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iii.

By blood sucking insects: Filariae


NEMATODES iv. By inhalation of dust containing
eggs: Ascaris,
Enterobius
NEMATODES CLASSIFICATION BASED ON THEY LAY EGGS/LARVAE
LOCATION OF ADULT IN BODY i. Oviparous: Egg laying nematodes
• INTESTINAL NEMATODES: a. Unsegmented eggs: Ascaris, trichuris
a. Small intestine: Ascaris, Ancylostoma, b. Segmented eggs: Ancylostoma,
Necator, Necator
Strongyloides, Trichinella. c. Eggs containing larvae: Enterobius
b. Large intestine: Enterobius, Trichuris ii. Viviparous: Producing larvae
Ex: Trichinella, Wuchereria, Brugia,
• TISSUE NEMATODES (Somatic Dracunculus
nematodes): iii. Ovoviviparous: Laying eggs
a. Lymphatic: Wuchereria, Brugia containing fully

b. Sub-cutaneous: Loa loa, Onchocerca, formed larvae which hatch out


Dracunculus immediately: Strongyloides.

c. Mesentry: Mansonella spp.,


d. Conjucntiva: Loa loa NEMATODES:

e. Zoonotic filariasis: Dirofilaria spp. “Roundworms”

Multicellular with internal organs


MODE OF INFECTION 3 morphologic forms: Eggs, larvae
i. By ingestion: and adult worm

a. Eggs: Ascaris, Enterobius, Trichuris Separate sexes (Dioecious)

b. Larvae within intermediate host:


Dracunculus
LIFE CYCLE:
c. Encysted larvae in the muscle:
Pinworms – ingestion/ inhalation of
Trichinella
infected eggs
ii. By Penetration of Skin:
Ancylostoma, Necator, Hookworm (larvae) – burrow through
skin of the foot
Strongyloides
Adult female worm – lay eggs in the
intestine

Larvae – inside the eggs; require


moist soil to continue development

Trichinella spiralis, Dracunculus


medinensis (reside in tissues)

Facultative parasites (free-living)

LABORATORY DIAGNOSIS:

Recovery of eggs, larvae and adult


worms

Cellophane tape preparation

Stool samples, tissue biopsies and


skin ulcers

Concentration techniques:
1. FECT (Formalin Ether)
2. AECT (Acid Ether)
1.Enterobius vermicularis LIFECYCLE
• Humans are the only known host.
Enterobiasis: Pinworm infection
• Adult worms (reside in the colon)
Common name: Pinworm,
Seatworm • Copulation (mating), pregnant] (gravid)
female worm
EGGS:
• RETROINFECTION – migration of
• Oval egg flattened on one side newly hatched larvae
• Unfertilized egg from anal skin back into the rectum
(unembryonated)
• AUTOREINFECTION – reinfect
• Fertilized egg (embryonated) themselves
ADULT:
1. FEMALE:
• Yellowish-
white,organ
systems
• Clear pointed
tail “pinhead”
2. MALE:
• Yellowish-white
• Smaller than females

LABORATORY DIAGNOSIS:
• Cellophane tape preparation
EPIDEMIOLOGY AND
❑ “Scotch tape swab”
TRANSMISSION:
❑ Perianal region
• Hand to mouth contamination
❑ Collect samples before defecation/
• Responsible for transmission
washing
Of Dientamoeba fragilis
• Recovered in stool samples (rare)
CLINICAL SYMPTOMS:
• Intense itching and inflammation of
anal/ vaginal areas. Intestinal irritation,
mild nausea, vomiting, irritability and
difficulty in sleeping. Mild intestinal
inflammation and abdominal pain.

TREATMENT:
• Albendazole, Mebendazole and
Pyrantel Pamoate

PREVENTION A N D CONTROL:
• Practicing proper personal hygiene,
application of ointment in the infected
perianal area, cleaning of potentially
infected environmental surfaces (linens)
and avoid scratching the infected area.
2.Trichuris trichiura • Complete maturation (Cecum)

Trichuriasis: Whipworm infection

Common name: Whipworm

EGGS:
• “Barrel/ football-shaped”
• “Japanese lantern”
• Yellow-brown color
• Prominent
hyaline polar
plug

ADULT:
EPIDEMIOLOGY:
• Anterior end
• 3rd most common helminth
❑ Colorless with slender esophagus
• Defecating into the soil/ using human
• Posterior end feces as fertilizers

❑ Pinkish-gray color CLINICAL SYMPTOMS:

