INTESTINAL NEMATODES CLIN.PARA.

 Non-segmented, elongate, cylindrical

worms with a well-developed digestive
tract and reproductive system.
 The adult worms have separate sexes,
with the male generally smaller than the
female.
 Have very diverse life cycles providing
different routes of transmission as well as
disease symptoms.  Infertile eggs: 88 to 94 μm x 39 to 44
μm, longer and narrower
INTESTINAL NEMATODES: : with a thin shell
Ascaris lumbricoides and irregular mammilated coating filled
Trichuris trichiura with refractile
Necator americanus granules.
Ancylostoma duodenale  Fertile eggs: 45 to 70 μm x 35 to 50 μm
Strongyloides stercoralis  has a thick, transparent, hyaline shell with
Enterobius vermicuralis a thick outer layer
Capillaria philippinensis  have an ovoid mass of protoplasm

Ascaris lumbricoides  Diagnostic stage: Fertilized and

 Causes ascariasis in humans Unfertilized eggs
 The most common intestinal nematode  Infective stage: Fully embryonated eggs
 “Giant roundworm”  MOT: Contaminated food and water
 Is a soil-transmitted helminth (STH)  Hand to mouth route contaminated
 STH infections are diseases of poverty, with
and contribute to malnutrition and
impairment of cognitive performances
 Primary hosts: Humans and Swine

Parasite biology
 Polymyarian type - cells are numerous
and project well into the body cavity
 The whitish or pink worms are large
 Male: 10-31 cm
 Female: 22-35 cm
Have a terminal mouth with three lips and
sensory papillae

Male: ventrally curved posterior end width two

spicules. Pathogenesis
 have a single, long, tortuous tubule Ascariasis pathogenesis involves:
Female: paired reproductive organs in the  tissue reactivity to invading larvae
posterior two-thirds.  intestine irritation caused by the
mechanical and toxic action of the adult
worm

MIDTERM DESO-ACIDO, G.
INTESTINAL NEMATODES CLIN.PARA.
 complications caused by the parasite's Bile Duct - Obstructive Jaundice
extraintestinal migration. Liver - Liver Abscess
The majority of Ascaris infections are Pancreas - Pancreatitis
asymptomatic. A typical infection of 10 to 20 Appendix - Appendicitis
worms may not show symptoms unless detected Brain - Ascaris Encephalopathy (rare)
by stool testing or the spontaneous passing of
worms in the stool. Diagnostic tests
 Microscopic Examination of a Stool Sample
1. Lung Migration Phase - During lung  Direct Fecal Smear (DFS)
migration, several larvae penetrate  Kato Thick Smear
through the lung capillaries as they enter  Kato-katz Techniques
the air sacs this may cause host
sensitization resulting in allergic Formalin Ether/Ethyl Acetate Concentration
manifestations, difficulty of breathing, and Techniques
fever similar to pneumonia.
Treatment
Main Penetrator: Migrating Larvae Anthelmintic Medications:
 Albendazole - (400 mg single dose)
2. Intestinal Phase - In intestinal 200 mg for children
migration, the larvae have matured into adults,  Mebendazole - 500 mg single dose
invading the digestive tract and causing serious  Pyrantel Pamoate
disease when they migrate into other organs. A  Ivermectin
few Ascaris adults' constant biting or pricking of  Nitazoxanide
the intestinal mucosa for food may irritate nerve
endings, resulting in intestinal spasm and Trichuris trichiura
obstruction.  causal agent of TRICHURIASIS
 “Whipworm”
Main Penetrator: Adult Worms  soil-transmitted helminth
 children are most frequently infected
Clinical manifestations
Due to larvae in Lung Migration Phase:
 Loeffler's syndrome - A type of
eosinophilic pneumonia mimicking
community-acquired pneumonia and
asthma.
 Ascaris Pneumonitis
Due to adult worm in Intestinal Phase:
 Biliary Ascariasis - severe colicky
abdominal pain caused by worms inside.
 Acute Peritonitis or Chronic Parasite biology
Granulomatous Peritonitis.  Holomyarian type - muscle layer
 Loss of appetite, weight loss, continuous or divided into two longitudinal
intestinal spasm zones
 ATTENUATED ANTERIOR THREE-
Moderate infections - may produce lactose FIFTHS traversed by a narrow esophagus
intolerance and vitamin A malabsorption. resembling a string of beads.
ROBUST POSTERIOR TWO-FIFTHS contains
Heavy infections - are likely to cause bowel the intestine & a single set of reproductive organs
obstruction (due to bolus formation),  secrete TT47 - a pore-forming protein
intussusception, or volvulus that may result in
bowel infarction and intestinal perforation. Adult Male Adult female
Size 30 to 45 mm 35 to 50 mm
Adult worms does erratic migration in different Anterior end Whip-like
organs: Posterior end Coiled blunt

