tissue)
- As the Adult dead worms calcify there it would cause immune response, it will
elicit’s a hypersensitivity or the immune system would try to clear out the calcified
dead worms. Immunologic responses like “Inflammation” or recruitment of
immunologic cells like “Eosinophils & WBC’s”
- The Inflammation & Accumulation of cells will form “Abscess” (Pus)
- One main causes of abscess is is the “Accumulation of Pus”

- This may also leads to Lymphatic Blockage, Lesions (Fibrotic), Fibrosis, and
Cellular Hyperplasia

ELEPHANTIASIS Hydrocoele/Chylocoele

TREATMENT

● Diethylcarbamazine (DEC)- The Drug Of Choice (DOC)

- Drug of Choice for Lymphatic Filariasis (Both Wuchereria bancrofti & Brugia
malayi)
● Ivermectin (Stromectol) when used in combination with albendazole
- “Ivermectin with Albendazole” is also use as treatment
● Surgical removal of excess tissue may be appropriate for the scrotum.
- Surgical removal of excess tissues particularly the “Scrotal Tissues”
● Use of special boots or elastic bandage
- The use of “Special Boots” if ever the Elephantiasis happens on the lower
extremities (Ex. Foot)
- “Elastic Bandage” can also alleviate the disease
PREVENTION AND CONTROL

● Use personal protection when entering known endemic areas

● Destroy breeding areas of mosquito
● Using insecticides
● Mosquito netting
● Insect repellants
● Educating the inhabitants of endemic areas

- We can easily remember the prevention & control if we know the mode of transmission
- If the mode of transmission is the “Injection of the L3” via vector (Mosquito). We need to
target the mosquito
- If how can we kill the mosquito or how we can Eliminate the mosquito
- Prevention is better than cure (Preventing the spread of vector is better than the cure for
the disease)

BRUGIA MALAYI
COMMON NAME: MALAYAN FILARIA, MALAYAN FILARIAL WORM
DISEASE ASSOCIATED: MALAYAN FILARIASIS, ELEPHANTIASIS

- The Elephantiasis that it cause is mostly seen on the “Upper Lymphatics”

- Wuchereria bancrofti’s common habitat is at the “Lower Lymphatic Extremities”,
While the the Brugia malayi’s common habitat is at “Upper Lymphatic Extremities”
ADULTS

• Adult B. malayi resemble those W. bancrofti.

• Typical adult female worm measures 53 mm in length
• Adult male measures 24 mm in length

Brugia malayi (Microfilaria)

Parameter Description

Size range 200-280 um long

Sheath Present

Arrangement of Nuclei in tail Presence of two distinct nuclei in the tip of

the tail; The organism tissue tends to bulge
around each of the two nuclei

- We do not have pictures of the adult forms because we cannot view them, we only see
its Microfilariae forms (Larvae Forms)
- It is the Microfilariae that we view for the specie identification

ADULT Brugia malayi

- It resembles Wuchereria bancrofti (They are almost the same). It is difficult for us to
differentiate the adult stages of this parasites

MICROFILARIAE Brugia malayi

- It’s size range is at 200-280um long
- The Sheath is present (SHEATHED)
- As for the tail morphology there is a presence of “Two distinct Nuclei present on the tip of
the tail” of Brugia malayi (Microfilariae Form). There’s a nuclei although it is not
continues but there is still presence of a 2 distinct nuclei at the tip of the tail and also
there's a sheath
- Brugia malayi’s tissue tends to “Bulge around each of the 2 nuclei”

🌓
LABORATORY DIAGNOSIS
● Nocturnal/Subperiodic periodicity
 - Diethylcarbamizine: stimulates microfilariae to come out even during daytime

🔬 Examination of fresh Giemsa-stained blood

🔬 Nuclepore filter: heparinized blood
●

🔬 Knott Technique
●
●
- Using 10ml of 2% Formalin and 1ml blood

● 🖥 Serologic Test
- PCR
- detection of Circulating Filarial Antigen (CFA)

- As for Brugia malayi’s periodicity it is “Nocturnal or Subperiodic”

- It is usually seen at night like the Wuchereria bancrofti but some some times it has a
Subperiodic Periodicity
- “Diethylcarbamizine” would be the treatment also, but in low doses it can stimulates the
presence of Microfilariae to come out even during day time
- The Low Doses of Diethylcarbamizine can stimulate the microfilariae to come out even
during day time
- We can also use the laboratory diagnosis or the test described from the Wuchereria
bancrofti (Examination of Thick & Thin Smear that is Stained with Giemsa, the use of
Membrane Filtration Method, The use of Knott’s concentration Method where in we are
using 10mL of 2% Formalin & 1mL of blood (Increases the sensitivity on detecting the
microfilariae), PCR, and the Detection of “Circulating Filarial Antigen”)

EPIDEMIOLOGY

● Areas of the world in which the mosquitoes breed are the primary locations in which B.
malayi may be found including philippines
- Common again on the Philippines (Regions of Visayas & Mindanao)
● Although humans are considered to be the primary definite host, it is also known to
infect felines and monkeys

● Transmitted by the mosquito

- Mansonia sp.
- Anopheles
- Aedes

- Generally they are all mosquitoes

CLINICAL SYMPTOMS

● Asymptomatic
● Fevers may take months to years to develop after initial infection
● Adenolymphagitis/Dermatolymphagioadenitis: formation of granulomatous lesions
following microfilarial invasion into lymphatics, chills, lymphadenopathy, lymphangitis,
and eosinophilia.
● Elephantiasis of the legs
● Tropical pulmonary eosinophilia (TPE)
● Milky urine: rupture of lymphatics

- The clinical Symptoms of Mayi Filariasis are almost similar to Bancroftian Filariasis.
There are also cases of Asymptomatic patients and if it is Symptomatic “Fevers may
take months or years to develop after the initial infection.
- We can also describe the ADLA or the Dermatolymphagio Adenitis
- Malay Filariasis is common to seen at the upper Lymphatics but the Elephantiasis of the
Legs are also possible
- Hydrocoele/Chylocoele is not common on cases of Malayan Filariasis. But allother
clinical symptoms are similar to Bancroftian Filariasis
- We can also describe the Tropical Pulmonary Eosinophilia (TPE) like on the Bancroftian
Filariasis

TREATMENT

● Treatment for B. malayi is similar to that for W. bancrofti

● Most useful medication is Diethylcarbamazine (DEC) DOC

- Treatment for Malayan Filariasis is similar to the treatment described for the Bancroftian
Filariasis

PREVENTION AND CONTROL

● The prevention and control measures for B. malayi are identical to those for W. bancrofti
- Prevention & Control for Brugia malayi is also identical to those prevention and control
describe for Wuchereria bancrofti
LOA LOA
COMMON NAME: AFRICAN EYE WORM, OCULI HUMANIS
DISEASE ASSOCIATED: LOAISIS

ADULTS

● Typically white in color and exhibit a cylindrical threadlike appearance

Loa loa (Microfilaria)

Parameter Description

Size range 248-300 um long

Sheath Present

Arrangement of Nuclei in tail Distinct continuous row of nuclei; extend

to tip of tail

MICROFILARIAE Loa loa

- Size range of the Loa loa Microfilariae is “248-300um long”
- Loa loa is a Sheathed Microfilariae (SHEATHED).
- Loa loa is like the first two parasites (Wuchereria bancrofti & Brugia malayi) which is a
“Sheathed Microfilariae”
- Loa loa Microfilariae’s tail morphology and arrangement of nuclei is a “Distinct
Continues Row of Nuclei that Extends at the Tip of the Tail”

LABORATORY DIAGNOSIS

● 🌞 Diurnal periodicity: collection is done during the midday hours between 10:15 am
to 2:15 pm
- Loa loa is have a “Diurnal Periodicity” that means Filarial worms are active during
“Day Time”
- Loa loa Microfilariae can be seen in high amounts on the blood sample during
day time
 - The recommended time of collection for Loa loa Microfilariae is during the mid

💉
day hours at “10:15am-2:15pm”
● Specimen of choice for the recovery of Loa loa microfilariae is Giemsa-stained
blood
- Specimen of choice is “Blood” stained with “Giemsa Stain” for us to recover Loa

👀
loa Microfilariae
● The migrating adult worms may be extracted from a variety of body location
including the eye.
- The habitat of Loa loa is our “Subcutaneous Tissue”
- Subcutaneous Tissues can be found through out of our body (Subcutaneous
Tissues are the “Deepest Layer’s of our Skin” that is composed with Fat cell &
Connective Tissues)
- Loa loa can be found through out of our body as long as there’s “Subcutaneous
Tissues”
- There are cases that adult Loa loa worms migrates to different sites of the body
such as “Conjunctiva of the Eye” or can be seen “Under the Skin Bridge of Nose”
(Loa loa can be extracted at those locations)
- The Loa loa is noticeable and can be extracted at the Eyes of the patient
- Loa loa is also known as the “Eye Worm”
- When we talk about the Loa loa microfilariae this can be seen at the “Blood”.
While the Adult Loa loa’s are can be seen at the “Eyes”
● Knott technique
- Knott’s Concentration Technique can also be use for the concentration of the Loa
loa microfilariae present in the blood

