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PLASMODIUM MORPHOLOGY

INTRODUCTION  Immature schizonts –

 The term malaria comes from “mal’aria or active chromatin

bad air” replication

 Malaria is a mosquito-borne infectious  Mature schizonts –

disease of human and other animals caused emergence of the

by parasitic protozoan belonging to merozoites

Plasmodium spp.  Microgametocytes –

 Infections is characterized clinically by male sex cell, which is

fever, anemia, and splenomegaly roundish in shape (except P. falciparum

 The defining clinical features of malarial “ crescent-shaped”)

attack or paroxysm consist of, in order,  Macrogametocytes – female sex cell,

shaking chills, fever (up to 40℃ or higher) which is round to oval shape (except P.

and generalized diaphoresis, followed by falciparum)

resolution of fever.
LIFE CYCLE

TYPES OF PLASMODIUM CAUSING - Plasmodium spp. have two life cycle phases.

MALARIA a. Sporogony: Sexual phase

1. Plasmodium falciparum – Welch (1922) that occurs within the

2. Plasmodium vivax – Grassi and Felet intestinal tract of the

(1980) mosquito

3. Plasmodium ovale – Laveran (1881) b. Schizogony: Asexual phase

4. Plasmodium malariae – Stephens (1922) that occurs in the human host

5. Plasmodium knowlesi
LIFE CYCLE

 Ring forms (Early trophozoites) – refers

to a ring-like appearance of the malarial
parasitie following invasion into a
previously healthy RBC.

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TRANSMISSION OF MALARIA  Aestivoautumnal malaria

 Occurs with the bite of a female Anopheles  Subperiodic malaria
mosquito that harbors the infective
sporozoites in the salivary gland
 Other forms of transmission include
contaminated blood products, contaminated
SMEAR | OOKINETE | RING FORM
needles, and congenital malaria.

Plasmodium falciparum morphological stage

 Plasmodium vivax (worldwide)
 RELAPSING MALARIA/ BENIGN
TERTIAN MALARIA
 Infects young RBC
 Benign tertian malaria

OOKINETE | RING FORM

P.
P.
Plasmodium vivax Stage P. vivax falciparu P. ovale
malariae
m
Benign Malignant Benign
Quartan
Malaria tertian tertian tertian
malaria
malaria malaria malaria
Enlarged
Infercted with
Young All Old
RBC fragmenta
tion
SCHUFF MAURER ZIEMAN
JAMES
Stipplings NER'S 'S N'S
DOTS
DOTS DOTS DOTS
 Plasmodium falciparum (common in Accole
Trophozoi Amoeboi Band and
and Small
Philippines) tes d compact
applique
 Malignant tertian malaria Schizonts 12-24 8-36 6-12 6-12
 Cerebral malaria Length of
36-48
erythrocyt 36 hours 72 hours 48 hours
 Subtertian malaria hours
ic cycle
 Tropical malaria

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3 STAGES OF CLASSICAL MALARIA

PAROXYSM
1. Cold stage
2. Hot stage
3. Sweating stage

PREVENTION
 Prevent man-vector contact
MALARIA  Reduce vector density
 PRE-PATENT PERIOD – period between  Reduce parasite infection
sporozoites injected by the mosquito until  Symptoms of MALARIA
the diagnosis in the blood sample of the
patient.

Plasmodium falciparum 11-14 days

Plasmodium vivax 11-15 days
Plasmodium ovale 14-26 days
Plasmodium malariae 3-4 weeks

 INCUBATION PERIOD – start of signs

and symptoms.

Plasmodium falciparum 8- 15 days

Plasmodium vivax 12-20 days
Plasmodium ovale 11-16 days
Plasmodium malariae 18-40 days

 PRODROMAL SYMPTOMS –
symptoms felt by the patient 2-3 days BABESIA
before malarial paroxysms attack. Brief history of babesia:
 Weakness, exhaustion, nausea &  Babesial organisms were first described in
vomiting, aching limbs, desire to the 1880s as being responsible for Texas
stretch and yawn, loss of appetite. cattle fever or RED WATER FEVER.
 Babesia microti (Theileria microti),
Babesia divergens are two most commonly
isolated from clinical specimen.