MIDTERM DESO-ACIDO, G.
INTESTINAL NEMATODES CLIN.PARA.

posterior  Anemia is strongly correlated to heavy

which a single intensity trichuriasis
spicule and
refractile Diagnosis
sheath  FLOTAC technique
 Direct Fecal Smear (DFS)
EGG:  Kato-katz technique
Size:
Length: 50 to 54 um Treatment
Width: 23 um  Mebendazole 100mg (once a day) 500mg
Shape: Lemon or football- (twice a day)
shaped with plug-like  Albendazole 400mg
translucent polar prominences
Shell: yellowish outer shell HOOKWORMS:
and transparent inner shell Necator americanus
 Females lay approximately 3,000 to Ancylostoma duodenale
10,000 eggs per day
 Larvae escape & penetrate intestinal villi Necator americanus
(remain for 3 to 10 days)  Soil-transmitted helminths
 A blood sucking nematodes that attach to
Pathogenesis the mucosa of the small intestine
 Lumen may be filled with worms  “New World hookworm”
 Cause intestinal bleeding  Anterior end forms a conspicuous bend
 Cause petechial hemorrhages

Clinical manifestations
 Light infections are moderately with
anemia
 Heavy infections can lead to Trichuris
dysentery

MIDTERM DESO-ACIDO, G.
INTESTINAL NEMATODES CLIN.PARA.
Parasite biology  Zinc Sulfate Centrifugal
HOOKWORM EGGS Flotation/Formalin-Ether Acetate
 Length: 65-75 um  Harada- Mori
 Width: 35-40 um  Direct Fecal Smear
 Bluntly rounded ends
 Thin,smooth, colorless shell Treatment
 Unsegmented at oviposition  Albendazole (400mg) - DRUG OF CHOICE
 Undergoes two-eight cell stage of division  Mebendazole (500mg)
 Iron supplement

Ancylostoma duodenale
 One of the primary intestinal hookworm
species
 A blood sucking nematodes
 Found in tropical and subtropical countries

Parasite biology
Hookworm eggs
 Bluntly rounded ends
Rhabditiform larva  Transparent
 Newly hatched: 15 by 270 um  unsegmented at oviposition
 Actively feeding: 540 to 700 um  Size: 55-60 µm by 35-40 µm

Filariform larva Rhabditiform larvae

 Appears after the second molt of  hatch from eggs are 250-300 µm long and
rhabditiform approximately 15-20 µm wide.
 Similar to Strongyloides stercoralis  long buccal canal
 They resemble those of Strongyloides
Adult stercoralis
 Rarely seen
Filariform larvae
Small adult  Inscopicouus buccal spear
 Appears grayish-white to pink  500—700 µm long.
 Long buccal cavity and short esophagus
 Small genital primordium
 pointed tail
Clinical manifestations  Unsheathed, with about a 1:2 ratio in
 ITCHING, EDEMA, ERYTHEMA length of esophagus to intestine
 PAPULOVESICULAR ERUPTIONS
 BRONCHITIS OR PNEUMONITIS Adult form
 ABDOMINAL PAIN  Male: 8—12 mm long,
 STEATORRHEA  females : 10—15 mm long
 DIARRHEA WITH BLOOD AND MUCUS  Single-paired male or female reproductive
 EOSINOPHILIA organs
 Head: continues in the same direction as
HEAVY HOOKWORM INFECTION the curvature of the body
 progressive , secondary, microcytic,  Buccal capsule: 2 pairs of curved ventral
hypochromic teeth
Anemia
 Hypoalbuminemia  Diagnostic stage: Hookworm eggs
 Infective stage: Filariform larva
Diagnostic tests  Definitive host: human
 Kato Thick or Kato-Katz method