LIFE CYCLE
- Life cycle is similar to the life cycle described at Wuchereria bancrofti & Brugia malayi.
The difference is the “Vector” and the “Common Habitat”

TRANSMISSION

● Human infection of Loa loa is initiated by the bite of an infected Chrysops fly, Tabanid,
mango fly.
- Causes Eosinophilia and Calabar Swelling or Transient Subcutaneous
Swelling.
- It is because of the bite of the Arthropod vector that causes “Eosinophilia &
Calabar Swelling”

● Adult worms multiply throughout the subcutaneous tissues

 ● The microfilariae are present in the blood but not until years after the initial infection
making the diagnosis more difficult. (Means that after many years of infection we cannot
view the Microfilariae Loa loa in the blood)

- The Arthropod that is responsible for the transmission of Loa loa is called “Chrysops
Fly, Tbanid, & Mango Fly or Deer Flies”
- Chrysops Species is the “Genus of the Fly”
- Within the Chrysops Species we have the “Mango Fly or Deer Fly”

EPIDEMIOLOGY

🌍 The endemic regions of infection correlate with the areas where the vector flourishes
- 🐝 Chrysops fly inhabits africa especially the rainforest belt region
●

- The Infection with Loa loa is common to some places that that has a plenty of “Chrysops
Fly”
- Chrysops fly is very common in “Africa”

CLINICAL SYMPTOMS

● After initial bite, individuals infected with Loa loa may experience pruritis and localized
pain.
- Initially patients that is bitten by the Chrysops Fly will experience “Pruritis &
Localized Pain” and this bit is also “Itchy”
- Generally it is Itchy when you are bitten by this type of vectors
- Aside from the Pruritis, Localized Pain, & Itchy, because of the secretion of the
flies patients can also have “Immunologic Reaction against the secretion of the
flies”
● Development of calabar swelling at the site of initial discomfort.
- Because of the Immunologic reaction against the secretion of the flies “Calabar
Swelling” will Arise
- There would be development of Calabar Swelling at the site of Bite Wound
- It is termed as Calabar Swelling because there would be “Localized
Subcutaneous Edema”
● Localized subcutaneous edema
- Subcutaneous means that the layer of the skin will have an “Accumulation of
Fluid” because of the Inflamation
● Adult worms may only be noticeable when seen migrating under the conjunctiva of the
eye or crossing under the skin of the bridge of nose
TREATMENT

● Surgical removal of adult worms

- Surgical Removal of the adult worms from the Subcutaneous Tissues
● Diethylcarbamazine (DEC)

PREVENTION AND CONTROL

● Personal protection
● Destroy vector breeding areas
● Prophylactic DEC

- To prevent infection we need to block the mode of transmission

- Target the vector & Protect yourself from being bitten by the vectors

ONCHOCERCA VOLVULUS
COMMON NAME: BLINDING CONVULATED WORM or BLINDING FILARIA
DISEASE ASSOCIATED: RIVER BLINDNESS, ONCHOCERCIASIS

- Another name is “Blinding Filariae” because when the Onchocerca volvulus migrated
into our eyes it causes blindness
- The cause of blindness will be the presence of Microfilariae in the eyes, Secondary
bacterial Infection, & Productions of Lesions
 - This picture is the Microfilariae Onchocerca volvulus which as we can see that it has a
tendency to coil up and they are “Unsheathed”
- This is a type of parasite that do not have a sheath
- The Nuclei of the tail “do not extend to the tip of the tail”

ADULTS

● Thin and wirelike in appearance

● Typically coil up in knots inside infected nodules
● Adult females may measure up to 500 mm in length, adult males are 25-50 mm long

- For us to remember that Conchocerca volvulus “Coils up in Knots” we need to

associated it with its own name which is “Volvulus to word Convoluted”
- The Volvulus association with the word Convoluted can link to the Coiling up in Knots of
the adult worms

Onchocerca volvulus (Microfilaria)

Parameter Description

Size range 150-355 um long

Sheath Absent

Arrangement of nuclei in tail Do not extend to tip of the tail

💉
LABORATORY DIAGNOSIS
● Skin snips (SOC)
- specimen of choice. Because the parasite tends to reside at the subcutaneous
tissue
- Skin Snips is a type of tissue biopsy or skin biopsy where in Adult worms may
recovered from infected nodules

● 💡 Organisms residing in the eye are best seen by ophthalmologic examination using
slit lamp
 - This “Slit Lamp” is a special apparatus or equipment used by the ophthalmologist
to observe the eye
- This Slit Lamp helps on observing the presence of the migrating larvae on the
eyes of the patients

● 😵 Presence of Eosinophilia and ocular discomfort

- The migration of the parasite in the eyes is very antigenic and can cause

🖥
discomfort to the patient
● Serologic examination
- PCR

LIFE CYCLE

- Same as the Wuchereria bancrofti & Brugia malayi the difference is the vector

🕷
TRANSMISSION
● Vector: Simulium or Black fly

🌍
EPIDEMIOLOGY
● O. volvulus is distributed primarily in equatorial Africa and central america.

CLINICAL SYMPTOMS
● Patient experience localized symptoms caused by the development of infected nodules.
● Some patients may also suffer severe allergic reactions to the presence of the
microfilariae
● When the eye becomes involved, lesions may lead to blindness.

- Patients can have infected nodules specially on the parts that we can see the
Onchocerca volvulus (Filarial worms or Microfilariae worms) such as the subcutaneous
tissue or areas
- The Onchocerca volvulus presence and migration to one area to another can cause
antigenic reaction & severe allergic reaction
- The eyes is can be reach by the Onchocerca volvulus microfilariae and can cause
“Blindness” (The lesions that produced on the eyes can cause blindness that why the
disease is also known as the “River Blindness”)

TREATMENT
● Ivermectin – DOC
● Surgical removal of adult worms

PREVENTION AND CONTROL

 ● Personal protection
● Controlling the vector breeding grounds with the use of insecticides

- Prevention & control is same as the first other parasites that we need to prevent the
affection of vectors

MANSONELLA OZZARDI
COMMON NAME: NEW WORLD FILARIA or OZZARD’S FILARIA
DISEASE ASSOCIATED: NONE

ADULTS
● Generally, it is described that the common habitat would be body cavities
● The location of the adults in humans is currently unknown
● Adult female may range in length from 65-80 mm average of 70 mm
● Male worm measures 32 mm

Mansonella ozzardi (Microfilaria)

Parameter Description

Size range 150-355 um long

Sheath Absent (unsheathed)

Arrangement of nuclei in tail Do not extend to tip of the tail

LIFE CYCLE
● Life cycle of Mansonella ozzardi is similar to the filarial worms that was mentioned earlier

LIFE CYCLE NOTES

● Transferred by the injection of infective larvae to the human definitive host.

● The transmission is carried out by the culicoides sucking midges and simulium
blackfly
● Microfilaria is found in the blood as well as in the capillaries and intravascular spaces
of skin
 ● The emerging adults may take up residence in the body cavities, visceral fat and
mesenteries

🔬
LABORATORY DIAGNOSIS
● Examination of fresh Giemsa-stained blood
● ☁ nonperiodic: no known optimum time for collecting the blood sample

🌎
EPIDEMIOLOGY

📌
● Found exclusively in western hemisphere
● Known to exist in North, central, and south america, as well as part of west indies

🕷
and carribean.
● The parasite may be transmitted by culicoides midges or simulium blackfly

CLINICAL SYMPTOMS
● Asymptomatic infections are common, symptoms such as urticaria, lymphadenitis(skin
itching), and arthralgias may occur
○ Urticaria - hypersensitivity reactions due to the inoculation of the parasites
○ Lymphadenitis - pangangati
● Eosinophilia
○ Increased numbers of eosinophil in the blood

TREATMENT
● Asymptomatic patients are not treated
● Ivermectin - drug of choice (DOC)
● Diethylcarbamazine (DEC) - ineffective

MANSONELLA PERSTANS
● Also known as perstans filaria or persistent filaria

COMMON NAME: PERSTANS FILARIA or PERSISTENT FILARIA

DISEASE ASSOCIATED: NONE or NOT WELL DESCRIBED
ADULTS
● They reside in peritoneal and pleural cavities as well as the mesentery
○ Body cavities (Peritoneal, Pleural, & Mesentery Cavities)
● Adult female worm measures 82 mm in length
● Adult male 43 mm in length

Mansonella perstans (Microfilaria)

Parameter Description

Size range about 200 um in length

Sheath Absent (unsheathed)