• Male is smaller than female. • 500 to 5000 worms (heavy infection),


chronic dysentery, severe anemia and
growth retardation. Rectal prolapse,
LABORATORY DIAGNOSIS: Tenesmus and peristalsis. Abdominal
tenderness, pain, weight loss,
• Stool sample weakness, mucoid or bloody diarrhea.
• Zinc Flotation method
• Adult worms (intestinal mucosa)
• Rectum (heavy infections)

LIFE CYCLE:
• Infective stage: Embryonated ova
• Diagnostic stage: Unembryonated ova
• Larvae – small intestine
3.Ascaris lumbricoides
ADULT:
Ascariasis: Roundworm infection
• Creamy-white color
Common name: Large intestinal
roundworm • Cuticle – surface
covering
• Largest intestinal
UNFERTILIZED EGGS: (Vitelline nematode
layer is absent.)
• Female: Larger and
• Thin-shell (protection of amorphous pointed tail
mass of protoplasm)
•Male: Slender and curved tail
• Corticated – Outer mamillated,
albuminous coating
• Decorticated – Outer layer is absent LABORATORY DIAGNOSIS:
• Stool sample
• Others: Small intestine, gallbladder,
liver and appendix
• Adult worms - present in stool, vomited
up or removed from the external nares
• ELISA, DFS, Kato-katz/ Kato-thick and
Conc.techniques
FERTILIZED EGG: (Vitelline later is
present.) • During the lung phase of larval
migration, pulmonary symptoms
• More rounded than unfertilized egg can occur (cough, dyspnea,
• Chitin hemoptysis, Loeffler’s syndrome)
• Diagnosis is done by microscopic
❑ Thick Nitrogen-containing identification of eggs in the stool.
polysaccharide coating

❑ Between the embryo and mammillary


LIFE CYCLE:
albuminous material
Liver-lung migration
❑ Less evident in corticated eggs
Infective stage: Embryonated
eggs

Diagnostic stage: Fertilized,


unfertilized egg and adult worms
Maturation of larvae – small LOEFFLER’S SYNDROME
intestine • Simple pulmonary eosinophilia is
250,000 eggs per day are inflammation of the lungs associated
passed in the feces with an increase in eosinophils
• Causes
– Most cases of simple pulmonary
eosinophilia are due to an allergic
reaction, either from a drug, such as
sulfonamide, or infection with a fungus
or parasite, including Ascaris
lumbricoides.

Animal Ascarids:

• Toxocara cati Visceral Larva Migrans

• Toxocara canis

CLINICAL SYMPTOMS:
• Vague abdominal pain, vomiting, fever
and distention.
Obstruction of the intestine, appendix,
liver or bile duct and malnutrition.
• Discomfort from adult worms exits in
the body through the anus, mouth or
nose.
• Lungs – low-grade fever, cough,
eosinophilia and Pneumonia.
• Asthmatic reaction (presence of
worms).
4.HOOKWORMS RHABDITIFROM
LARVAE:
Most common STH (Soil Transmitted
Helminths). • Non-infective (feeding)
stage
Necator americanus
• Buccal cavity/ capsule
Ancylostoma duodenale (oral cavity)
Most common STH (Soil Transmitted • Genital primordium
Helminths).
FILARIFORM
Ancylostoma caninum LARVAE:
Ancylostoma braziliense • Shorter esophagus
than S.stercoralis

◾Tropical anemia • Distinct pointed tail

ADULT:
Necator americanus
• Buccal capsule:
• Common name: New World
hookworm
• Necatoriasis 1. Necator
americanus
Ancylostoma duodenale
❑ Pair of cutting
• Common name: Old World
plates. “S-shaped”
hookworm
• Ancylostomiasis
2.Ancylostoma
EGGS:
duodenale
• Unsegmented
❑ Consist of actual/
• Embryonic sharp teeth
cleavage
❑ “C-shaped”
❑ 2,4,8 cell
stage
• Thin, smooth, colorless shell LABORATORY DIAGNOSIS:
• Stool samples
• Recovery and examination of buccal
capsule
• “Harada-Mori technique”
LIFE CYCLE: CLINICAL SYMPTOMS:
• Infective stage: Filariform larvae • Ground itch– Intense itching at the site
of infection
• Diagnostic stage: Egg/ ova
• Sore throat, bloody sputum, wheezing,
headache and
mild Pneumonia with cough (larvae
migration to lungs).
• Mild gastrointestinal symptoms, mild
anemia.
loss, weakness Diarrhea, anorexia,
edema, pain, enteritis
• Microcytic hypochromic Iron deficiency,
weakness and hypoproteinemia.
HUMAN HOOKWORM Mortality – enormous loss of blood.