MIDTERM DESO-ACIDO, G.
INTESTINAL NEMATODES CLIN.PARA.
MOT: Skin penetration, Trans mammary - FLOTAC
transmission and Trans placental transmission
4.Culture methods
Clinical manifestation - Harada-Mori

Maculopapular lesions & localized erythema 5. Molecular approaches which includes:

 Penetration of the filariform larvae a. PCR-based detection
through skin b. Enzyme-Linked Immunoabsorbent Assay
 “Ground itch” or “dew itch” (ELISA)
 Related to contact with soil
 Can Last for 2 weeks Treatment
 light infection: no symptoms  MASS DRUG ADMINISTRATION
 heavy infection: abdominal pain, diarrhea,  Recommended by WHO
loss of appetite, weight loss, fatigue and  ALBENDAZOLE
anemia - Drug of choice
- Is larvicidal and ovicidal against N.
Bronchitis or Pneumonitis americanus & Ancylostoma duodenale
 Larvae migrating through the lungs - Adults: 400 mg once a day
 produce minute hemorrhages with - Children (2 yrs old): chewable tablets or
eosinophilic and leukocytic Infiltration suspension preparations
 Maturation stage: abdominal pain,  MEBENDAZOLE
steatorrhea, or sometimes diarrhea with - For children and adults (500 mg 1x a day)
blood, mucus, eosinophilia  DERIVATIVES: BENZIMIDAZOLE
- derivative of Mebendazole
Progressive, Secondary, microcytic - Drug resistance to benzimidazole
hypochromic anemia (of the iron deficient) derivatives has not been done in local
 Due to continuous blood loss setting

Hypoalbuminemia ADVERSE EFFECTS: rare and are usually mild

 Low-level of albumin due to combined loss and transient
of blood, lymph and protein
 Other symptoms: Exertional dyspnea, IRON SUPPLEMENTS AND ADEQUATE DIET:
Weakness,Dizziness and Lassitude Patients that has anemia and hypoproteinemia
 Signs: Rapid pulse, Edema and
Albuminuria
Strongyloides stercoralis
 “threadworm”
Diagnostic tests  Causes STRONGYLOIDIASIS or
 Clinical picture threadworm infection
 Characteristic is not  Free living rhabditiform and parasitic
pathognomonic to permit filariform stages
differentiation from other helminth  Naturally pathogenic to human
infections  Soil-transmitted helminth
 Final diagnosis Definitive hosts: Humans, dogs and cats
 Depends on the identification of
parasite ova in the feces Parasite biology
S. stercoralis eggs
Individual and Mass screening  Size: Ave. 48 by
1. Direct fecal smear 35 um
2. Kato thick or Kato-Katz Method  Typical growth
3. Concentration technique phase: contains
- Zinc Sulfate Centrifugal flotation well-developed
- Formalin-ether/ethyl acetate concentration larvae
methods

MIDTERM DESO-ACIDO, G.
INTESTINAL NEMATODES CLIN.PARA.
 Embryonic cleavage: Two-, four-, or  Parasitic males have not been reliably
eight-cell stage, when present identified
 Contains 8-12 thin-shelled segmented ova
 Shell: Thin hyaline shell  Diagnostic stage: Rhabditiform larva
 Infective stage: Filariform larvae
Rhabditiform larva
 “Actively feeding”
 Size: 224 um by 16
um
 Appearance:
elongated esophagus
with a pyriform
posterior bulb,
shorter buccal capsule and a larger genital
primordium
 Differs from the hookworm in being
slightly smaller and less attenuated
posteriorly