Arrangement of nuclei in tail Numerous; extend to the tip of tail

- Like Loa loa on the Arrangement of nuclei on the tip of the tail

LIFE CYCLE NOTES

🦇
● The life cycle of M. perstans is similar to that of M. ozzardi
● Culicoides sucking midges is the only known vector
● Humans are the primary definitive host in the life cycle
● The incubation period of this organism once inside the host is unknown

🏥
EPIDEMIOLOGY

🙉
● Infection rates are high in areas endemic to the culicoides sucking midges.
● Primates or monkeys are thought to harbor M. perstans or a closely related species
as reservoir hosts
○ Life cycle can be continuous even if there is no human involvement

CLINICAL SYMPTOMS
● Adult M. perstans worms usually appear singly.
● Minor allergic reactions or no symptoms at all, are experienced by the infected
individuals.
● These individuals may exhibit moderate eosinophilia
 ● Presence of calabar swelling (similar to Loa loa), headache, edema, and lymphatic
discomfort are also associated with this infection
● Responsible for joint and bone pain, as well as enlargement and associated pain in the
liver (Mansonella perstans can be disseminated in the liver due to blood circulation)

- M. ozzardi & M. perstans can only cause minimal damage on the areas that we can see
them

TREATMENT
● Diethylcarbamazine (DEC) - treatment of choice (DOC)
● Effective alternative is mebendazole
● Ivermectin has not proven effective
- Prevention and control is reverse to Mansonella ozzardi

PREVENTION AND CONTROL

● Insecticides targeted against the vector
● Measures of controlling the vector population
● Personal protection

MANSONELLA STREPTOCERCA (MUST KNOW)

● Microfilariae
○ Unsheathed
○ Appearance: Shepherd’s crook or Hooked tail (Tail Morphology)
○ Recommended specimen to obtain is skin snips (LSame as Onchocerca
volvulus)
○ Periodicity: non-periodic
○ The Nuclei on the tip of the tail is “Not Describable”
● Also considered as filarial worm

INTESTINAL-TISSUE NEMATODES
● They develop in the intestine and the produced larvae will migrate to specific tissues
● Under the Intestinal-Tissue Nematodes are the Trichinella spiralis & Dracunculus
medinensis

TRICHINELLA SPIRALIS
● DISEASE: TRICHINOSIS, TRICHINELLOSIS
● Common name: PORK MUSCLE ROUNDWORMS
 ● Name is associated wherein the larvae within the muscle cells is spiral-like
● Anterior tip of the larvae is spear-like (Patusok ang nguso)

- As we can see on the picture surrounding the nurse cell would be the “Inflammatory
Infiltrates”
- The Nurse cells is the actual “Muscle cells Infected” and within the Nurse cells are the
larvae of Trichinella spiralis that is coiled
- The name Trichinella spiralis implies its spiral like coiled formation inside the cell

Trichinella spiralis (Larva)

Parameters Description

Average juvenile size (Young) 75-120 um long

4-7 um wide

Average mature size up to 1 mm in length

Appearance Coiled within the muscle cell

Encysted in Nurse cells of striated muscle (they will

serve as the house of the larva)
Notable features Inflammatory infiltrate present around nurse
cell

- It is called Nurse cell because it already infected the muscle cell

- When the Trichinella spiralis is on the muscle cell it is now called the “Nurse Cells”
(Parang magiging bahay ng Trichinella spiralis na nag aalaga and nag nunuture)
- Possible notable feature is “Inflammatory Infiltrates” due to the inflammatory reaction
that clear out or eliminate the larva that infects the cell

Trichinella spiralis (Adults)

Characteristics Adult female Adult male

Size 4 by 0.5 mm 2 by 0.04 mm

Notable features Blunt, round posterior end; curved posterior end with
single ovary with vulva in two round appendages
anterior fifth of body

COMMON TO BOTH MALES AND FEMALES

Thin anterior end

Small mouth

Long slender digestive tract

Anterior tip - has spear-like morphology; mouth of the worm can be seen
Posterior end - anus can be seen
 ● At the posterior end (Blunt or Round) of the female Trichinella spiralis we can see the
“Anus & Ovary”. Single ovary found at the posterior end. On the other hand the Vulva is
found at the “Anterior fifth” of the body
● Adult Male Trichinella spiralis has a “Curved Posterior End”. At the posterior end of the
male we can view the “Cloaca” and it has a “two round appendages (Copulatory
appendage)”. On its mid portion near the posterior end we can see its “testes”
● Notable commonality for both female and male Trichenella spiralis there have “Thin
Anterior End” (Habang papunta sa anterior end numinipis ang circumference ng adult
worm), “Small Mouth” (It is described that both female and male has an Anterior tip that
is Spear-like), “Long slender Digestive Tract”
● Female and male Trichinella spiralis are also common on having Stichocytes in the
esophagus(Disk like struct ure found at esophagus); collective term is stichosomes

LIFE CYCLE

● Involves only the animals

● Main host of Trichinella spiralis
● Each host would be harboring the complete life cycle of the parasite
● Pigs - rats, Pigs - pigs, Rats-pigs, Rats - rats transmission
● Mode of Transmission: ingestion of encysted larvae in striated muscles
(Cannibalism)
● Life cycle can also revolve in the life cycle in predators such as bears etc.
 ○ Eating improperly cooked meat of rats and pigs that has encysted larva in the
striated muscle
● Complete life cycle can happen within one host (No intermediate Host)
● Man is incidental or accidental host
● The complete life cycle of trichinella spiralis can happen in one host
● Infective Stage: Encysted larvae on Striated Muscle
● Trichinella spiralis can also be a part of a scavenger (Kumakain yung animal ng namatay
na na mammal). If the meat of the dead animal is infected with the Encysted larvae
Trichinella spiralis and eaten by another animal. This animal who eats the meat will be
infected
● The life cycle of Trichinella spiralis is same happens to the man
● Pork Muscle Roundworms- Pigs are the primary host of the Trichinella spiralis and the
man is just a accidental host
● Not properly cooked or raw pork meat can infect the man if the pork or pic is infected
with trichinella spiralis
● Females that lay eggs are considered larviparous because it not lays egg it is just called
encysted because of the Nurse cells (Striated muscle) that surrounds the larvae

Life Cycle into Humans

● Human acquire the infection by accidental ingesting the encysted larvae and the larvae
inside will be digested and it will excyst and the covering will be digested by the stomach
and will liberate in the small intestine so the larva will borrow the subepithelium of the
small intestines and will develop into adults and male and female worms will mate
(Females must be Gravid). Females will deposit the larva in the mucosa of the
intestine. Moreover, larvae will penetrate the mucosa of the Intestine and will go to
striated muscle (The primary location is on the digestive circulation & Striated muscle)
and within the striated muscle it will form a cyst and will encapsulate (Nurse cells).
Larvae can be viable for years (It can be infectious for years). Since man is the incidental
or accidental host, they will be considered as the final host because the larvae will not
find another host (If cannibal ka pwede).
● Humans cannot transmit the infection of Trichinella spiralis that why we are the “Final
Host”. The larvae or larva just die inside the human body
● Always remember that if animals or man are infected with Trichinella spiralis the end
result will be the infection on the “Striated Muscles”
● Presence of the Trichinella spiralis on the Intestine is also common but the end result or
location of this parasite will always be the Muscle Celss

DIAGNOSIS
● Examination of the affected skeletal muscle
○ Muscle biopsy (Direct examination of the larvae using muscle biopsy)
● Serologic methods
○ Bentonite flocculation test
○ Latex flocculation test
 ○ IFAT
○ ELISA
● Eosinophilia (Presence of eosinophilia is very remarkable on infection with Trichinella
spiralis)
○ very remarkable; it described that T. spiralis infection causes one of the highest
eosinophilia (Trichinella spiralis infection is very Eosinophilic)
● Leukocytosis (Presence of plenty WBC’s)
○ Can also find plenty of leukocytes in the site of infection
○ Presence of larva in the muscle is inflammatory (Inflammation due to Allergic
Reaction)
● Elevated serum muscle enzyme level (CK [Creatine Kinase], LDH [Lactate
Dehydrogenase], Myokinase)
○ Due to destruction on Muscle cell & proceeding on becoming “Nurse Cells”
○ Subsequent liberation of enzymes is an indication that subsequent destruction on
the striated muscles happens

EPIDEMIOLOGY
● T. spiralis is found worldwide, particularly in members of the meat-eating population
● Not endemic in the Philippines
● The Angiostrongylus cantonensis is the most common infection of Intestinal
Nematodes on the Philippines

CLINICAL SYMPTOMS
● Trichinosis or Trichinellosis is the infection to Trichinella spiralis
● T. spiralis is known as the great imitator
○ Mimic the symptoms of other diseases (Mimics Intestinal symptoms and Muscle
infection)
● Light infection (Intestinal Symptoms)
○ Diarrhea
○ Slight fever
○ Flu

