Lesson 6: Coccidian Parasites
Coccidian parasites
- Under class Sporozoa (Phylum Apicomplexa)
In class Sporozoa, the life cycle is characterized by an
alternations of generation:
1. Sexual : Sporogony – production of oocyst
2. Asexual : Schizogony (Merogony) – producing
merozoites (meronts)
COMMON COCCIAN PARASITES:
Cystoisospora belli (Isospora belli)
Cryptosporidium hominis
Cyclospora cayetanensis
Toxoplasma gondii
Sarcocystis hominis and Sarcocystis suihominis
 Cystoisospora belli
MORPHOLOGY
Infective stage: sporulated oocyst
MOT: ingestion of oocyst (contains 2 sporocyst with 4
sporozoites each) = 8 sporozoites
- Disease is common to children and male
homosexuals with AIDS
- Oocyst are being passed out by feces
LIFE CYCLE
Oocysts in feces  Immature oocysts with sporozoblast
 Immature oocysts with sporozocysts  Mature
oocysts with sporozoites (infective stage)  Human 
sporozoites will release (asexual reproduction) 
Macrogamete and microgamete (fertilization) 
Oocysts
PATHOLOGY
 Infection is usually asymptomatic. (among
immunocompent individuals or it may present
itself a self-limiting gastroenteritis)
 Symptomatic: diarrhea, fever, malaise,
abdominal pain and flatulence
 In AIDS patients, reports on dissemination of
parasite to other organs are present
*Stool – may contained Charchot-Leyden crystals
compared to Entameoba histolytica
- Flattened or damaged villi as compared to Gargia
lamblia
DIAGNOSIS
1. Direct microscopy
2. Concentration technique (FECT, ZnSO4 and
sugar floatation)
3. Staining techniques (Iodine, Kinyoun,
Auramine-Rhodamine)
4. Enterotest and duodenal aspirate
5. Molecular testing
NOTE:
- Ziehl-Neelsen method: granular red color
against a green background
- Almost all coccidian are acid-fast positive
TREATMENT
Asymptomatic: bland diet (soft foods) and bed rest
Symptomatic: Trimethoprim/Sulfamethoxazole
PREVENTION AND CONTROL
• Good sanitary practices
• Thorough washing and cooking of food
• Provision for safe drinking water
 Cryptosporidium hominis
MORPHOLOGY
Infective stage: oocyst (thick-walled)
NOTE:
- Thin walled oocyst: infect other enterocytes thus
resulting to autoinfection
- Thick walled oocyst: passed out with the feces
- 4 sporozoites
LIFE CYCLE
Thick walled Oocyst (4 sporozoites)  attach to
the surface of the epithelial cells of GIT  small
tropozoites (divide by schizogony) 
Merozoites  Gametocytes  Microgamete and
macrogamete  (fertilization)  Zygote  either
thin walled or thick walled oocysts (repeat)
PATHOLOGY
• Immunocompetent: self-limiting diarrhea within
2-3 weeks
• Immunocompromised: severe diarrhea, bile duct
and gallbladder maybe heavily infected, blunted
intestinal villi, varying degrees of malabsorption
land excessive fluid loss
• AIDS patient: severe form of diarrhea,
progressively worse and life-threatening
SOURCES OF INFECTION
• Faulty water purification system
• Swimming in contaminated recreation water
• One person to another: infected food handlers
• Nosocomial infection
DIAGNOSIS
1. Sheather’s sugar floatation or FECT
2. Kinyoun’s modified acid-fast stain (oocyst
appear as red-pink doughnut-shaped circular
organisms) – cheapest and simplest method of
diagnosis
3. IFA
4. DNA probe
TREATMENT
 No acceptable treatment yet
 Nitazoxanide – said to be effective in preliminary
studies
 Bovine colostrum, paromomycin and
clarithromycin  treatment of severe diarrhea
PREVENTION AND CONTROL
• Chlorination is NOT effective
• Use of multiple disinfectant and combined water
treatment
• Proper disposal of human and animal excreta
 Cyclospora cayetanensis
MORPHOLOGY
Infective stage: oocyst
Disease is usually self-limiting
MOT: ingestion
- Auto-fluorescent when viewed under ultraviolet
microscopy
 (A) An unsporulated oocyst, with undifferentiated
cytoplasm, is shown (far left), next to a sporulating
oocyst that contains two immature sporocysts.
(B) An oocyst that was mechanically ruptured has
released one of its two sporocysts.
(C) One free sporocyst is shown as well as two free
sporozoites, the infective stage of the parasite.
(D) Oocysts
(E) Auto-fluorescent when viewed under ultraviolet
microscopy