CLINICAL SYMPTOMS:
• Wakana disease (Pneumonitis)
• Miner’s anemia (IDA) (Microcytic
hypochromic)
• Animal hookworm: Creeping Eruption,
Cutaneous Larval Migrans (CLM)

ANIMAL HOOKWORM
5.Strongyloides stercoralis • Colorless body (transparent)

PARTHENOGENIC

Strongyloidiasis – ❑ Male is not required for


Threadworm infection fertilization.
Common name:
Threadworm
LABORATORY DIAGNOSIS:
• Stool samples (severe diarrhea)
EGGS:
• Duodenal aspirates and stool
• Smaller than (rhabditiform larvae)
hookworms
• Enterotest
• Well developed larvae is contained.
• Sputum (disseminated infection)
• “Chinese lantern”
• Threadworm larvae (higher recovery in
• Thin hyaline shell conc. samples)
• ELISA
RHABDITIFORM LARVAE: LIFE CYCLE:
• Short buccal cavity • Direct – Similar to hookworms
• Prominent genital primordium • Indirect – Rhabditiform larvae are
passed into the outside environment
(soil) and mature into free-living adults.
FILARIFORM LARVAE:
• Autoinfection – Rhabditiform
• Long, slender develop into filariform larvae inside the
intestine and may enter the lymphatic
• Long esophagus
system/ bloodstream.
• Notched tail

ADULT FEMALE:
• Short buccal
cavity
• Long and slender
esophagus
CLINICAL SYMPTOMS:
• Diarrhea and abdominal pain, Urticaria
and eosinophilia.
• Vomiting, constipation, weight loss,
anemia and Malabsorption syndrome.
Site of larvae penetration (itchy and
red), recurring allergic reactions,
pulmonary symptoms (larvae to lung).
• Immunocompromised (suffer from
severe autoinfection).
• “Cochin China Diarrhea/Vietnam
Diarrhea”

TREATMENT: Ivermectin with


Albendazole

PREVENTION AND CONTROL:


• Proper handling and disposal of fecal
material.
• Adequate protection of skin from
contaminated soil.
• Thorough treatment of infected person
(prevent autoinfection)

Differentiate Hookworm from


Strongyloides
• T.spiralis larvae in the intestine →
matures into adult rapidly
6.Trichinella spiralis • Gravid adult female → intestinal
mucosa (lay eggs)
• Infant larvae → bloodstream → striated
muscle (encyst)
• N O EGG STAGE

◾Trichinosis, Trichinellosis

◾Common name: Trichina worm

◾ENCYSTED LARVAE:
• Coiling up in the muscle fiber
• Striated muscle cell (nurse cell)

❑ Surrounds the coiled larva

◾LABORATORY DIAGNOSIS:
• Examination of infected skeletal
muscle.
• Laboratory findings: Eosinophilia and
leukocytosis, elevated Lactate
Dehydrogenase (LDH), Aldolase and
Creatinine Phosphokinase (serum ◾CLINICAL SYMPTOMS:
muscle enzymes) • Light infection: Diarrhea, headache
• Bentonite Flocculation test, Beckman and fever
Intradermal test • Heavy infection: Vomiting, nausea,
◾LIFE CYCLE: abdominal pain, diarrhea, headache and
fever (intestinal phase)
• Zoonosis – accidental infection, normal
host is an animal. • Eosinophilia, pain in pleural area,
fever, blurred vision, edema, cough and
• Consuming undercooked, death (larval migration through the body)
contaminated meat (striated
• Muscular discomfort, edema, local
muscle) inflammation, overall fatigue and
weakness (larvae settled into the
striated muscle)
7.Dracunculus medinensis
◾One of the largest adult nematodes

◾Dracunculosis, Dracunculiasis:
Guinea worm infection

◾Common name: Guinea worm

◾LARVAE:
• 1st stage/ Rhabditiform larvae
(Diagnostic stage)
• 3rd stage larvae

◾LIFE CYCLE:
• Ingestion of contaminated drinking
water with infected COPEPODS
(freshwater fleas – Intermediate host).
• Copepods contain the 3rd stage larvae
→ intestine → larvae mature into adult
worm → penetrate the intestinal wall →
connective tissue/ body cavities.
• Copulation → subcutaneous tissue (lay
1st stage larvae) → infected ulcer at the
site of larvae deposit
8.Capillaria philippinensis TAKE NOTE:

◾Pudoc’s Mystery ◾UNHOLY THREE/ TRIAD OF


disease: Capillariasis INFECTION:
• Hookworm, Ascaris
◾Common name:
lumbricoides,T.trichiura
Pudoc worm
◾HABITAT:
• Small intestine – T. trichiura,
◾EGGS:
C.philippinensis, A.lumbricoides
◾Flattened bipolar S,stercoralis and hookworms
mucus plugs • Large intestine – E.vermicularis,T.
◾ “Guitar/ peanut-shaped” trichiura
• Muscle – T.spiralis
◾Striated
• Lymph nodes – W.bancrofti, B.malayi

◾HEART A N D LUNG MIGRATION:


◾LIFE CYCLE:
• Intermediate host: Fresh water fish ◾A.lumbricoides, S. stercoralis and
(Birot, Bagsang, Bagsit) Hookworms

• Diagnostic stage: Ova


• Infective stage: Larvae
• Autoinfection
• MOT: Ingestion of raw/ undercooked
infected fish

◾CLINICAL SYMPTOMS:
• Abdominal pain
• Diarrhea
• Borborygmi (abdominal gurgling
sound)
FILARIAL WORMS ◾MORPHOLOGY:

◾Two morphologic forms:

Classification of Human filarial 1. ADULT WORMS


worms • Creamy white
A. Lymphatic filariasis: • Thread-like appearance
a. Wuchereria bancrofti (Bancroftian 2. MICROFILARIAE (LARVAE)
filariasis)
• Distribution of nuclei within the tip of
b. Brugia malayi (Malayan filariasis) the nuclei.
c. Brugia timori • Presence of sheath (transparent
B. Subcutaneous filariasis: covering)

a. Loa loa (Calabar swelling/Fugitive


swelling)
◾LIFE CYCLE:
b. Onchocerca volvulus (River
• Larvae → tissues (complete
blindness, dermatitis) &
development)
c. Mansonella streptocerca (Skin • Adult worms → lymphatics,
diseases) subcutaneous tissue, body
cavities
C. Serous cavity filariasis:
• Adult female worms lay live
a. Mansonella ozzardi (Non-pathogenic) microfilariae in blood or dermis.
• Microfilariae exit the body through
b. Mansonella perstans (Non-
blood meal (vector).
pathogenic)
• Intermediate host: Vectors
(Mosquitoes/ flies)
FILARIAE:
◾LABORATORY DIAGNOSIS:
◾Adult worm (tissue/ lymphatic
system) ◾PERIODICITY
◾Larvae (microfilariae - blood) • Presence of parasites in bloodstream
during a specific
◾Periodicity (nocturnal, diurnal and
time (nocturnal, diurnal or subperiodic).
sub periodic)
• Helpful for specimen collection
◾Viviparous/ larviparous
◾Giemsa-stained blood smear/ tissue
◾Vector: Mosquitoes and flies of infected nodule

◾Knott technique
1. Demonstration of microfilariae in the
peripheral blood
a. Thick blood smear: 2-3 drops of free-
flowing blood by finger prick method,
stained with JSB-II
b. Membrane filtration method: 1-2 ml
intravenous blood filtered through 3µm
poresize membrane filter
c. DEC provocative test (2mg/Kg): After
consuming DEC, mf enters into the
peripheral blood in day time within 30 -
45 minutes.

PATHOGENESIS & CLINICAL


SYMPTOMS:

◾Lesions, eosinophilia, fever and chills

◾ELEPHANTIASIS
• Enlargement of the skin and
subcutaneous tissue

◾CALABAR SWELLINGS
• Transient swelling of subcutaneous
tissue

◾Blindness
1.Wuchureria bancrofti ◾TREATMENT:
• Diethylcarbamazine (DEC) and
◾Elephantiasis
Ivermectin with Albendazole
◾Common name: Bancroft’s filaria • Surgical removal of abscess
◾MICROFILARIAE: • Use of special boots “Unna’s phase
• Thin and delicate sheath boots”

• Numerous nuclei • Elastic bandages (reducing size of


enlarged limb)
• Anterior end – blunt and round
• Posterior end – pointed, free from
Nuclei