CLINICAL SYMPTOMS
● Heavy infection
○ Vomiting
○ Nausea
○ Abdominal pain
○ Headache
○ Fever
○ Migration of larvae
○ Eosinophilia
○ Pain in pleural area
 ○ Fever
○ Blurred vision
○ Edema
○ Cough
- Incases of Heavy Infection. The Signs and Symptoms would still not be limited to either
intestinal symptoms since adults are found on the intestine. Other Symptoms would be
attributed to the migration of the larvae & Presence of the larvae on the muscle cells

TREATMENT
● Get plenty of rest
● Adequate fluid intake
● Fever reducer
● Pain relievers
● Prednisone
- These pain relievers are considered on the “Muscle Pain” due to the presence of the
larvae encysted on the Muscle cells (Nurse cells or Striated Muscle)
● Thiabendazole - may also be given but according to reference the medication is quite
questionable

🍲
PREVENTION AND CONTROL

🍖
● Thorough cooking of meats

🥓
● Proper storage of meat
● Avoidance of feeding pork scraps to hogs
DRACUNCULUS MEDINENSIS
● COMMON NAME: GUINEA WORM , FIERY SERPENT OF THE ISRAELITES, MEDINA
WORM, DRAGON WORM or LITTLE DRAGON WORM
○ Fiery Serpent - it is called a fiery serpent of the Israelites because as stated by
the bible, in the Ancient Egypt & time of Moses, this worm causes a significant
guinea worm infection.
○ The described worm or serpent that is surrounding the rod can be seen in
medicine logos (WHO Logo).
● DISEASE: DRACUNCULIASIS, DRACUNCULIASIS, GUINEA WORM INFECTION

○ It is called “Guinea Infection” because it is found on the western africa where this
worm infection said to be endemic (Dracunculus medinensis is very common at
the western Africa that why it is called “Guinea Infection”)

Larval stages
● First stage or rhabditiform larvae (L1)
○ diagnostic stage (We can see on the Labs)
● Third stage larvae (L3)
○ which reside in an intermediate host, have not been well described
○ L3 is the “Infective Stage” for the Dracunculus medinensis
○ If the L3 is ingested by the humans it will be directly develop into adult worm

Dracunculus medinensis (Larva)

Parameters Description

Average size 620 by 15 μm

Tail characteristics Consumes one third of body length;

culminates in a point

Dracunculus medinensis (Adult)

Characteristics Adult female Adult male

Size 840 by 1.5 mm 21 by 0.4 mm

Other features Prominent rounded anterior Anterior end coils itself at

end least once
 - On the Trichenella spiralis the posterior end identifies the different sexes, while on the
Dracunculus the Anterior end identifies the different sexes of the parasite

LIFE CYCLE
Intermediate host
● COPEPODS - these are crustaceans; very small and cannot be seen by the naked eye

● Infective Stage is the Ingestion the L3

● Humans can drink contaminated water containing copepods. This Copepods is
infected with L3 larvae of Dracunculus medinensis (Waters like stagnant water, lakes,
streams where commonly copepods can be found)
● Copepods- This are “Prostatians” family of shrimp (very small)
● We are also can be infected when we eat freshwater fish or frogs that recently eat
copepods that is infected with L3 larvae
● Lave are released when copepods die
 ● The copepods will die on the digestive tract and the larvae will penetrate the host
stomach and the intestinal walls as well. This larvae will reproduce on the subcutaneous
tissue of the digestive tract.
● Male and female Dracunculus medinensis will develop and populate at the
subcutaneous tissues of our digestive tract
● After reproduction of the female Dracunculus medinensis it will go to the surface of the
skin more likely ate the “feet”
● This Dracunculus medinensis is larviparous, they don't reproduce eggs and directly a
larvae which they reproduce L1
● Female Dracunculus medinensis try to emerge to the skin 1 year after the infection & L1
larvae will be released on the water (One release reaction of the larvae from the female
is the “exposure to water”)
● L1 larvae are consumed by the copepods. When it is already L3 larvae, this copepod
once ingested by the host, will be in an infective stage.
● Fish and frogs will not develop the L3 larvae.
● The man is the developing area for the L3 larvae
● Intermediate host: Copepods
● Indefinitive Host or Transient: Freshwater fish & Frogs
● Definitive host: man and dog
● Dracunculus medinensis does not invade the blood when it is already in the
subcutaneous tissue
● After ingestion it will go to the subcutaneous tissue of the intestine and after that it will
develop and travel to the skin surface
● D. medinensis (Guinea worm) is the longest nematode that humans are definitive
host
● If the man is accidental host by the nematodes it is the Trichinella spiralis
● If we are talking about the “Largest Nematodes” it is the “Ascaris lumbricoides”

EPIDEMIOLOGY
● Guinea worm is found in parts of Africa, India, Asia, Pakistan, and the Middle East
- Copepods & Dracunculus transmission are common on the fresh
● Copepods reside in freshwater, located particularly in areas called step wells, from
which people obtain drinking water and bathe
● First-stage D. medinensis larvae escape from the ulcers of infected persons who come
into contact with this water.
- Once the ulcers is exposed to the water will give arise toDracunculus larvae
● Ponds, human-made water holes, and standing water may also serve as sources of
infection.
● There are a number of known reservoir hosts, including dogs. Like humans, these
animals become infected via contaminated drinking water.
CLINICAL SYMPTOMS
● This parasite can cause Dracunculiasis, Dracunculiosis, or Guinea worm infection
● allergic reactions: as migration of the organism occurs (Migration of the adult worms
from the subcutaneous tissues to the skin surface)
● secondary bacterial infections: may cause disability or even death
● painful ulcer: gravid female settles into the subcutaneous tissues and lays her larvae.
○ Should be treated immediately and disinfected
● unsuccessful attempts to remove an entire adult female worm may result in a partial
worm being left at the site and subsequent Toxic & Allergic reactions in the ulcer
(Unsuccessful extraction can worsen the infection)
- On removing we need to use a stick or rod on coiling the parasite
- The whole adult female worms should be properly eliminated or removed from
the procedure
● additional allergic reactions and nodule formation may develop on the death and
calcification of an adult worm (Worst condition) (Toxic to our body)

TREATMENT
● no specific dracunculiasis medicines available
● successful treatment typically consists of total worm removal
● Five steps: (Direct removal of the entire worm from the site of infection by using a stick
or rod)
● The removal of the Dracunculus medinensis is described on the “Medicine Logo”
○ Step 1: Place the affected body part, in the form of a blister, in cool water
○ Step 2: In this step, the adult worm breaks through the blister
○ Step 3: It is important at this juncture to clean the resulting wound thoroughly.(If
not properly remove it can cause “Secondary Bacterial Infection”)
○ Step 4: Manual extraction of the entire worm by winding it around a stick
○ Step 5: Once the worm is removed, apply topical antibiotics to the wound site
to prevent emergence of secondary bacterial infections

🥃
PREVENTION AND CONTROL

☕
● properly treated water for consumption

🛀
● boiling water suspected of contamination

🐛
● prohibiting the practice of drinking and bathing in the same water
● copepods may be removed from suspected water is to filter it using a finely meshed

📖
filter
● educate the entire population in endemic areas
 ZOONOTIC NEMATODES

NEW NAME: PARASTRONGYLUS CANTONENSIS

OLD NAME: ANGIOSTRONGYLUS CANTONENSIS

● COMMON NAME :
● DISEASE: ANGIOSTRONGYLOSIS, ANGIOSTRONGYLIASIS
● New name is Parastrongylus cantonensis
● First described by “Chen” in “1935” at the rat the he nurtures
● Canton, China- Place first identified
● Chen discovered that the rats that he nurtures are infected with the Angiostrongylus
cantonensis
● Main Definitive host of this Angiostrongylus cantonensis are the “RATS or RODENTS”
● Humans are “Accidental or Incidental Host”
● The infection of Angiostrongylus cantonensis is commonly seen on the Philippines
compare to Trichenella spiralis
● Trichenella spiralis is not endemic in the Philippines it is the Angiostrongylus that is
endemic in the Philippines

Angiostrongylus cantonensis (Adults)

Characteristics Adult female Adult male

Size 21 to 25 mm by 0.30 to 0.36 16 to 19 mm by 0.26mm

mm

Notable features uterine tubules (Worm) are “kidney shaped” caudal

spirally around the intestine bursa and single lobed
arrangement is described as
“barber’s pole” can lay up
to 15,000 eggs daily

(Eggs)

Characteristics

Size 46 to 48 μm by 68 to 74 μm

Notable features thin hyaline shell embryonated when

oviposited (Oviviparous)
 (Larva)

Characteristics

Notable features L1: distinct small knob near the tip of the
tail
L3: 2 well developed chitinous rods (knob
like tips) below buccal cavity