Infective Filariform larva

 “Non-feeding”
 Appearance: Slender and 550 um in
length
 Autoinfection: It results when an
 Similar to hookworm filariform larva but is
infected individual becomes his own direct
usually smaller, with a distinct cleft at the
source of infection
tip of the tail
 M.O.T: Contact with soil that is
 Eggs: thin shells and similar to those of
contaminated with free living larvae/ skin
hookworm except that they measure only
penetration
about 50-58 um by 30-34 um
 Life cycle last apprx. 3-4 weeks
Parasitic Filariform female
 Size: 2.2 mm by 0.04 mm
Pathogenesis
 Appearance: colorless, transparent with
 3 Phases of Acute Infection
finely striated cuticle, short buccal cavity;
 First Phase - Invasion of the skin by
long and slender esophagus
filariform larvae (causes Erythema and
 Vulva: located one-third the length of the
pruritic elevated hemorrhagic papules)
body from the posterior end
 Second Phase - Migration of larvae
 Uteri: single file of 8-12 thin shelled,
through the body (causes Lobar
transparent, segmented ova
Pneumonia)
 Parthenogenetic
 Third Phase - Penetration of the
intestinal mucosa by adult female worms
Free-living female
 Size: 1mm by 0.06 mm (smaller than the
Clinical manifestations
parasitic female)
 Light Infection - does not cause intestinal
 Appearance: has a muscular double-
symptoms
bulbed esophagus, and the intestine is a
 Moderate Infection - diarrhea alternating
straight cylindrical tube
with constipation
 Heavy Infection - intractable, painless,
Free-living male
and intermittent diarrhea (Cochin China)
 Size: 0.7 mm by 0.04 mm
 Appearance: smaller than female,
Immunocompromised
ventrally curved tail, 2 copulatory
 Hyperinfection
spicules, a gubernaculum but no caudal
alae

MIDTERM DESO-ACIDO, G.
INTESTINAL NEMATODES CLIN.PARA.
Diagnostic tests ❏Eggs
 Baermann funnel gauze method ❖50-60 μm by 20-30 μm
 Harada - Mori Culture (average 55 by 36 μm)
Other laboratory methods : Asymmetrical, has a
 Beale’s string test translucent shell, tadpole-
 Duodenal aspiration like embryo (inside)
 Small bowel biopsy

Treatment
 Albendazole
 Thiabendazole ❏Diagnostic stage: Eggs on perianal folds
 Ivermectin ❏Infective stage: Embryonated Eggs
 Contraindicated in pregnant women and ❏MOT: Ingestion
those with known hypersensitivity to ❏Host: Human
drugs - Albendazole and Thiabendazole

Enterobius vermicularis
Also known as human pinworm
❏Causes enterobiasis or oxyuriasis in humans
❏Perianal itching or pruritus ani
❏“meromyarian”
❏2-5 cells per dorsal or ventral half
❏Most common parasite in temperate regions

Parasite biology Clinical manifestation

❏Adult Worm  Mild catarrhal inflammation of the
intestinal mucosa
- cuticular alar expansions at the anterior
 Inflammation of the deeper layers of the
end and a prominent esophageal bulb
intestines
 Location: Cecum and Adjacent portions
 Irritation of Perineal region
of the small and large t intestines
 Secondary Bacterial infection
❖Male: 2-5 mm by 0.1-0.2 mm
 Insomnia
: curved tail and single spicule
 Appendicitis, Endometritis, Salpingitis,
❖Female: 8-13 mm by 0.4 mm
and Peritonitis
: long pointed tail and uteri is distended with
 Familial or Group Disease
eggs
Diagnosis
 Adult worms or eggs on microscopic
❏Rhabditiform larva
examinations
❖140-150 μm by 10 μm  Graham’s scotch adhesive tape swab
: Esophageal bulb, but has no cuticular expansion
on the anterior end

MIDTERM DESO-ACIDO, G.
INTESTINAL NEMATODES CLIN.PARA.
Treatment Treatment
 Mebendazole (100 mg) or Albendazole  Electrolyte replacement and high protein
(400 mg) diet
 Pyrantel pamoate (11 mg/kg)  Anthelminthic Drugs
(secondary drug)
DRUG OF CHOICE:
Capillaria philippinensis  Mebendazole- 200mg twice a day for 20
 From the superfamily Trichinelloidea days
 Male worms: 1.5 - 3.9 mm  Albendazole- 400mg may be given once
 Female worms: 2.3 - 5.3 mm daily for 10 days
 Natural hosts: Fish-eating birds
 Incidental hosts: Humans Relapses may occur if the treatment regimen is
not followed and completed.