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INTESTINAL NEMATODES EGGS:

 Fertile eggs:
 round/oval
1. Ascaris lumbricoides (Giant
 45–70 µm x 35–50 µm
Roundworm)
 thick shell
 embryonate in ~14 days
 infective when fully embryonated
 Infertile eggs:
 larger (88–94 µm x
39–44 µm)
 thin shell
MORPHOLOGY:
 filled with granules
 Most common intestinal nematode of
 non-infective
humans
 Soil-transmitted helminth (STH)
LIFE CYCLE:
 Adults:
 Humans ingest embryonated eggs from
 Female: 22–35 cm
contaminated soil, food, or water.
 Male: 10–31 cm
 Eggs hatch in small intestine; larvae
 Mouth with 3 lips
penetrate intestinal wall.
 Humans mainly infected; pig Ascaris (A.
 Larvae migrate via liver, heart, lungs.
suum) may infect humans
 In lungs, larvae enter air sacs → move up
 Large worms:
trachea → swallowed back.
 females 22–35 cm
 Mature into adults in intestine.
 males 10–31 cm
 Duration: 9–11 weeks; adult lifespan ~1
 Whitish or pinkish, smooth outer cuticle.
year.
 Females have two long reproductive tubes;
males have one.

SPECIES:
 A. lumbricoides primarily infects humans.
 A. suum (pig-derived) can infect humans
too

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DIAGNOSIS:  Mass Deworming: WHO recommends

a. Direct Fecal Smear (DFS): simple but less preventive chemotherapy in high
sensitive. prevalence areas (>20%).
b. Kato-Katz Technique: quantitative,  Health education and school-based
measures eggs per gram (epg), high programs (e.g., War on Worms).
sensitivity (up to 99.9% with double smear).
c. Formalin-Ether Concentration EPIDEMIOLOGY:
Technique (FECT): more sensitive than  Worldwide distribution:
DFS.  Mostly Southeast Asia
 Africa
TREATMENT:  Central & South America
 Drugs:  Transmission linked to:
 Albendazole (400 mg)  Poor sanitation
 Mebendazole (500 mg)  Crowded living
 Pyrantel pamoate  Use of untreated fertilizer
 Ivermectin
 Nitazoxanide. 2. Trichuris trichiura (Whipworm)
 Effectiveness:
 Mebendazole (96.5%)
 Albendazole (93.9%)
 Pyrantel pamoate (87.9%)
 Side effects:
 Mild GI symptoms
 Headache MORPHOLOGY:
 Dizziness.  Male: 30–45 mm; female: 35–50 mm.
 Whip shape: attenuated anterior, robust
PREVENTION & CONTROL: posterior.
 Personal hygiene: handwashing, clean  Female lays 3,000–10,000 eggs/day.
nails. Eggs:
 Environmental sanitation: proper latrines,  Size: 50–54 µm x 23 µm.
safe feces disposal.  Lemon or football-shaped with polar
 Safe water: boil or filter. plugs.
 Outer yellowish shell, inner transparent.

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 Susceptible to desiccation compared to  Concentration techniques (formalin-ether)

Ascaris eggs.  FLOTAC/Mini-FLOTAC (more sensitive)

LIFE CYCLE: TREATMENT:

 Unembryonated eggs passed in feces.  Mebendazole 100 mg twice daily for 3
 Eggs embryonate in soil (15–30 days). days (most effective).
 Humans ingest embryonated eggs.  Albendazole 400 mg daily for 3 days
 Eggs hatch in small intestine → larvae (alternative).
migrate to cecum and ascending colon.  Combination with ivermectin improves
 Adults mature in colon → produce eggs. cure rates.

EPIDEMIOLOGY:
 604–795 million infected worldwide.
 More common in warm, moist climates.
 High prevalence in children 5–15 years.
 Coinfection with Ascaris common.

PREVENTION & CONTROL:

 Similar to Ascaris.
CLINICAL MANIFESTATIONS:  Personal hygiene: handwashing,
 Light infection: asymptomatic or mild washing/cooking produce, wearing shoes.
anemia.  Sanitation: toilets, safe feces disposal.
 Heavy infection (>5,000 eggs/g stool):  Food and water safety.
Trichuris Dysentery Syndrome (chronic  Community education on hygiene and
diarrhea, rectal prolapse, anemia, growth fecal-oral transmission.
retardation in children).  Mass drug administration depending on
prevalence.
DIAGNOSIS:
- Clinical diagnosis only in heavy infections.

LABORATORY:
 Direct Fecal Smear (DFS)
 Kato-Katz Technique (quantitative, WHO
recommended)

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3. Hookworms (Necator americanus and LIFE CYCLE:

Ancylostoma duodenale)  Adult worms attach to small intestine →
eggs passed in feces.
 Eggs hatch in soil → rhabditiform larvae
→ molt to filariform larvae (infective).
 Filariform larvae penetrate skin →
bloodstream → lungs → trachea →
swallowed.

MORPHOLOGY:  Mature in small intestine → lay eggs.

 Necator americanus (New World

hookworm)
 Ancylostoma duodenale (Old World
hookworm)
 Hookworms have meromyarian muscles
(2–5 muscle cells per half of the body).
 Blood-sucking worms
 Infection via skin penetration
 Cause iron-deficiency anemia
 Small, cylindrical worms.
 Female: N. americanus 9–11 mm; CLINICAL FEATURES:

male: 5–9 mm.  Skin: itching, rash (“ground itch”).