Larval stages
● L1: found in the rodent host (RATS)
● L3: found in mollusk (Slugs or Garden Snails)
● Adult worms: found in pulmonary arteries of rat, gravid females lay eggs which are
carried into smaller vessels of the lungs
○ Rats, snails
○ Common Name of Angiostrongylus cantonensis is “RAT LUNGWORMS”
○ Definitive host is the rats and it infects rats lungs

LIFE CYCLE

Intermediate host
● slugs and snails
○ Achatina fulica (giant african snail)
 ○ Hemiplecta sagittifera
○ Helicostyla macrostoma
○ Vaginilus plebeius
○ Veronicella altae

● Rodents are the definitive host and snails are the intermediate hosts.
● Embryonated eggs will be passed out in the feces of the rodents. The first stage larvae
shed from the definitive host and are ingested by the gastropod (Snail). Infective in the
snail is the first stage larvae. It will then be ingested by the snail and the larvae will reach
its third stage larvae after molting two times. After that, third stage larvae will emerge
inside the intermediate host (snail), and subsequently ingested by the rodent. Within the
rat, specifically the rat's lung, adults (either male or female) will develop there. They will
mate and will produce an egg and when they are capable of producing eggs they will lay
an embryonated egg and the cycle will continue. Humans acquire the infection by
ingesting gastropods (Snail). Within the snail, there is a third stage larva.
● Mode of Transmission to man: Ingestion of L3 from mollusk or fresh-produced plants
and fruits have secretion of snails
● Infective Stage to Human: Ingestion of L3 from the Snails
● If man ingested the L3 it will not develop into an adult form since we are just accidental
● The L3 Larvae will go to brain, Eyes, or in lungs
● If the L3 Larvae goes to the Bain of the man and it will cause Eosinophilic
meningoencephalitis
○ Very deadly and fatal disease
○ The larvae will lodge to the brain tissue and will cause inflammation of the
meninges in the brain
○ Brains of the man is the usual habitat of the Angiostrongylus cantonensis and will
cause Eosinophilic Meningoencephalitis that is very severe or deadly

EPIDEMIOLOGY
● First reported by Nomura and Lin from Taiwan
● Nishimura and Yogore in the Philippines
● Mechanism:
○ Ingestion of raw mollusk
○ Ingestion of leafy vegetables containing mollusk secretion
○ Ingestion of paratenic host (freshwater prawn and crab)
○ Drinking contaminated water

CLINICAL SYMPTOMS
● stiffness of the neck, weakness of the muscles, abdominal pain, nausea, vomiting,
peripheral eosinophilia, facial paralysis and low grade fever
○ Stiffness of the neck - CNS involvement
● eosinophils, monocyte and foreign body giant cells in the spinal cord and fluid
● CSF contain 100-2000 leukocytes per μl
 ● Charcot-Layden crystals in the meninges
- Degradation products of the eosinophils. If there is eosinophilia there is also
Charcot-leyden crystals

TREATMENT
● No treatment recommended at present
● Successful in animal experiment
○ Mebendazole
○ Thiabendazole
○ Albendazole
○ Ivermectin

🥃
PREVENTION AND CONTROL

☕
● properly treated water for consumption

🛀
● boiling water suspected of contamination

🍽
● prohibiting the practice of drinking and bathing in the same water

📖
● proper eating habits

🐌
● educate the entire population in endemic areas
● elimination and eradication of intermediate host

Additional notes:
ANGIOSTRONGYLUS COSTARICENSIS
● Related to A. cantonensis is A. costaricensis
● Almost similar life cycle to A. constarinensis
● In humans, it causes eosinophilic enteritis
○ Goes to mesenteric arterioles of abdominal tract (abdomen)
INTESTINAL & INTESTINAL-TISSUE NEMATODES
- All of the nematodes have “cephalic chemoreceptors” (Sensory organ used by the
parasite). They do not have eyes, nose, etc. they just using the cephalic
Chemoreceptors as their sensory organ
- When we say Cephalic the receptor is can be seen at the head or anterior portion of
the intestinal nematodes
- When the parasite have the Cephalic Chemoreceptor it is called the “Amphids”
- When the Chemoreceptors are located at the posterior end of the intestinal nematodes it
is called “Caudal Chemoreceptors” or also known as the “Phasmids”
- We can classify the Intestinal Nematodes by the presence or absence of “Caudal
Chemoreceptors”
- Not all the Intestinal Nematodes have Caudal Chemoreceptors. There is an exemption
like on the “Class Adenophorea” and order “Trichurida”

- Caudal Chemoreceptors are located at the posterior ends of the parasites

- On the Order Trichurida we can also observe the presence of “Stichocytes”

GENERAL CHARACTERISTICS

● According to habitat
- Intestinal Nematodes (We can see the adult worms usually on the cases of
Capillaria philippinensis, Ascaris lumbricoides, Strongyloides stercoralis, & 2
Hook worms that infect humans)
- Extraintestinal Nematodes (Large Intestine the adult worms of this parasites
resides at the large intestine which are the Trichuris tichura & Enterobius
vermicularis)

1. Roundworms are elongated, cylindrical in shape with bilaterally

symmetry and unsegmented
2. Have complete digestive system, no circulatory system
3. With sensory organ known as chemoreceptor
4. Provided with separate sexes although some are parthenogenic
5. Female maybe oviparous or viviparous
6. Developmental stages(5)
EGG> 1st larvae>2nd larvae>3rd larvae>ADULT

● Roundworms are can be classified according to the presence or absence of “Caudal

Chemoreceptors
- Those that with Caudal Chemoreceptors are called “Phasmids”
- Phasmids are under subclass “Secernentea” from the taxonomy

● Nematodes are can be classified according to the presence of Caudal receptor

- Phasmids: with caudal chemoreceptors (subclass “Secernentea”)
- Hookworm
 - S. stercoralis
- W. bancrofti
- B. malayi

- Aphasmids: Lacks phasmids or caudal chemoreceptors (Class Adenophorea)

- “TCT”: Trichuris-Capillaria-Trichinella

LIFE CYCLE
- Some roundworms do not have an intermediate host

2 Cycles:
● Direct life cycle: no intermediate host (1 host)
● Indirect life cycle: with intermediate host (At Least 2 Host)

- Generally males of most species have curved tail end and provided with special
structure such as copulatory bursa
- At the curved tail end of the male intestinal Nematodes we can view the Copulatory
Bursa
- Male Intestinal Nematodes usually smaller than females and have a curved tales ends
- Male uses their curve tail to catch the female during copulation
- Females Intestinal Nematodes usually have Round tale ends

ASCARIS LUMBRICOIDES
COMMON NAMES: GIANT ROUNDWORM, GIANT INTESTINAL ROUNDWORM
DISEASE: ASCARIASIS

- Ascaris lumbricoides is the “Largest Intestinal Nematode”

- One of the most common Intestinal Nematode that causes intestinal infection worldwide
- Ascaris lumbricoides is a “Geohelminths”. This Geohelminths are also called “Unholy
three”
- Geohelminths- means they are transmitted through soils (Usually obtained from the soil)
- The Geohelminths or Unholy Three is composed of Hookworms, Ascaris Lumbricoides,
& Trichuris Tichra (HAT). these are the Geohelminths that is usually transmitted from the
soil (Eggs are obtained from the soil)
- Also common for the Ascaris lumbricoides are the cells of the somatic muscle
arrangement are plenty & organized when observe. Thats why the Somatic Muscle
Arrangement is called “Polymyrian Type”
- “Polymyrian Type”-refers to the somatic muscle arrangement of the worms
 ● Diagnostic Stage: “UNEMBRYONATED EGGS”
- The unembryonated eggs of the Ascaris lumbricoides can be “Fertilized or
Unfertilized”
- When we say Fertilized it is fertilized by the “Male Genetic Material”
- Unfertilized is not fertilized by the male Ascarislumbricoides
- It is possible that even if we have males we can also see an unfertilized eggs on
the stool sample

● Human Stool: Specimen of Choice on diagnosing Ascaris lumbricoides

- Stool sample of humans is used in diagnosing the presence of the
“Unembryonated Eggs”
- Adult worm of the Ascaris lumbricoides resides on the “Small Intestine” thats why
the specimen of choice is the stool sample

● Infective Stage: Embryonated Eggs

● There are 3 Layers on the Unembryonated eggs of the Ascaris lumbricoides

Unembryonated Unfertilized Eggs

Ascaris lumbricoides (Unfertilized Egg)

Parameters Description

Size 85-95 um by 38-45 um

Shape Varies

Embryo Unembryonated; amorphous mass of

protoplasm (Blurred or Not detailed inside)