2.Brugia malayi
◾LABORATORY DIAGNOSIS:
• Giemsa-stained blood smear
◾Malayan
• Knott technique
Filariasis/
• Sample collected during night Elephantiasis
(NOCTURNAL).
◾Common name:
• Peak hours: 9:00pm to 4:00am Malayan filaria
• Antigen and antibody detection
• PCR
◾MICROFILARIAE:

◾LIFE CYCLE: • Sheathed, round anterior end


• Numerous nuclei
• Vector: Aedes, Anopheles and Culex
spp. • Presence of two nuclei (tip of the tail)
◾CLINICAL SYMPTOMS:
1. Asymptomatic – Self-limiting ◾LABORATORY DIAGNOSIS:
2. Symptomatic – fever, chills and • Giemsa-stained blood smears
eosinophilia, granulomatous lesions,
lymphangitis, lymphadenopathy, • Specimen collection during nighttime.
elephantiasis/swelling of lower • Knott technique
extremities (breasts/ genitals),
abscesses may occur.
◾LIFE CYCLE: 3.Loa loa
• Vectors: Mosquito (Aedes, Anopheles
or Mansonia spp.) ◾Loiasis

• Co-infection with W.bancrofti can be ◾Common name: African eye worm


possible
◾MICROFILARIAE:
• Sheathed
◾EPIDEMIOLOGY:
• Nuclei fill the organism
• Humans – Definitive host • Nuclei at the tip of the tail
• Infect felines and monkeys

◾CLINICAL SYMPTOMS: ◾LABORATORY DIAGNOSIS:


• Fever, lesions, chills, • Giemsa-stained blood
lymphadenopathy, lymphangitis and
eosinophilia, elephantiasis of the legs • Corneal scrapings (adult worm)
and genitals (rare).
• Knott technique
• Sample collection: 10:15am to 2:15pm
◾TREATMENT: DEC (DIURNAL)
(Diethylcarbamazine) ◾LIFE CYCLE:
◾N E W TREND:
• Bite of Chrysops fly (vector)
• Brugia timori – can also cause
Malayan filariasis
◾CLINICAL SYMPTOMS:
• Tropical Eosinophilia (Occult Filariasis)
• Pruritus/ itchiness or localized pain,
Calabar swelling (anywhere in the
body).
• Circulating adult worms in the tissue
(no discomfort).
• Noticeable adult worms in the
conjunctiva of the eye/crossing under
the skin of the bridge of the nose.
– Pulmonary and asthmatic symptoms.
Microfilariae resides in the lungs.
Treatment is DEC. 4. Onchocerca volvulus
◾River Blindness, • Changes in skin appearance (loss of
Onchocerciasis elasticity and location of nodules)

◾Common name:
Blinding filaria

5. Mansonella ozzardi
◾MICROFILARIAE: ◾Common name: New
• Unsheathed World Filaria

• Numerous nuclei ◾MICROFILARIAE:

• Found in subcutaneous tissue • Unsheathed


• Numerous nuclei that
do not extend
◾LABORATORY DIAGNOSIS:
at the tip of long, narrowed, tapered tail.
• Giemsa-stained tissue biopsies
• Do not exhibit periodicity.
• Skin snips
• Ophthalmologic examination using a
slit lamp. 6.Mansonella perstans
• PCR (low infection) ◾Common name: Perstans filaria
◾LIFE CYCLE:
• Vector: Black fly (Simulium spp.) ◾MICROFILARIAE:
• Adult worms encapsulate in the • Unsheathed
subcutaneous fibrous tumors.
• Nuclei extend at the tip of the tail.
• Adult worms coiled and microfilariae
emerge. ◾ADULT:

• Microfilariae → infected nodules → • Female is


subcutaneous tissues → skin → eyes longer than
male.
• Resides in
◾CLINICAL SYMPTOMS: pleural and
• Severe allergic reactions, scratching peritoneal cavities
(leading to secondary bacterial
infection).
• Lesions → blindness (eyes)
7.Dirofilaria immitis
◾Common name: Dog heartworm

◾Common filarial parasite in dogs

◾Causes pulmonary diseases in humans


• Dead worms lodge in the pulmonary
vessels, these infarcts are referred as
“coin lesions” in chest radiography.

SUMMARY

1. LYMPHATIC FILARIASIS:
• Wuchureria bancrofti,Brugia malayi,Brugia timori
2. SUBCUTANEOUS FILARIASIS:
• Loa loa,Onchocerca volvulus
3. SEROUS/ BODY CAVITY FILARIASIS:
• Mansonella perstans, Mansonella ozzardi

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