Parasite biology
 Peanut-shaped with
striated shells and
flattened bipolar plugs
 Size: 36 - 45 um by 20
um

 Diagnostic stage: Unembryonated eggs

 Infective stage: Larvae
 M.O.T: Ingestion of raw/uncooked fish

Clinical manifestations
 Causes Capillariasis
 Usually have abdominal pain and
borborygmi
 Initially experience intermittent diarrhea
 Progress to 8-10 voluminous stool
per day
 Intestine shows
 Flattened and denuded villi
 Dilated mucosal glands

Diagnosis
 Direct smear or wet mount
 Stool Concentration methods
 Enzymed-linked immunosorbent assay
(ELISA)
 ELISA using T. spiralis antigen has been
tested and shown to have a sensitivity of
100% in the diagnosis of capillariasis.

MIDTERM DESO-ACIDO, G.
TISSUE NEMATODES CLIN. PARA.
TISSUE NEMATODES - Undergo 2 molts to reach maturity –
Parastrongylus cantonensis Adult worm
Trichinella spiralis - After final molt (Host: Rat) the young
Toxocara canis and cati adult migrate in pulmonary
Dracunculus medinensis arteries to complete development
- After 2 weeks adult female will
Parastrongylus cantonensis start laying eggs
 RAT LUNGWORM
 1st described in Canton, China by Chen in HOSTS
1935 from domestic rats  Definitive hosts: RATS
 Normally lives in the lung of the Rats  Intermediate hosts: MOLLUSKS
 Formerly under genus Angiostrongylus but - Acatina fulica (GIANT AFRICAN
now under genus Parastrongylus SNAIL)
 HUMANS: cause eosinophilic - Hemiplecta sagittifera
meningoencephalitis - Helicostyla macrostoma
- Vagiilus plebeius
- Veronicella altae

 Paratenic host: Freshwater Prawn/Crab

 Accidental host: HUMANS
 transmission is via
- Ingestion:
o Raw mollusk (ESCARGOT)
o Leafy vegetables (with mucus of
mollusks)
o Ingestion of prawn/crab
o Contaminated water

APPEARANCE
 MALES
 Single-lobed, kidney
 Shaped: well-developed caudal bursa
(use for grasping into the body to the
female body during copulation)

 FEMALES
 15, 000 eggs daily
 “BARBER’S POLE”
o Appearance: uterine tubules wind
spirally in the intestine
 WHITE – UTERUS
 RED – DIGESTIVE TRACT

 LARVAE
 1ST stage larvae
- Infective stage of Molluscan Ih
(intermediate host of Parastrongylus)  Adult worm lives in the pulmonary arteries
and right ventricle of normal definitive
 3rd stage larvae (12 DAYS) host – RATS
- Infective stage of rats and humans  Female worm lays egg and it will hatched
- Occur in the brain in the terminal branch of pulmonary
- Penetrates the stomach to reach arteries of the rats – yield the 1st stage
bloodstream to access CNS larvae

PREFINAL DESO-ACIDO, G.
TISSUE NEMATODES CLIN. PARA.
 In humans, after ingestion, it will migrate Trichinella spiralis
in the brain where it develops as young  TRICHINA WORM,
adults MUSCLE WORM,
 Young adult will return to the venous GREAT IMITATOR
system via bloodstream, to the  Most important cause
pulmonary arteries and become of TRICHINELLOSIS
sexually matured (rats) in humans
 Most adaptive in
Infective stage (humans & rats): 3rd stage domestic and wild
larvae pigs