Shell Thin
Other feature Usually corticated (Outer Mammillary
Coating)
- The Ascaris lumbricoides Unembryonated unferlized eggs has a color of “Yellow Brown”
& “Ovoidal in Shape (mas pahaba compared to fertilized eggs)”
- This Unembryonated Unfertilized Eggs of Ascaris lumbricoides is “Narrower & Longer”
than the fertilized eggs
- Unembryonated Fertilized eggs of Ascaris lumbricoides has a round shape and smaller
than the Unfertilized eggs
- The Inner shell of the Unembryonated Unfertilized Ascaris lumbricoides is “Thin”
- The Unfertilized eggs will die soon and not develop furtherly into a larvae. The fertilized
eggs is the one that will going to be a larvae

● There are 3 Layers on the Unfertilized eggs

3 Shell layers:
1. Outer mammillary coating
2. Middle glycogen layer
3. Inner vitelline membrane

Unembryonated Fertilized Eggs

- There are 2 types of Fertilized eggs the “Corticated & Decorticated”

- If the egg is corticated there is a presence of “Coarse Mammilated Albuminous Material”

(Outer mammillary Coating)
- If we see Fertilized eggs have irregular mamillary coating it is Corticated

Ascaris lumbricoides (Fertilized egg)

Parameters Description

Size 40-75 um by 30-35 um

Shape Rounder than non-fertilized

Embryo Undeveloped unicellular embryo

Shell Thick chitin

Other feature May be corticated or decorticated

- Decorticated: absence of outer coarsely mammilated covering

- If the fertilized egg is smooth and we do not see any coating that is ragged edges it is
the Decorticated eggs

● The difference between the fertilized and Unfertilized eggs. Unfertilized is narrower then
the fertilized eggs. Inside (Embryo) the Fertilized eggs we can view much detailed
structures. The shell is Thicker into the Fertilized eggs than the Unfertilized eggs
● The Unembryonated eggs should be embryonated on the soil
● The Unembryonated egg is still not infective, the infective is the Embryonated eggs
● When patient release an egg on the stool it is still Unembryonated because it needs
embryonation process outside the environment particularly the soil
● The coating of the fertilized eggs are used as protection from the harsh environment.
Thats why this fertilized eggs cansurvive the environment and undergo to embryonation
● Eggs can remain viable for a long period of time
● Eggs can survive the environment for about months to few years
 Adult Ascaris lumbricoides

Ascaris lumbricoides (ADULTS)

Characteristics Female Adult Male Adult

Size 22-35 cm Up to 30 cm

Color Creamy white pink tint

Other feature Pencil lead thickness Prominent incurved tail

● Adults may lay a number of undeveloped eggs up to 250,000/day that are passed in the
feces
● Terminal mouth: trilobate lips and a sensory papillae
● Superficial resembles the earthworms but but the earthworms are segmented, while the
Large roundworms or Ascaris lumbricoides are “unsegmented”
● The male adult Ascaris lumbricoides is smaller & have a prominent curve tail
● The female adult Ascaris lumbricoides has a thick tail or “Pencil Lead Thick” tail
LIFE CYCLE

● Diagnostic Stage: UNEMBRYONATED EGG (Either Fertilized or unfertilized Eggs)

- Unferfilized eggs will not undergo biological development and eventually
disintegrate and will not continue to develop
- Fertilized eggs will continue to develop tobe a larvae
● Infective Stage: EMBRYONATED EGGS
- Mode of Transmission: Ingestion of the Embryonated egg
- The embryonated eggs is ingested when the person is exposed to a
contaminated soil with an Embryonated egg
- Inside the Embryonated egg we have a fully develop larvae
- The fully develop larvae will start to emerge and go to our intestines
- After going to the intestine it will migrate to “Liver, Heart, & Lungs”
- It will firstly migrate to the liver by the portal circulation and will proceed to the
lungs up to the heart (Liver Heart Lung Migration)
- On the lungs it will go to our pulmonary vessels and the it will penetrate the
“Alveoli (Air Sacks)”. After penetration it will go to our “Pharynx & Larynx”
- When the Ascaris lumbricoides go to our Pharynx and Larynx, we can ingest
again the parasite
 - When it is on the digestive tract the the Ascaris lumbricoides will further mature to
become an adult worm
- It is possible that there is a liver & lung migration
- On the migration we can have different infections due to allergic reaction, tissue
destruction, etc.
- After maturation the adult worms will mate and the female may produce 250,000
eggs per day
- Unembryonated eggs can be past out the stool
- When Unemryonated eggs is exposed to the soil it will undergo Embryonation to
become Embryonated
- On the environment Unembryonated eggs will become Embryonated due to
Suitable temperature, moisture, ect.
- When it become Embryonated it will be infective for the next host

● Sample of Choice(SOC): STOOL SAMPLE (Usually we see fertilized eggs but there's a
possibility that we see Unfertilized eggs)

🔬
DIAGNOSIS (Stool examination)

🔬
● Direct fecal smear (DFS)

🔬
● Kato technique or cellophane thick smear method (Mass Stool Examination)

🤢
● Kato-Katz technique (Quantitative)
● Adult worms may be present in the stool, vomitted up, or removed from the external
nares. (Possible that Ascaris lumbricoides will go out on the mouth of out on the nose)

🖥
- Adult worms can lodge on the intestine
● Serologic techniques: ELISA

🌍
EPIDEMIOLOGY
● Ascariasis is considered as the most common intestinal helminth infection in the

🌎
world

👋
● The region s of the world and of the United State most susceptible to harbor.
● A. lumbricoides infection in children who place their contaminated hands into their

👧
mouths
● Sources of contamination range from children’s toys to the soil itself

CLINICAL SYMPTOMS

● Asymptomatic
- Patients infected with a small number of worms will often remain asymptomatic.
- No signs & symptoms. Patients will only know that they are infected when the
stool is examined
 ● Symptomatic
- Tissue damage
- Vague abdominal pain
- Vomiting
- Fever
- Distention
- Obstruct the intestine
- Appendix
- Liver
- Bile duct
- Infected children may develop protein malnutrition (Childrens are susceptible)
- Low grade fever
- Cough (Pulmonary vessels)
- Eosinophilia (Possible findings on the blood due to migration)
- Pneumonia (resembles Loeffler’s syndrome)- Difficulty on Breathing

TREATMENT

● Albendazole (DOC)
● Mebendazole
● Pyrantel pamoate

PREVENTION AND CONTROL

💩 Avoidance of using human feces as fertilizer

🚿Exercising proper sanitation and personal hygiene practices
●

📖 Health education
●

💊 Mass chemotherapy
●
●
ENTEROBIUS VERMICULARIS
COMMON NAMES: PINWORM, SEATWORM
DISEASE: ENTEROBIASIS, PINWORM INFECTION, OXYURIASIS

Enterobius vermicularis (Egg)

Parameters Description

Size 48-60 um long

20-35 um wide

Shape Oval, one side flattened

Embryo Stage of development varies may be

unembryonated embryonated, mature

Shell Double-layered, thick colorless

● 🐣 Shell: outer triple albuminous covering (mechanical protection)

and inner embryonic lipoidal membrane (chemical protection)
 Enterobius vermicularis (Adults)

Parameters ADULT Female ADULT Male

Length 7-14 mm 2-4 mm

Width Up to 0.5 mm <0.3 mm

Color Yellowish-white

Tail Pointed; resembles Curved tail and a single

pinhead spicule

● 💁 Single female lays 4,672 to 16,888 per day with an average of 11,105 eggs and dies
after deposition
LIFE CYCLE

TRANSMISSION

● 🌫 Eggs can be acquired through air

● Retroinfection
- Infective pinworm that migrates back into the host body, develop and reproduce

● Autoreinfection/Autoinfection
- Infective pinworm eggs are ingested via hand-to-mouth contamination

● 👪 Familial disease: spread within the family

● E. vermicularis may be responsible for the transmission of Dientamoeba fragilis
CLINICAL SYMPTOMS

● Asymptomatic
● Pruritus ani: Intense itching and inflammation of the anal or vaginal areas
● Intestinal irritation
● Mild nausea
● Vomiting irritability
● Insomnia: due to pruritus
● Minute ulcer
● Mild intestinal inflammation
● Abdominal pain

DIAGNOSIS

🔬 Fecal Smear
🔬 Graham’s scotch adhesive tape swab/scotch tape method/perianal cellulose
●
●
tape swab: highest percentage of eggs seen

TREATMENT

● Albendazole
● Mebendazole
● Pyrantel pamoate (DOC)

- Cure is considered if:

- 7 perianal smears using scotch tape swab are all found negative

PREVENTION AND CONTROL

🚿 Practicing proper personal hygiene

👋 Particularly hand washing
●

💅 Fingernails should be cut short

●
●
● Avoid scratching the infected area

💊
● Cleaning of all potentially infected surface
● Chemotherapy of entire family
TRICHURIS TRICHIURA
COMMON NAMES: WHIPWORM
DISEASE: TRICHURIASIS, WHIPWORM INFECTION

Trichuris trichiura (Egg)