TREATMENT
• No treatment needed
• If pharmacologic treatment is warranted,
Cotrimoxazole is given.
- Immature oocysts are released –
PREVENTION AND CONTROL
ENVIRONMENTAL CONTAMINATION 
Sporolated oocysts • Good sanitary practices
• Access to safe and clean drinking water
PATHOLOGY
• Proper food preparation
• Chronic and intermittent watery diarrhea occurs in
early infection and may alternate with
constipation.  Toxoplasma gondii
• Fatigue, anorexia, weight loss, nausea, abdominal
pain, flatulence, bloating and dyspnea may MORPHOLOGY
develop. Infections are usually self-limiting.
Infective stages: tachyzoite, bradyzoite and the oocyst
• No death is associated
- Can be passed from mother to baby and blood Definitive host: Cats
transfusion
Complete life cycle occurs in cats
DIAGNOSIS
Humans – accidental/ incidental host
1. DFS
2. Concentration techniques
3. Kinyoun stain Clinical manifestation is apparent if immune system is
4. Fluorescent microscopy suppressed  AIDS patient
5. Safranin staining
- Cats are members of the Felidae family
6. PCR
  Sarcocystis hominis & Sarcocystis
suihominis
• S. hominis from cattle
• S. suihominis from pigs
• Definitive host: humans

LIFE CYCLE
Sporocysts  ingested by cow or pigs  enters
endothelials cell of the blood vessels (Schizogony)
 schizonts  Merozoites  penetrate muscle
cells  cysts with bradyzoides (infective stage)

LIFE CYCLE
Sporozoite  Tachyzoite (found during initial and - Ingestion of undercooked meat
acute stages of infection) – fast multiplying  - Ingestion of sporocysts
small multiplying bradyzoites (slow)  oocysts
PATHOLOGY
• Toxoplasmosis commonly asymptomatic, if
immune system is good.
• Encephalitis-most common manifestation

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

TREATMENT
• Pyrimethamine and Sulfadiazine
• These drugs keeps the Toxoplasma under control PATHOLOGY
but does not kill it.
• Sarcosporidiosis and sarcocystosis
PREVENTION AND CONTROL • Gastroenteritis, diarrhea, myalgia, weakness, fever
• For intermediate host, brain, muscle and kidney
• Good sanitation and hygiene
tissues maybe
• Proper food preparation
• damaged
• Pregnant women should avoid contact with cats • May cause abortion to cows
DIAGNOSIS
1. Fecal floatation methods  sporocysts will be
seen
2. Necropsy  schizonts will be seen
3. Western blot
4. Serologic tests (IFA, ELISA)
5. PCR (amplification of the 18S rRNA)

NOTE:

• Fecal flotation wet mount: to visualize sporocysts

using bright-field microscopy
• Flotation methods based on high density solutions
incorporating sodium chloride, cesium chloride, zinc
sulfate, sucrose, Percoll, Ficoll-Hypaque and other
density gradient media
• Identifiable with hematoxylin and eosin staining.
• Confirmatory staining: Periodic Acid Schiff (PAS)

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

PREVENTION AND CONTROL

• Uncooked animal carcass should not be fed to other
animals
• Thoroughly cooking and freezing meat to kill
bradyzoites
Lesson 7: Filarial Worms MOT: Skin penetration through a vector

Habitat: Lymphatic vessels (lymph nodes)

Eight known species of filarial nematodes: Vector: Aedes spp., Culex spp. and Anopheles spp. (W.
bancrofti)
Serous cavity filariasis
Mansonia spp. eg. M. bonnae and M. uniformis (B.
• Mansonella
malayi)
Subcutaneous filariasis (fat under the skin):
Infective stages: L3 larva or filariform larva (man)
• Loa loa
microfilariae (mosquito)
• Mansonella streptocerca
• Onchocerca volvulus Diagnostic stage: microfilariae

Lymphtatic filariasis Definite host: man

• Wuchereria bancrofti NOTE:

• Brugia malayi
- With adult worms become lodge in the lymphatic
• Brugia timori
system, these worms causes lymphedema,
lymphangitis and elephantiasis in chronic cases.

 FILARIAL WORMS Parameter Wuchereria Brugia malayi

bancrofti
Common name Bancroft’s Malayan filarial
filarial worm worm
1. Sheathed microfilaria – retains embryotic sheath
Vector Anopheles, Mansonial spp.
 Wuchereria bancrofti Aedes, Culex
 Brugia malayi spp.
 Loa loa Area affected Lower Upper
lymphatics lymphatics
2. Unsheathed microfilaria – does not retain Periodicity Nocturnal Subperiodic
embryotic sheath (8pm-2am)
 Onchocerca volvulus
 Mansonella perstans - Periodicity: rhythmical appearance of the
 Mansonella ozzardi microfilaria in the PBS