Diagnostic stage: Larvae migrate to brain APPEARANCE

DISEASE ASSOCIATION  ADULT WORMS
 Primary Eosinophilic  In small intestine
Meningoencephalitis  MALES – conical papillae (copulatory
 Incubation period: 6 – 15 days appendage)
 Acute or severe intermittent occipital or  FEMALES
bitemporal headache - Coiled/ club shaped uterus
 Paresthesia, blurred vision/diplopia - Viviparous (gives birth to live
 Confusion, incoherence, disorientation, larvae): lives on 30 days
memory lapses, coma - 1,500 larvae (lifetime)
 Infection is self-limited
 Rare cases: can cause death  ENCYSTED LARVAE
- Diagnostic and infective stage
DIAGNOSIS - In muscle fibers
 Meninges - Spear-like, burrowing anterior tip
 Charcot-Leyden Crystals

 Blood
 Eosinophilia (7% – 36%)

 CSF
 Eosinophils (>10%) and monocytes
 100-1000 WBC/uL
 Mildly elevated proteins
 Normal glucose

 Post-mortems
 Immature worms in cerebrum/cerebellum

 ELISA
 Dot-blot ELISA (100% sensitive)
specimen: blood (used in epidemiological
survey)
 PCR

TREATMENT
 Mebendazole and Albendazole (China,
Taiwan and Thailand)

HOSTS
 HUMANS, RATS, DOGS, CATS, PIGS,
BEAR, FOXES AND ANY OTHER
CARNIVORE/OMNIVORE
PREFINAL DESO-ACIDO, G.
TISSUE NEMATODES CLIN. PARA.
 Definitive and Intermediate hosts DIAGNOSIS
 Via ingestion of:  MUSCLE BIOPSY
o Raw/ Undercooked meats  0.2 – 0.5g of muscle tissue
 (+) larva
 In humans: after exposure to gastric acid  HCI and PEPSIN – digestive muscle
and pepsin, larvae will released from cyst (limited to larvae 10-12 days old or 2-3
and will invade the small bowel mucosa – weeks post-infection)
sub epithelium villi of intestine  Definitive diagnosis
 Maturation: 2 days
 Adult worm: 5-7 days post-infection  BLOOD
 Life span in small bowel: 4 weeks (after  Eosinophilia
1 week, female will released larvae and
this will migrate to striated muscle where  ENZYMES
they encyst  Increased muscle enzymes:
 After 3 weeks, they will start to coil into o Creatine phosphokinase
their individual cyst o Lactate dehydrogenase
 Encapsulation: 4-5 weeks after o Myokinase
infection
 Ave. life span of encysted larvae: 5-6
years and survived for up to 40 years in  OTHER CHEMISTRIES
humans  Total IgE – elevated

Domestic cycle: pigs and anthrophophilic  LATEX AGGLUTINATION

(human-loving) rodents/ horses  Rapid diagnosis (<1HR)

Sylvatic cycle: bears, moose, wild boars  ELISA

 RECOMMENDED
DISEASE ASSOCIATION
 TRICHINELLOSIS  WESTERN BLOT
 Cardinal signs (primary or major  Confirmation of ELISA results
symptoms):
- Severe myalgia  BACHMAN INTRADERMAL TEST
- Periorbital edema  Skin test made from Trichinella LARVAE
- Eosinophilia ANTIGEN + SALINE
 > 10 larvae – asymptomatic (light  (+) WHEAL AND FLARE REACTION
infection) (reddiness and inflammation)
 150 – 500 larvae – (symptomatic)
 1,000 – 3,000 larvae – (severe infection) TREATMENT
 MEBENDAZOLE
THREE PHASES:  ALBENDAZOLE
1. ENTERIC PHASE – incubation and
intestinal invasion PREVENTION AND CONTROL
2. INVASION PHASE – larval migration and  COOKING OF THE MEAT
muscle invasion (immunological,  77C (170 F)
pathological and metabolic reaction –
inflammatory reaction) eosinophilia,  STORAGE (freezing)
releasing of inflammatory substances:  -15 C for 20 DAYS
histamine, serotonin, bradychinin,  - 30 C for 6 DAYS
prostaglandins – which result in increased  SMOKING, DRYING MEAT IS
vascular permeability INEFFECTIVE
3. CONVALESCENT PHASE – encystment
and encapsulation (fever, weakness, pain  ANIMAL MONITORING
of patient)  Meat inspection
 Serological tests for animals