Parameters Description

Size 50-55 by 25 um

Shape Barrel, football, Lemon Hyaline polar plug

at each end Japanese latern appearance

Embryo Unicellular; undeveloped

Shell Smooth; yellow-brown color because of bile

contact
 ● Compared to Ascaris eggs, Trichuris eggs in the soil are more susceptible to desiccation

Trichuris trichiura (Adult)

Parameters Description

Size 2.5-5 cm long; males usually smaller than

females

Anterior end Colorless; resembles a whip handle; contains

a slender esophagus

Posterior end Pinkish-gray; resembles whip itself; contains

digestive and reproductive systems; males
possess prominent curled tail; female has
a bluntly rounded tail

● A female lays approximately 3,000 to 10,00 eggs per day

● Each female worm can produce a total of over 60 million eggs over an average life span
of 2 years

LIFE CYCLE
DIAGNOSIS

● Direct fecal smear

● Kato thick smear
● Kato-Katz technique
● Concentration technique:
- Zinc Sulfate flotation method
- Formalin-ether concentration technique
EPIDEMIOLOGY

● The life span of the adult worms in untreated infections may be from 4 to 8 years
● The female lays her undeveloped eggs. Passed into the feces, 1 month outside the
human body, the egg embryonate and become infective, and ready to initiate a new
cycle.
● Considered the 3rd most common helminth
● Found primarily in warm climates

CLINICAL SYMPTOMS

● Asymptomatic: patients who suffer from slight whipworm infection.

● Ulcerative colitis
● Chronic dysentery
● Severe anemia
● Growth retardation
● Rectal prolapse
● Peristalsis
● Mimic the inflammatory bowel disease

CLINICAL SYMPTOMS

● Common symptoms
- Abdominal tenderness
- Pain
- Weight loss
- Weakness
- Mucoid or bloody diarrhea

TREATMENT

● Mebendazole (DOC)
● Albendazole
● Benzimidazole derivative
PREVENTION AND CONTROL

🚿 Exercising proper sanitation practices

💩 Avoidance of defecating directly into the soil
●

🤷 Avoid placing potentially infective hands into the mouth

●

📖 Educating children in their personal hygiene and sanitation practice

●
●

ANCYLOSTOMA DUODENALE
● COMMON NAME: OLD WORLD HOOKWORM
● Prevalent in Europe, Southwestern Asia
○ About 1% hookworm cases

NECATOR AMERICANUS
● COMMON NAME: NEW WORLD HOOKWORM
● Prevalent in African and America
● Most common in the Philippines
○ About 97% of hookworm cases

● These are the hookworms that can cause major infections to humans
● Hookworms - soil transmitted helminths
○ Geohelminths
○ Blood sucking nematodes
○ All hookworms have the meromyarian type in terms of the arrangement of the
somatic muscle
● Eggs and larval stages of hookworm is indistinguishable
● Adult - head, number of hooks, copulatory bursa

Egg: Morula ball appearance

Hookworm Egg

Parameter Description

Size

Length Necator: 60-75 um

Width Ancylosttoma: 55-60 um/35-40 um

Embryonic Cleavage Two, four, or eight-cell stage

Shell Smooth, colorless

Hookworm Rhabditiform Larva (L1)

Parameter Description

Size

Newly-hatched 270 by 15 um
5 days old 540-700 um long

Other features Long buccal cavity; small genital primordium

Length of esophagus Short

Tail Pointed

Hookworm Filariform Larva (L3)

Parameter Description

Length of esophagus Short (¼ the length of the body)

Tail Pointed

● Size: 700 um
● Sheathed
● This filariform larva is the infective stage of the hookworm parasite
● Mode of Transmission: skin penetration of the filariform larva

2 notable characteristics (Hookworms vs S. stercoralis)

a. Hookworm has slender larva has a shorter esophagus than that of Strongyloides
stercoralis
b. Hookworm filariform larvae have a distinct pointed tail.
Hookworm Adults

General Characteristics

Color Grayish-white to pink

Cuticle Somewhat thick

Anterior End Conspicuous bend, hook

Characteristics

Size Female Adults: 9-12 mm long, 0.25-0.50 mm

wide
Male Adults: 5-10 mm long, 0.2-0.4 mm wide

Other Features Male: Prominent posterior copulatory bursa

Buccal Capsule Characteristics

Necator Contains pair of cutting plates

Ancylostoma Contains actual teeth

N. americanus A. duodenale
COPULATORY BURSA OF MALE HOOKWORM
● Located at the posterior end
● Used by male to impregnate the female

N. americanus
● Dorsal rays
○ Cleft - deep
○ Tip - bifurcated
○ Copulatory spicules - fused/barred

A. duodenale
● Dorsal rays
○ Cleft - shallow
○ Tip - trifurcated
○ Copulatory spicules - not fused

LIFE CYCLE

● Generally, adult females lay 10,000 to 20,000 eggs/day

● They are said to be oviparous
 ● Diagnostic Stage: Unembryonated egg (4-8 germ cells)
● Rhabditiform larva can be seen in some cases and can be considered as diagnostic
stage in old stool

1. Eggs are passed in the stool and under favorable conditions, larvae will hatch.
a. Favorable conditions such as moisture, warmth, and soil.
2. Rhabditiform larva is released from the egg and will grow in the feces or in the
environment with favorable conditions.
3. After a week or 5-10 days, it will undergo molting stages until it becomes filariform.
4. Filariform larva, L3 or 3rd stage larva is considered as the infective stage to humans.
5. Mode of Transmission: Skin penetration of the filariform larvae
6. Ancylostoma duodenale can gain entry to humans by oral ingestion
a. Human is the only host
7. After penetration in the skin, larvae can enter the blood vessels and can be carried
through the heart, lungs, and trachea.
8. After that, they can be swallowed and develop into adult worms in the small intestine.
a. Adult worms reside in the small intestine
b. Adult worms that live in the small intestine can also attach to the mucous
membrane of the gut and they will get the nutrients from it.
c. Adult female can deposit their eggs in the gut → large intestine –> feces
9. Unembryonated egg is deposited in the feces and later on will become rhabditiform larva
and cycle will continue.

🔬
DIAGNOSIS

🔬
● Direct fecal smear (DFS) - recommended test

🔋
● Kato technique or Kato-Katz method
● Concentration methods:
○ ZnSO4 floatation method

🖥
○ Formalin-ether concentration technique
● Culture methods:
○ Harada-Mori
■ test tube culture method;
■ stool specimen is cultured particularly the eggs
■ Filter paper strips and test tube
● Stool is placed in the filter paper and then the filter paper will be
placed in the test tube with 7mL water. Filariform larvae of
hookworms will generally move downward.
● Hookworms filariform larva will be recovered from the water
● On the other hand, if it is said to be Strongyloides species, the
larvae will be deposited on the upper portion
● Larvae may mature and hatch from the eggs in stool
● Examination of the buccal capsule
 🤔
EPIDEMIOLOGY
● The frequency of hookworm infection is high in warm areas in which the inhabitants

💃
practice poor sanitation practices.
● Person at risk for contracting hookworm in areas are those who walk barefoot in
feces contaminated soil
● N. americanus – primarily found in North and South America
● A. duodenale – may be found in europe, china, africa, south america and caribbean.

CLINICAL SYMPTOMS

Asymptomatic Hookworm Infection

● Some person infected with light hookworm burden do not exhibit clinical symptoms
● Hookworm Disease: Ancylostomiasis, Necatoriasis
● Ground itch/Dew itch/Water sore/Mazza mora/Coolie itch: patients who are
repeatedly infected may develop intense allergic itching at the site of hookworm
penetration.
○ Pertains to the cutaneous manifestations
○ Localized erythema
● A number of symptoms experienced by infected persons are associated with larvae
migration into lungs, including sore throat, bloody sputum, wheezing, headache, and
mild pneumonia with cough
● In chronic infection, patients may experience vague mild, gastrointestinal symptoms,
slight anemia, and weight loss or weakness.
● In acute infection, may develop a number of symptoms including diarrhea, anorexia,
edema, pain, enteritis, and epigastric discomfort
● Adult hookworms compete with the human host for nutrients as they feed, infected
patients may develop a microcytic hypochromic iron deficiency, weakness, and
hypoproteinemia.