 Mouth: N. americanus has cutting plates.  Lungs: mild bronchitis/pneumonitis.

 A. duodenale has curved teeth  Intestines: blood-sucking causes anemia,

(two pairs of ventral teeth). abdominal pain, diarrhea.

 Chronic infection can cause iron-

EGGS: deficiency anemia, weakness.

 Oval/elliptical, 65 µm x
40 µm, colorless. DIAGNOSIS:

 Diagnostic stage: 1. Stool examination: Kato-Katz,

unembryonated eggs in concentration techniques.

feces. 2. Culture (Harada-Mori) for species ID.

3. Molecular methods (PCR, ELISA).

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TREATMENT: 4. Strongyloides stercoralis

 Albendazole
 Mebendazole

EPIDEMIOLOGY:
 Over 900 million infected worldwide. BIOLOGY:
 N. americanus common in tropical Africa  Has free-living rhabditiform and
& Americas. parasitic filariform stages.
 A. duodenale in Europe, SW Asia.  Autoinfection possible → lifelong infection
 Transmission: contaminated soil, skin  Female filariform: ~2.2 mm, semi-
penetration. transparent.
 Parasitic males rarely identified.
PREVENTION:  Eggs similar to hookworms but smaller
 Sanitation, footwear, health education. (50–58 µm x 30–34 µm).
 Treat infected individuals.  Autoinfection - occurs when rhabditiform
 Mass treatment if prevalence >50%. larvae pass down the large intestine and
develop into filariform larvae.
Necator Ancylostoma
Feature
americanus duodenale
LIFE CYCLE:
Adult size 7-11 mm 10-13 mm
Cutting  Autoinfection possible: rhabditiform
Mouthparts Two pairs of teeth
plates larvae develop into infective filariform
Skin Skin penetration
Infection routes larvae inside host → reinfection.
penetration and oral ingestion
Blood ~0.03
~0.2 mL/day
consumption mL/day
Mediterranean,
Geographic Americas,
Europe, North
distribution Africa, Asia
Africa, Asia
Larval dormancy Absent or
Present
(hypobiosis) rare
Usually
Severity of anemia Often more severe
milder

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CLINICAL MANIFESTATIONS: PREVENTION & CONTROL:

 Skin invasion: erythema, pruritic papules.  Environmental sanitation.
 Lung  Health education.
migration:  Screen and treat immunocompromised
lobar patients.
pneumonia.
 Intestinal phase: diarrhea, constipation. 5. Enterobius vermicularis (Pinworm)
 Heavy infection: chronic diarrhea,
malabsorption.
 Hyperinfection syndrome in
immunocompromised.

DIAGNOSIS:
 Baermann funnel method (larvae
detection).  Most common nematode in temperate
 Harada-Mori culture- considered one of the regions.
most successful methods in parasite  Causes perianal itching at night
identification.  Highly contagious (households, schools)
 Beale’s string test, duodenal aspiration,
 Female: 8–13 mm with pointed tail.
biopsy.
 Male: 2–5 mm with curved tail.
 Eggs: D-shaped, 50–60 µm x 20–30 µm.
TREATMENT:
 Ivermectin preferred.
LIFE CYCLE:
 Albendazole
 Adults in cecum and colon.
 thiabendazole also used.
 Gravid females migrate at night to
perianal skin → lay eggs (~11,000/day).
EPIDEMIOLOGY:
 Eggs embryonate in ≤6 hours.
 Worldwide distribution similar to
 Transmission: hand-to-mouth,
hookworm.
contaminated bedding, surfaces, inhalation.
 More common in male children.
 Linked to poor sanitation.

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CLINICAL FEATURES: 6. Capillaria philippinensis (Pudoc Worm)

 Perianal itching at night.
 Scratching causes excoriations, secondary MORPHOLOGY:
infection.  Adult male: 1.5–3.9 mm.
 Children: irritability, insomnia, bruxism.  Eggs: similar to Trichuris but
smaller, guitar or peanut-shaped
DIAGNOSIS: with striated shells.
 Graham’s scotch  Esophagus contains rows of stichocytes
tape test: perianal (stichosome).
cellulose tape
swab (best test).
 Eggs rarely found
in stool.

TREATMENT: LIFE CYCLE:

 Mebendazole 100 mg single dose.  Transmission: ingestion of infective larvae
 Albendazole 400 mg single dose. through undercooked fish.
 Pyrantel pamoate alternative.  Habitat: small intestine.
 Treat whole household.  Birds are definitive hosts; freshwater fish
intermediate hosts.
EPIDEMIOLOGY:
 Worldwide; common in school-aged
children.
 Not controlled by fecal sanitation.