PREFINAL DESO-ACIDO, G.
TISSUE NEMATODES CLIN. PARA.
 Rat free pens  CATS
 Proper disposal of carcasses  Toxocara cati (CAT ASCARID)
- HUMANS are ACCIDENTAL HOSTS
Toxocara canis and cati - Ingestion of embryonated egg
 DOG & CAT
ROUNDWORM Diagnostic stage: 3RD STAGE LARVAE migrate
 TOXOCARIASIS in tissues
 Zoonotic diease
 From stray dogs Infective stage: Embryonated eggs
(T. canis) and
Cats (T. cati)  Unembryonated eggs will embryonate – 1
to 4 weeks in the environment
 Embryonated eggs – 3rd stage larvae
APPEARANCE (infect hosts via ingestion)
 WORMS AND EGGS  Larvae will now penetrate the dogs and
cats gut wall
 EMBRYONATED EGGS (resistance to  Younger cats & dogs: larvae will
freezing, moisture and pH levels – 1 year) migrate to lungs (bronchial tree) and
- INFECTIVE STAGE esophagus where they will be swallowed
back to gastrointestinal tract
 Gastrointestinal: Adult worm developed
 ADULT FEMALES and lay eggs in small intestine
- 200,000 EGGS DAILY  Older dogs:
 ENCYSTED STAGES - Patent: egg producing infection
- Can be transmitted transplacental or - Larvae goes to tissue (encyst)
transmammary routes  Female dogs
- Mainly for predation transmission - Encysted larvae can reactivate during
late gestation (pregnant)
HOSTS - Transplacental: major route
 DOGS - Transmammary: minor route
 Toxocara canis (DOG ASCARID)  Humans: larvae will penetrate the
- PARATENIC HOSTS (non-canid): intestinal wall and carry through
Rabbits, chicken, cattle, sheep circulation (liver, heart, lungs, brain,
- Earthworms, ants, other muscle and eyes)
invertebrates
DIEASE ASSOCIATION
 TOXOCARIASIS
- T. canis CASES ARE FEWER

VISCERAL LARVA MIGRANS/ VLM

- Migration and death of larvae to
tissues and organs
- Inflammation and eosinophilic
granulomas
- Liver, lungs, CNS, eyes

OCULAR LARVA MIGRANS/ OLM

- May coexist with VLM
- Unilateral visual impairment
- Strabismus (duling)
- Blindness (most serious)

COVERT TOXOCARIASIS/ CoTOX

- Less specific and Asymptomatic

PREFINAL DESO-ACIDO, G.
TISSUE NEMATODES CLIN. PARA.
- Less frequent eosinophilia  3RD STAGE
- In the intermediate host
NEUROLOGIC TOXOCARIASIS - INFECTIVE STAGE
- One causes of ENCEPHALITIS
- migration of larva to the brain, may HOSTS
show in CSF  HUMANS
- DEFINITIVE HOSTS
DIAGNOSIS AND TREATMENT - Via ingestion of water contaminated
 BIOPSY (time consuming and difficult) with infected copepods (FRESHWATER
- Definitive diagnosis FLEAS)
 SEROLOGIC
- IgG ELISA KITS for Toxocara  COPEPODS
- EXCRETORY-SECRETORY (TES) - INTERMEDIATE HOSTS
ANTIGENS - Harbors 3rd stage larvae
 PCR (used animal models)
TREATMENT
 MEBENDAZOLE
 ALBENDAZOLE
Combined with anti-inflammatory medications

Dracunculus medinensis
 DRAGON WORM, MEDINA WORM,
GUINEA WORM
 “FIERY SERPENT” of the Israelites
plagued in the red sea
 Longest nematode of man

LIFE CYCLES:
After the copepods die, Larvae will penetrate the
stomach and intestinal wall, enters the abdominal
cavity and retroperitoneal space and mature