TREATMENT
● Albendazole (DOC)
● Mebendazole
● Pyrantel pamoate
● Dietary therapy Proteins
● Iron

🚿
PREVENTION AND CONTROL

💩
● Proper sanitation practices
● Appropriate fecal disposal
 ● 💁 Personal protection of person: avoid walking barefoot
STRONGYLOIDES STERCORALIS
● COMMON NAME: THREADWORM
● This parasite is characterized by its alteration between free living and parasitic cycles
○ Free-living: capable of living even outside the host; it has to infect a human or a
host
● Chinese lantern ova
● Specimen of choice: stool
○ But can also be seen in duodenal aspirate

Strongyloides stercoralis (Egg)

Parameter Description

Size Average, 48 by 35 um

Typical growth phase Contains well-developed larvae

Embryonic cleavage Two, four, or eight-cell stage when present

Shell Thin, hyaline

 Strongyloides stercoralis Rhabditiform Larva

Parameter Description

Average size 220 by 15 um; 225

Other features Short buccal cavity; prominent genital

primordium; ½ the width of the body

Strongyloides stercoralis Filariform larva (unsheathed)

Parameter Description

Average length 690 um or 550 um

Length of esophagus Long; ½ the length of the body

Tail Notched
Filariform Larva: S. stercoralis vs Hookworm
a. S. stercoralis has a long esophagus, compared with that of the hookworm
b. The tail of S. stercoralis is notched, unlike that Hookworm which is pointed.

Strongyloides stercoralis Adult Female

Parameter Description

Approximate size 2 by 0.4 mm

Other features Colorless, transparent body; finely striated

cuticle Short buccal cavity; Long slender
esophagus

● Probably because no adult male S. stercoralis is known to exist, the adult female is considered
as parthenogenic, because there are no obvious morphologic structures to indicate that a male
is not required for fertilization.
○ Parthenogenesis - capable of producing eggs even without the help of male

LIFE CYCLE

● Diagnostic stage: Rhabditiform larvae

 1. Adult females that are found in the intestine are capable of producing eggs that are already
embryonated.
2. Eggs that are deposited in the intestinal mucosa can hatch inside the intestine
a. When conditions are unfavorable, it will molt and will become filariform larvae and
that will be our infective stage.
b. MOT: skin penetration of filariform larva
3. Rhabditiform larvae, when the environment is favorable, transform into free-living adult worms.
4. This can be called indirect life cycle
5. If there’s a possibility that it can infect humans, it transforms into filariform larva as an infective
stage.
6. In the indirect cycle, this threadworm larva is passed outside the environment and mature into
free-living adults that are non-parasitic.

What will happen to humans?

1. Once the filariform larva penetrates the skin, it enters the circulation and undergoes lung
migration. Then eventually, it will be found in the larynx and swallowed to the digestive tract and
from there it will become an adult. Usually female worms.
2. Females will generally reproduce parthenogenesis. They invade intestinal mucosa and deposit
the embryonated eggs there. That possibly after a few hours, rhabditiform larvae will go out and
hatch an egg.
a. There can be internal autoinfection - rhabditiform larvae in the intestine became filariform
larvae

3 possible routes
● Direct life cycle - rhabditiform larvae transformed into filariform and filariform penetrates the
skin and infect human
● Indirect life cycle - rhabditiform larvae became adult worm
● Autoinfection - di na nakalabas si rhabditiform larvae into the large intestine and it transformed
into filariform and infecting again the same host

EPIDEMIOLOGY
● Strongyloides is found predominantly in the tropical and subtropical regions in the world.

🔬
LABORATORY DIAGNOSIS

🔋
● Direct fecal smear (DFS) - observance of rhabditiform larvae
● Stool concentration:

💉
○ zinc sulfate
● Enterotest™, Duodenal aspirates, Small bowel biopsy

🎈
○ Duodenal aspirates - observe the presence of embryonated egg

🖥
● Beale’s string test
● Culture:
○ Harada-Mori
 🔋
○ Baermann funnel

🖥
● Flotation Technique
● Serological Test: cross reaction with filarial worm antigens
○ ELISA

CLINICAL SYMPTOMS

Asymptomatic
Strongyloidiasis: Threadworm Infection
● Cochin China Diarrhea: series of watery and bloody diarrhea
● Abdominal pain
● Urticaria accompanied by eosinophilia
● Vomiting
● Constipation
● Weight loss
● Variable anemia
● Heavy infection
● Malabsorption syndrome
● When the larvae migrates into the lungs patient may develop pulmonary symptoms
○ It can cause lobar pneumonia (bronchitis)
● In cutaneous manifestation, it causes localized dermatitis

TREATMENT
● Ivermectin oAlbendazole (DOC)
● Thiabendazole

🚿
PREVENTION AND CONTROL

💩
● Proper sanitation practices

💁
● Appropriate fecal disposal
● Personal protection of person: avoid walking barefoot
CAPILLARIA PHILIPPINENSIS
● DISEASE: MYSTERY DISEASE
● Discovered in the Philippines
● Reported in Northen Luzon, Barangay Pudoc
● Also known as PUDOC WORM

Capillaria philippinensis (Adults)

Characteristics Adult female Adult male

Length 1.5 to 3.9 mm 2.3 to 5.3 mm

Notable Features Blunt, round posterior end; Curved posterior end with two
single ovary with vulva in round appendages
anterior fifth of body

COMMON TO BOTH MALES AND FEMALES

Thin filamentous anterior end

Small mouth

Long slender digestive tract

● Stichocytes: rows of secretory cells present in the esophagus

● Stichosome: entire esophageal structure
 Capillaria philippinensis (Egg)

Parameter Description

Size Average, 48 by 35 um

Typical growth phase Laid unsegmented

Shell Pitted shell that is slightly constricted

● Egg: peanut shaped/guitar shaped with striated shells and flattened bipolar plugs
○ Bipolar plugs are flattened

DIAGNOSIS
● Direct smear or wet mount
● Stool concentration method
● Duodenal aspiration
● Specimen of choice: Stool

LIFE CYCLE
● Diagnostic stage: Unembryonated egg
● Typical female roundworm - oviparous (lays unembryonated egg)
● Atypical female roundworm - larviparous (lays unembryonated or larva)
○ Diagnostic stage is larvae
 ● Mode of Transmission: Ingestion of infected larvae from the infected fish
● Definitive Host: man
● Reservoir Host: Birds
● Intermediate Host: Freshwater/Brackish Water Fish
● Incidental Host: Humans

1. Female worm produced an embryonated egg (from the soil or in the water)
a. In the water: embryonated egg is ingested by the fish
b. Eggs passed out by birds or man, it will embryonate in the water and become infective.
This will be eaten by the fish and then the infective larvae will develop inside the fish.
2. In the intestine, the larvae will develop into an adult worm
3. Some female worms will produce larvae
4. 1st generation of adults will become the atypical type of adult female worms wherein they are
larviparous producing larvae that can re-invade the intestinal mucosa resulting in internal
autoinfection
5. Infective larvae will become an adult without developing outside the environment
6. From infective larva, it became an adult worm that is capable of producing another set of
offspring.
7. This will lead to hyperinfection and result in internal autoinfection.

CLINICAL SYMPTOMS
● Severe protein losing enteropathy
● Malabsorption of fats and sugars
● Decrease excretion of xylose
● Low electrolyte level (especially potassium)
● High levels of immunoglobulin E
 ● Gurgling stomach - borborygmi

EPIDEMIOLOGY
● Intestinal capillariasis was first recorded in Northern Luzon in the philippines.
● Migratory fish-eating birds are considered the natural host.

TREATMENT
● Albendazole (DOC)
● Mebendazole

PREVENTION AND CONTROL

● Discourage people from eating raw fish
● Good sanitary practices
● Educational programs
● Proper excreta disposal

ZOONOTIC NEMATODES
● The usual host is the animals and man is considered as incidental host

TOXOCARA CANIS
● Host: Dog ascaris
● Habitat in the animals: intestine
● Habitat in the humans: visceral organs or eyes
● Mode Of Transmission: ingestion of embryonated egg
● Disease: Visceral larva migrans or ocular larva migrans

TOXOCARA CATI
● Host: Cat ascaris

ANCYLOSTOMA BRAZILIENSE
● Same life cycle
● Primary host: Cat
● Cat hookworm
● Man: resides in the subcutaneous tissue
● MOT: Skin penetration of filariform larvae
● Arrested at the larval stage
● Cutaneous larval migrans
● During adult stage
○ Number of hook: 1 pair
ANCYLOSTOMA CANINUM
● Dog hookworm
● Primary host: Dog
● Man: resides in the subcutaneous tissue
● MOT: Skin penetration of filariform larvae
● During adult stage
○ Number of hook: 3 pairs

DIROFILARIA IMMITIS
● Dog heartworm
● Animal: Heart
● Humans: Lungs
○ Granulomatous nodules in the lungs
■ Characteristic lesions: coin lesions in x-ray
● Skin inoculation of L3 by mosquitoes

POINTS TO REMEMBER

Triad of infection/Unholy 3 Habitat: Large intestine Visceral Larva Migrans

Hookworm Enterobius Toxocara canis

Ascaris Trichuris Toxocara cati
Trichuris

Habitat: Small intestine Heart-to-lung migration Cutaneous Larva Migrans

(Creeping eruption)
Capillaria Ascaris
Ascaris Strongyloides Ancylostoma braziliense
Strongyloides Hookworm Ancylostoma caninum
Hookworms