PREVENTION:
 Personal hygiene, nail trimming.
 Wash bedding/clothes.
 Household treatment.
 School hygiene education and mass drug
administration.

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CLINICAL SIGNIFICANCE: PERSONAL HYGIENE:

 Causes intestinal capillariasis (“Mystery  Wash hands after defecation and before
Disease”). eating.
 Symptoms:  Keep nails trimmed and clean.
abdominal pain,  Avoid geophagia (soil eating).
diarrhea, weight loss,  Wear shoes to prevent skin penetration.
edema.
 Lab findings: protein-losing enteropathy, ENVIRONMENTAL MEASURES:
hypoalbuminemia, malabsorption,  Use proper sanitation facilities.
electrolyte imbalances, increased IgE.  Safe disposal of human feces.
 Ensure clean soil and play areas.
DIAGNOSIS:  Safe water supply (boiling/filtering).
 Stool examination, duodenal aspirate.  Mass Drug Administration (MDA):
 Direct fecal smear, concentration
techniques, ELISA.  Targeted to high-risk groups: children,
women of childbearing age.
TREATMENT:  Frequency depends on prevalence.
 Mebendazole 200 mg twice daily for 20
days. HEALTH EDUCATION:
 Albendazole 400 mg daily for 10 days.  Teach life cycles and transmission.
 Supportive: electrolyte replacement, high  Promote hygiene and sanitation.
protein diet.  Encourage participation in deworming
programs.
PREVENTION:  Integrated Approach: WASHED
 Avoid eating raw or undercooked fish.  Water, Sanitation, Hygiene, Education,
 Sanitary disposal of feces. Deworming.
 Treat infected persons promptly. School-Based Programs:
Example: War on Worms (WOW) program.
EPIDEMIOLOGY:
 Endemic in parts of the Philippines,
Thailand, Iran, Japan, and other Asian
countries.
 Summary of Prevention and Control for
Intestinal Nematodes

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Capillaria philippinensis (Pudoc Worm) Sensitivity/Useful

Technique Parasite(s)
VS. Trichuris trichiura (Whipworm) ness
Culture larvae for
Feature Capillaria Ova Trichuris Ova Harada-Mori Hookworms,
More elongated Larger, barrel- species
Culture Strongyloides
Shape and Size and smaller (30- shaped or lemon- identification
55 µm in length) shaped (50-55 µm)
Thick, smooth Thick shell with Graham’s Best for detecting
Shell shell with less distinctive, Scotch Tape Enterobius pinworm eggs on
Characteristics prominent or prominent bipolar
absent polar plugs plugs Test perianal skin
Slightly striated Molecular
Surface or pitted surface Smooth and thick
Texture depending on shell surface Methods Hookworms, High specificity
species (PCR, Capillaria and sensitivity
Typically contains
May contain ELISA)
Internal a clear,
developing
Contents unsegmented
embryo or larvae
embryo

RECOMMENDED DIAGNOSTIC IMPORTANT DRUG DOSAGES

TECHNIQUES OVERVIEW
Drug Dose Parasites Treated
Sensitivity/Useful 400 mg single
Technique Parasite(s) Ascaris, Hookworm,
ness Albendazole dose (children
Trichuris, Capillaria
Ascaris, Simple, less 200 mg)
Direct Fecal
Trichuris, sensitive; good for 500 mg single Ascaris, Trichuris,
Smear (DFS)
Hookworms heavy infections Mebendazole dose or 100 mg Hookworm,
Ascaris, Quantitative, high BID for 3 days Enterobius
Kato-Katz
Trichuris, sensitivity; WHO Pyrantel 10 mg/kg (max 1
Technique Ascaris, Enterobius
Hookworms recommended pamoate g)
Formalin- Ascaris, Strongyloides,
Higher sensitivity Ivermectin 200 µg/kg
Ether Trichuris, Ascaris, Trichuris
than DFS
Concentration Hookworms 500 mg BID for
Nitazoxanide Ascaris
FLOTAC/Mi More sensitive for 3 days (adults)
Trichuris
ni-FLOTAC low egg counts
Baermann Detect larvae by
Strongyloides
Funnel motility

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TISSUE AND FILARIAL NEMATODES  Eggs hatch in lungs; L1 larvae expelled in

feces.
1. Parastrongylus cantonensis (Rat  Mollusks ingest L1 larvae → develop to L3
Lungworm) in ~12 days.