3. Dracunculus medinensis – unique nematode

Bancroftian filariasis
Vector Biology :
Lymphatic Filarial Parasites
Anopheles flavirostris
 Wuchereria bancrofti
 Brugia malayi Aedes poecillus

• Aquatic habitat: axils of abaca and banana plant

(sheathed)
• Adult biting: day and night biting, indoor and
• One of the “most debilitating disease” in tropical outdoor
countries • Adult resting: base of abaca plants (cool, shady
• Filariasis – parasitic infection caused by microscopic area)
threadlike worms acquired through a mosquito bite
(vector borne)
• Has its social and economic impact
 PATHOLOGY

Lymphatic Filariasis

PATHOLOGY

L3 larvae (enter the skin)  Adults in lower lymphatics

 sheathed microfilariae (migrate into lymphatic and
peripheral blood circulation  ingests microfilariae 
shed sheaths  L1 larvae  L3 larvae  Migration to
mosquito head and proboscis
Immune Response
(cell-mediated and humoral)
NOTE: Adult or Larval worm
- Adult worms are usually localized at in the lymph Causes lymphatic dilation
vessels of the lower extremities, inguinal lymph
nodes, epididymis of males and labia of females. 

Causing mechanical damage to the lymphatics



Dead worms

Elicit the most severe inflammation



Calcification of necrotizing granulomas


LYMPHATIC OBSTRUCTION

L3 larvae (enter the skin)  Adults in upper lymphatics
 sheathed microfilariae (migrate into lymphatic and
peripheral blood circulation  ingests microfilariae 
shed sheaths  L1 larvae  L3 larvae  Migration to
mosquito head and proboscis
NOTE:
- Lymph is less aggressive than blood: no platelets,
no complement system, incomplete coagulation
system, no granulocytes and the flow is much less
violent.

PATHOLOGY
Lymphatic Filariasis
A. Acute Filarial Disease
• Adenolymphagitis (ADL) or
Dermatolymphangioadenitis (DLA)
• Pain, tenderness & swelling of affected areas, with
or without fever
• Epididymo-orchitis in males may occur
B. Chronic Filarial Disease – more commonly
encountered than its acute form
• Lymphedema: fibrosis and cellular hyperplasia in
and around the lymphatic walls postulated to
render lymphatic endothelial cells less effective in
transporting interstitial fluid, abnormal
accumulation of lymph in tissues causing swelling of
legs, arms, breast, and genitals
• Lymphangitis and lymphadenitis with localized pain
and swelling
- Lymphangitis is defined as an inflammation of the
lymphatic channels that occurs as a result of
infection at a site distal to the channel
- Lymphadenitis is the inflammation of the lymph
node
• Elephantiasis: lower limbs are commonly affected
but upper limb and male genitalia may be involved,
breast and genitalia of females may be affected but
relatively uncommon. Disabling and disfiguring
lymphedema of limbs, breasts, and genitals
accompanied by marked thickening of the skin
• Hydrocele: results in the obstruction of the
lymphatics on tunica vaginalis. Clear or straw
colored hydrocele fluid typically accumulates in the
closed sac of the testis.
 Common chronic disease manifestation of
Bancroftian filariasis (W. bancrofti prefer
localization in scrotal lymphatics).
• Chylocele: milky appearance caused by the
presence of lymph
• Chyluria: kidney damage – “milky urine” due to
reflux of intestinal lymph to the renal lymphatics 
(proteinuria and hematuria)
PATHOLOGY
“Expatriate Syndrome”
- occurs to migrants who got infected from
endemic regions
- Characterized by clinical and immunologic
hyper-responsiveness to maturing worms
- Acute manifestations + allergic reactions
(hives, rashes and blood eosinophilia)
“Tropical Pulmonary Eosinophilia” (TPE)
- Classic example of occult filariasis, microfilaria
are not found in the blood but may be found in
tissues
“Weingartner’s syndrome”
- Marked increase of IgE and IgG antiparasitic Ab
as well as hypereosinophilia
- Nocturnal coughing, breathlessness, wheezing
Staging System for Chronic Lymphedema (Dreyer
et. al 2002):
• Stage 1: swelling increases during day but reversible
once the patient lies flat in bed
• Stage 2: irreversible swelling
• Stage 3: presence of shallow skinfolds
• Stage 4: knobs, lumps and protrusions
• Stage 5: deep skin folds
• Stage 6: mossy lesions with leaking of translucent
fluid
• Stage 7: foul-smelling infected area, patient is
unable to adequately or independently perform
activities of daily living
DIAGNOSIS
1. Microscopy
A. “wet smears” – demonstrate motile
microfilariae
B. “thick blood smears”
 Giemsa stain
 demonstration of the microfilaria (most
practical diagnostic procedure)
Differences in microfilariae Pathology:
Parameter Wuchereria Brugia malayi Loaisis, Fugitive swellings or Calabar swellings
bancrofti
Mean length 290 222 *causes localized subcutaneous edema as the
(μm) microfilaria die in the capillaries around the eye.
Cephalic space/ 1:1 1:1
breadth
Sheath affinity Unstained Pink
to
Giemsa
Body nuclei regularly irregular and
spaced overlapping
Terminal nuclei none 2 nuclei
Appearance in smoothly or kinky
blood gracely curve
film