Classification: Formerly Angiostrongylus

cantonensis; now Parastrongylus cantonensis.
Discovery: First described in 1935 in Canton,
China.
Hosts: Definitive host—rats (lungs);
Intermediate hosts—various snails and slugs.
Human Disease: Causes eosinophilic
meningoencephalitis.
HUMAN INFECTION ROUTES:
Geographical Distribution: Taiwan, Pacific
 Eating raw/undercooked infected mollusks.
islands, Philippines, and worldwide (~30
 Consuming contaminated vegetables or
countries).
paratenic hosts (prawns, crabs).
MORPHOLOGY:
 Drinking contaminated water.
 Adult worm: 17–33 mm; males smaller
than females.
CLINICAL FEATURES:
 Female uterus shows “barber’s pole”
 Incubation: 6–15 days (up to 47 days).
spiral pattern.
 Symptoms: Severe headaches, neck
 Eggs: elongated, ovoid, unembryonated
stiffness, paresthesia, vomiting, fever,
when laid.
blurred vision.
 Severe cases: confusion, coma, retinal
LIFE CYCLE:
detachment.
 Rats ingest L3 larvae from mollusks.
 CSF eosinophilia (>10%) diagnostic clue.
 Larvae migrate to Central Nervous
System, molt twice, then to lungs.

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DIAGNOSIS: Species: 8 species + 3 genotypes identified

 Based on clinical, epidemiologic history, worldwide.
CSF findings. 8 SPECIES:
 Imaging: CT/MRI show meningeal lesions. 1. Trichinella spiralis: found worldwide in
 Serology: Dot-blot ELISA (not widely domestic pigs, rats, and wild carnivores,
commercial), Immuno-PCR. the most common cause of human infection.
2. Trichinella britovi: common in wild
TREATMENT: carnivores across Europe, Asia, and Africa.
 No standard anthelminthic regimen. 3. Trichinella nativa: Found in Arctic bears,
 Albendazole or mebendazole used in wolves, and other predators in freezing
some countries. climates.
 Symptomatic relief: analgesics, lumbar 4. Trichinella murrelli: circulates in wild
puncture. carnivores in the United States and
 Steroids (prednisone) for severe cases. Canada.
 Surgical removal if ocular involvement. 5. Trichinella nelsoni: found in Africa,
particularly in predators and scavengers.
PREVENTION: 6. Trichinella pseudospiralis: found in
 Avoid raw/undercooked mollusks. mammals and birds worldwide.
 Proper washing of vegetables. 7. Trichinella papuae: found in wild and
 Molluscicide use and physical barriers in domestic pigs in Papua New Guinea and
farms. Thailand.
 Health education. 8. Trichinella zimbabwensis: found in
crocodiles in Africa
2. Trichinella spiralis (Pork Worm) 3 GENOTYPES:
a. Trichinella T6: Found in carnivores in
North America and parts of Canada. It
is similar to T. nativa in its resistance
to freezing.
b. Trichinella T8: Reported in Africa
Parasitic nematode (roundworm) and phylogenetically related to T.
Disease: Trichinosis (trichinellosis). britovi.
Discovery: Described in 1822; linked to raw c. Trichinella T9: Occurs in wildlife in
pork consumption. Japan and is differentiated from T.
britov.

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Hosts: Domestic pigs, wild carnivores, humans. DIAGNOSIS:

 Muscle biopsy (histology,
digestion).
 Eosinophilia and elevated
muscle enzymes.
 Serology: ELISA, Western
blot, latex agglutination.

LIFE CYCLE: TREATMENT:

 Ingestion of encysted larvae in meat.  Mebendazole or albendazole for 10–15
 Larvae released in intestine; mature into days.
adults.  Supportive therapy including
 New larvae migrate to muscles and encyst. corticosteroids and analgesics.
 Clinical Phases:
 Enteric Phase: GI symptoms (diarrhea, EPIDEMIOLOGY:
nausea).  Worldwide, 10,000 cases/year, mortality
 Invasion Phase: Larval migration ~0.2%.
causing muscle pain, edema, fever.
 Convalescent Phase: Recovery; PREVENTION:
neurological symptoms may persist.  Cook pork thoroughly (77°C).
 Severity: Depends on number of larvae  Proper freezing of meat.
ingested.  Avoid raw/undercooked meat.
 Meat inspection and sanitation.

3. Anisakis spp. (Herring Worm)

Hosts: Marine mammals; humans accidental

hosts.

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Transmission: Eating raw or undercooked  Allergic reactions: urticaria, asthma,

fish/squid containing L3 larvae. conjunctivitis.
Disease: Anisakiasis / Anisakidosis.
DIAGNOSIS:
LIFE CYCLE:  Gastroscopy to visualize and remove
Definitive hosts: Marine mammals (whales, larvae.
seals, etc.)  Serologic tests (ELISA, RAST).
 Adults live in stomach wall of marine
mammals → produce unembryonated eggs TREATMENT:
released into sea → eggs develop into 1st  Mechanical removal by endoscopy.
stage larvae inside eggs → larvae molt to  Corticosteroids for allergic reactions.
2nd stage → hatch into free-swimming  Albendazole used in some cases.
larvae → ingested by microcrustaceans →
develop into 3rd stage larvae → crustaceans EPIDEMIOLOGY:
eaten by fish or squid (paratenic hosts) →  Reported worldwide; common in coastal
humans infected by eating raw or Asia, Europe, Americas.
undercooked fish/squid containing L3  No documented cases in the Philippines.
larvae → larvae penetrate stomach or
intestinal wall causing anisakiasis. PREVENTION:
 Thorough cooking of marine fish and
CLINICAL MANIFESTATIONS: cephalopods.
 Gastric  Blast freezing fish products.
anisakidosis:  Health education.
abdominal pain,
nausea soon after 4. Toxocara canis and Toxocara cati (Dog and
ingestion. Cat Roundworm)
 Intestinal
anisakidosis:
mimics
appendicitis or
obstruction.
 Ectopic cases: larvae in oropharynx or
colon. Disease: Toxocariasis (zoonotic).

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Hosts: Dogs (T. canis), cats (T. cati); humans CLINICAL FORMS:
accidental hosts.  Visceral Larva Migrans (VLM): systemic
Transmission: Ingestion of embryonated eggs granulomatous inflammation.
from contaminated soil.  Ocular Larva Migrans (OLM): visual
Life Cycle: Adult worms in definitive hosts impairment/blindness, mainly children.
produce eggs; eggs embryonate in environment.  Covert toxocariasis: asymptomatic or mild.

LIFE: CYCLE: DIAGNOSIS:

Definitive hosts: Dogs (T. canis), cats (T. cati)  Clinical and serologic (ELISA) tests.
 Adult worms live in intestines → females  Detection of larvae by biopsy rare.
produce unembryonated eggs shed in feces  Imaging for granulomas.
→ eggs embryonate in environment (2  PCR available.
weeks to months) → infective eggs
ingested by definitive or accidental hosts → TREATMENT:
larvae hatch in intestine → migrate via  Albendazole or mebendazole.
bloodstream to various tissues (visceral  Treatment mandatory for neurological or
larva migrans) → larvae do not mature in severe cases.
humans but cause tissue damage.
Transmission: In dogs, vertical transmission PREVENTION:
transplacental and transmammary; humans  Deworming dogs and cats.
infected via ingestion of embryonated eggs  Prevent soil contamination.
from contaminated soil.  Wash vegetables; hand hygiene.

5. Dracunculus medinensis (Guinea Worm)

Disease: Dracunculiasis.

MORPHOLOGY:
 Female worm up to ~840 mm long.
 Larvae released in water through skin
ulcers.

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LIFE CYCLE: 5. Lymphatic Filariasis (Wuchereria bancrofti

 Infection via drinking water with infected & Brugia malayi)
copepods (water fleas).
 Larvae mature and migrate subcutaneously.

Disease: Lymphatic filariasis causing

lymphedema, elephantiasis, hydrocele.
Hosts: Humans definitive; Mosquitoes
intermediate (Aedes, Culex, Anopheles,
Mansonia).
CLINICAL FEATURES:
 Painful blister and ulcer at worm exit site. MORPHOLOGY:
 Secondary bacterial infections possible.  W. bancrofti adults: males 20–40 mm,
females 80–100 mm.
TREATMENT:  Microfilariae sheathed, circulate in blood
 No drugs available. (night periodicity).
 Manual extraction of worm by winding on
stick.
 Wound care and antibiotics to prevent
infection.

PREVENTION:
 Safe drinking water (filtering, boiling).
 Avoid drinking or bathing in infected water.
 Vector control (copepod removal). Differences between Wuchereria
bancrofti and Brugia malayi

Causative Organism:
 Wuchereria bancrofti is the most common
causative agent of lymphatic filariasis
worldwide.

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 Brugia malayi is less common and Morphological Differences (Microfilariae):