2. Knotts Concentration Method – for low intensity

infection
- employs Filtration method (Swinney filter)
- use of nucleopore filter *Vector = Fly (genus Chrysops)

3. Diethylcarbamazine citrate provocative test (3 mg

L3 larvae (enter the skin)  Adults in subcutaneous
per kg DEC single dose)
tissues  sheathed microfilariae (migrate into
- stimulates microfilariae to come out to
lymphatic and peripheral blood circulation  ingests
peripheral circulation
microfilariae  shed sheaths  L1 larvae  L3 larvae
 Migration to mosquito head and proboscis
4. RDT/Immunochromatography (ICT) – detects
circulating filarial antigens (CFA)

5. Molecular methods – xenomonitoring of parasites

in a pool of mosquitoes and PCR
UNSHEATHED MICROFILARIA
6. Ultrasonography – may demonstrate the live • Onchocerca volvulus -eyes
worms in the lymphatics - “Blinding worm”, “Gale filarienne”, “Craw
craw”
- causes Onchocerciasis, River blindness, Roble’s
 Loa loa- eyes disease
- destroys optic nerve
Parameter Loa loa
Common African eye worm
• Mansonella perstans
name
- old name: Acathocheilonema perstans
Vector Chrysops spp. –
deerflies - rare parasite of man
(aka mango flies or
mangrove flies) • Mansonella ozzardi
Area Subcutaneous - rare parasite of man
affected tissue
Periodicity Diurnal
 Parameter O. volvulus M. M. ozzardi  Dracunculus medinensis
perstans
Vector Black flies Small flies Small flies - Not a filarial worm
Simulium (gnats) (gnats)
- “Guinea worm”, “Worm of Medina”, “Dragon
damnosum Culicoides Culicoides
worm” or “Fiery serpent”
austeni furens
- Longest nematode to man (1 meter)
Habitat Subcutaneous Body Body - Causes “dracunculiasis” or “Guinea worm
tissues cavities cavities disease” (GWD)
Pathology Onchocerciasis, Non- Non- - Mature female worms migrate along the
River pathogenic pathogenic subcutaneous tissue to reach the skin below the
blindedness knee, forming a painful ulcerating blister
- Can also emerge to the head, torso, upper
Specimen Skin extremities, buttocks and genitalia
shadings/nips - No symptoms for one year
- Common symptoms: rashes, fever, nausea,
vomiting, diarrhea, dizziness
• I.S. to man : 3rd stage larva (L3)
- Until there is formation of blister and causes a
• I.S. to vector : microfilaria
burning sensation
• Covering : unsheathed
- Complications: cellulitis, abscess, sepsis, lock
• Periodicity : non-periodic
jaw (tetanus)
TREATMENT
1. Diethylcarbamazine citrate (DEC) – drug choice for
lymphatic filariasis, Bancroftian filariasis and
Tropical Pulmonary Eosinophilia
2. Ivermectin – found to be as effective as 12 days of
DEC in clearing microfilaremia
3. Surgery is the recommended treatment for
hydrocele

PREVENTION AND CONTROL

WHO targeted lymphatic filariasis to be eliminated by
2020

• Development of microfilaricidal regimens

(Moxidectin)
• Goal for endemic areas: Eliminate presence of LIFE CYCLE
microfilariae in blood Ingestion of L3 larvae (water)  Larvae released =
1. Personal protective measures (use of mosquito Copepodes die  Larvae penetrate the host’s stomach
nets) and intestinal wall (Mature and reproduce)  Fertilized
2. Residual spraying female worm migrated to surface of skin, causes a
3. Health education blister, and discharge of larvae  L1 larvae released to
water  comsumed by a Copepod L3 larvae

- Copepods are a group of small crustaceans

found in the sea and nearly every freshwater
habitat.
TREATMENT AND MANAGEMENT
1. Immersion of affected body part to water
2. Wound is cleaned
3. Worm extraction
4. Topical antibiotics are given to prevent infection
5. Aspirin and Ibuprofen are given to ease the pain

PREVENTION AND CONTROL

1. Surveillance and case containment

2. Provision for safe drinking water
3. Vector control – use of a chemical larvicide
(Abate™)
4. Health Education

Rod of Asclepius (the symbol which represents

medical practice since ancient times)