primarily found in certain regions of Asia.  Wuchereria bancrofti microfilariae are
larger, have a gently curved body, and a
Geographical Distribution: sheath that stains with Giemsa. The nuclei
 Wuchereria bancrofti is distributed in do not extend to the tail tip.
tropical and subtropical regions globally,  Brugia malayi microfilariae are smaller,
including Africa, Asia, the Pacific islands, have two distinct nuclei at the tip of the tail,
and parts of the Americas. and also possess a sheath.
 Brugia malayi is mainly found in Southeast
Asia, including countries like Malaysia, LIFE CYCLE:
Thailand, and the Philippines.  Mosquito takes blood meal; larvae develop
to L3 and infect humans.
Vectors:  Adults in lymphatics produce microfilariae.
 Wuchereria bancrofti is transmitted by
various mosquito species, CLINICAL MANIFESTATIONS:
mainly Culex, Anopheles,  Asymptomatic microfilaremia.
and Aedes mosquitoes.  Acute dermatolymphangioadenitis (ADLA).
 Brugia malayi is primarily transmitted  Chronic lymphedema, elephantiasis,
by Mansonia and Anopheles mosquitoes. hydrocele.
 Occult form: Tropical pulmonary
Clinical Manifestations: eosinophilia.
 Both cause lymphatic filariasis
characterized by lymphedema and DIAGNOSIS:
elephantiasis.  Detection of microfilariae in night blood.
 Wuchereria bancrofti infections tend to be  Circulating filarial antigen (CFA) tests
more widespread and severe. preferred.
 Brugia malayi infections often cause less TREATMENT:
severe symptoms and are less likely to  Diethylcarbamazine (DEC) drug of choice.
cause hydrocele.  Ivermectin and albendazole used in
combination.
 Doxycycline targets Wolbachia
endosymbionts.
 Surgery for hydrocele.

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PREVENTION: circulating in blood with diurnal periodicity

 Mass Drug Administration (MDA). → deerfly (Chrysops) ingests microfilariae
 Mosquito vector during bite → microfilariae develop into
control. infective L3 larvae in fly → infective larvae
 Personal protective transmitted to humans during fly bite →
measures. larvae mature into adults in subcutaneous
 Health education. tissues → cycle continues.

6. Loa loa (African Eye Worm)

Disease: Loiasis.
Transmission: Bite of Chrysops deerflies
(daytime biters).
Geographic Distribution: Central and West
Africa rainforests and wetlands.

MORPHOLOGY: CLINICAL FEATURES:

 Calabar swellings (localized edema).
 Adult worms visible migrating under
conjunctiva.
 Itching, localized pain.

 Adults: females 38–72 mm, males 28–35 DIAGNOSIS:

mm.  Blood smear (daytime).
 Microfilariae sheathed, show diurnal  Serology.
periodicity.
TREATMENT:
LIFE CYCLE:  Diethylcarbamazine (DEC); caution with
Definitive host: Humans high microfilarial loads.
 Adult worms live in subcutaneous tissues  Albendazole pre-treatment.
→ females produce sheathed microfilariae  Surgical removal of adult worms.

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PREVENTION: during bite → larvae mature into adults in

 Avoid deerfly bites with repellents, subcutaneous tissue → cycle continues.
protective clothing, window screens.

7. Onchocerca volvulus (Blinding Filaria)

Disease: Onchocerciasis (river blindness).

Transmission: Blackfly (Simulium) bite;
breeds in fast-flowing streams.

MORPHOLOGY: DIAGNOSIS:
 Adults: females up to 500 mm.  Skin snips microscopically.
 Microfilariae unsheathed, found in skin and  Ophthalmologic examination.
eyes.  Serology, PCR.

CLINICAL FEATURES: TREATMENT:

 Skin nodules, itching,  Ivermectin for microfilariae.
dermatitis.  Surgical removal of nodules.
 Eye lesions leading to
blindness. Prevention:
 Allergic reactions to microfilariae.  Personal protection.
 Vector control targeting blackfly breeding
LIFE CYCLE: sites.
Definitive host: Humans  Challenges in eradication.
 Adult worms live in subcutaneous nodules
→ females produce unsheathed
microfilariae that migrate through skin and
eyes → blackfly (Simulium) ingests
microfilariae during blood meal →
microfilariae develop into infective L3
larvae in fly → transmitted to humans

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8. Mansonella ozzardi (New World Filaria)

Disease: Usually asymptomatic; mild

symptoms possible.
Transmission: Biting midges (Culicoides) or
blackflies (Simulium).
 Symptoms: Mild itching, rash, joint pain,
Geography: South and Central America,
headache, fatigue.
Caribbean.
 Diagnosis: Blood smears, skin snips,
serology.
MORPHOLOGY:
 Treatment: Ivermectin single dose; DEC
 Microfilariae unsheathed, non-periodic.
and albendazole less effective.
 Adults in body cavities and subcutaneous
 Prevention: Insect repellents, protective
tissues.
clothing, insect-proofing homes.

LIFE CYCLE:
9. Mansonella perstans (Perstans Filaria)
Definitive host: Humans
 Adult worms inhabit subcutaneous tissues
and body cavities → females release
unsheathed microfilariae circulating in
blood → biting midges (Culicoides) or
blackflies (Simulium) ingest microfilariae
Disease: Usually mild or asymptomatic.
→ larvae develop into infective L3 larvae
Transmission: Culicoides midges.
in vector → transmitted to humans during
Geography: Africa, Caribbean, parts of Central
bite → larvae mature into adults → cycle
and South America.
continues.

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LIFE YCLE:
Definitive host: Humans
 Adults live in body cavities and
subcutaneous tissues → females release
unsheathed microfilariae in blood (non-
periodic) → Culicoides midges ingest
microfilariae → larvae develop into
infective L3 larvae in vector → transmitted
to humans during bite → larvae mature into
adults → cycle continues.

SYMPTOMS: Minor allergic reactions,

headaches, calabar swellings, edema.
DIAGNOSIS: Blood smear, concentration
techniques, serology.
TREATMENT: Often not treated if
asymptomatic; DEC, mebendazole, ivermectin
used.
PREVENTION: Vector control, personal
protection.

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PARASITES SUMMARY_SHAI

Microfilaria Nuclei Pattern (if Nocturnal/

Parasite Life Cycle Overview Vector Type Organ/Site of Infection Activity
Type microfilaria) Diurnal
Rats are definitive hosts; larvae
Parastrongylus mature in lungs; humans infected Intermediate hosts: Central nervous system Larvae migrate in
No microfilaria Not applicable Not applicable
cantonensis by ingesting contaminated snails/slugs (brain) tissues
snails/slugs
Humans infected by eating
undercooked pork with encysted
Trichinella No vector; food- Intestinal mucosa; Larvae encyst in
larvae; larvae mature in No microfilaria Not applicable Not applicable
spiralis borne skeletal muscle muscle
intestines, then migrate to
muscles
Marine mammals definitive
No vector; food- Stomach and intestinal Larvae invade GI
Anisakis spp. hosts; humans infected by eating No microfilaria Not applicable Not applicable
borne wall tract
raw/undercooked fish with larvae
Small intestine in
Dogs/cats are definitive hosts;
Toxocara No vector; direct definitive hosts; larvae Larvae migrate in
humans accidental hosts via No microfilaria Not applicable Not applicable
canis/cati fecal-oral migrate in humans tissues
ingestion of eggs
(visceral larva migrans)
Humans infected by drinking
Dracunculus water containing infected Copepods (water Subcutaneous tissue Adults migrate
No microfilaria Not applicable Not applicable
medinensis copepods; adults mature under fleas) (lower limbs) subcutaneously
skin causing ulcers
Nuclei do not
Wuchereria Mosquito vector transmits larvae; Mosquito (Culex, Lymphatic system Sheathed
extend to tip of Active in blood Nocturnal
bancrofti adults live in lymphatics Anopheles, Aedes) (lymph nodes, vessels) microfilariae
tail
Mosquito Nuclei extend
Mosquito vector transmits larvae; Sheathed
Brugia malayi (Mansonia, Lymphatic system close to tip but Active in blood Nocturnal
adults live in lymphatics microfilariae
Anopheles) last few separated
Deer fly (Chrysops) transmits
Deer fly Subcutaneous tissue, Sheathed Nuclei extend to
Loa loa larvae; adults migrate through Active in blood Diurnal
(Chrysops) conjunctiva of eye microfilariae tip of tail
subcutaneous tissues and eye
Nuclei do not
Onchocerca Blackfly vector transmits larvae; Blackfly Subcutaneous nodules, Unsheathed
extend to tip of Active in skin Diurnal
volvulus adults form nodules under skin (Simulium) skin, eyes microfilariae
tail
Biting midges
Biting midges and blackflies
Mansonella (Culicoides), Unsheathed Nuclei extend to Active in
transmit larvae; adults in Subcutaneous tissue Diurnal
ozzardi Blackflies microfilariae tip of tail blood/skin
subcutaneous tissue
(Simulium)
Mansonella Biting midges transmit larvae; Biting midges Serous cavities Unsheathed Nuclei extend to Variable
Active in blood
perstans adults in serous cavities (Culicoides) (peritoneal, pleural) microfilariae tip of tail (Nocturnal/Diurnal)
PARASITES SUMMARY_SHAI

Notes:
 Parastrongylus cantonensis, Trichinella spiralis, Anisakis spp., Toxocara canis/cati, and Dracunculus medinensis do not have microfilariae stages; their infection
involves larvae migrating through tissues or encysting.
 Lymphatic filariasis (W. bancrofti and B. malayi), Loa loa, Onchocerca volvulus, and Mansonella spp. are filarial nematodes with microfilariae circulating in
blood or skin.
 Vectors vary widely: mosquitoes for lymphatic filariasis, deer flies for Loa loa, blackflies for Onchocerca, biting midges for Mansonella; others are food-borne or water-
borne.
 Activity and periodicity: W. bancrofti and Brugia microfilariae show nocturnal periodicity, Loa loa and Onchocerca are diurnal, Mansonella may vary.
 Organ tropism influences clinical manifestations: CNS for P. cantonensis, muscle for T. spiralis, skin and eyes for Loa loa and Onchocerca, lymphatics for filariasis
parasites.