After copulation, male worm die and female

APPEARANCE migrate to subcutaneous tissue (skin surface),
 ADULT WORMS apprx. 1 year after infection, female worm will
 MALES – smaller and rare start cause blisters (skin) and eventually rupture.
 FEMALES
- Migrates to subcutaneous tissue DIEASE ASSOCIATION
after mating (skin of extremities) –  DRACUNCULOSIS/ DRACUNCULIASIS
DIAGNOSTIC STAGE  Symptoms associated with allergic
reactions
 LARVAE  Unsuccessful attempts to remove an
 1ST STAGE (rhabditiform larva) entire worm may result to partial worm
- Tail: 1/3 of body length being left – additional allergic reaction and
- DIAGNOSTIC STAGE nodule formation
- Ruptured ulcers immersed in cool
water reveals this larvae DIAGNOSIS
- Consumed by intermediate hosts  RECOVERY OF ADULT WORMS
- Observing ulcers for emergence of
worms

PREFINAL DESO-ACIDO, G.
TISSUE NEMATODES CLIN. PARA.
 RUPTURE OF ULCERS BY COOL WATER
- Reveals 1st stage larva

TREATMENT
- Total worm removal (winding of
stick)

CONTROL/ PREVENTION
- Properly treated water (boiling)

PREFINAL DESO-ACIDO, G.
THE FILARIAE CLIN.PARA.
THE FILARIAE – blood feeding arthropod  They penetrate the pro-ventriculous
vector-borne nematodes (stomach of the mosquito) and cardiac
portion of the midgut and reach thoracic
LYMPHATIC FILARIAE: muscle
1. Wuchereria bancrofti  Developed into 1st stage larvae
2. Brugia malayi  L3 migrate into hemocele or body cavity
to the proboscis of the mosquito
SUBCUTANEOUS FILARIAE:
3. Loa loa
4. Onchocerca volvulus

SEROUS CAVITY
- Filariae that causes infection in the
abdomen

LYMPHATIC FILARIAE
- Considered one of the most delabilating
diseases that is known in the man

Wuchereria bancrofti
 “BANCROFT’S FILARIAL WORM”
 Causative agent of BANCROFTIAN
FILARIASIS

FORMS:
 ADULT WORMS – creamy white, long
INTERMEDIATE HOSTS:
and have filiform shaped
 Aedes
 MALE: 20-40 mm in length
 Anopheles
 FEMALE: 80-100 mm
 Culex
MICROFILARIA
DEFINITIVE HOSTS:
 270-290 um
 Humans
 Small snake-like organism
 Moved along red blood cells
MODE OF TRANSMISSION:
 Enclosed in a hyaline sheath, Sheathed
 Mosquito bite
 Sheath of microfilaria is much longer than
the microfilaria itself
PERIODICITY:
 When stained, shows dark staining nuclei
 NOCTURNAL
(important identifying features) and tail
end culminates in a point that is free of
DIAGNOSTIC STAGE: Sheathed microfilariae
nuclei
INFECTIVE STAGE: 3rd STAGE LARVAE
LIFE CYCLE
Brugia malayi
 3rd stage larvae will developed into adults
 “MALAYAN FILARIAL WORM”
and resides in the lymphatics
 Causes MALAYAN FILARIASIS
 Adults produce microfilaria which are
FORMS:
sheath
 ADULT WORMS
 NOCTURNAL PERIODICITY: can see in
 MALE: 13-23 mm in length
peripheral blood during nighttime
 FEMALE: 43-55 mm
 Microfilaria migrates into the lymph and
blood
MICROFILARIA
 After ingestion of mosquito, the
 111-230 um
microfilaria will shed their sheaths
 Sheathed

PREFINAL DESO-ACIDO, G.
THE FILARIAE CLIN.PARA.
 When stained, shows 2 distinct nuclei at  LYMPHANGIOGENESIS
the end of the tail - Growth of lymphatic vessels due to the
inducement of proliferation of lymphatic
endothelial cells (because of the antigens
introduced by filarial parasites)

 Lead to LYMPHEDEMA – swelling of

lymph due to increased lymph fluid
 ELEPHANTIASIS – limbs like elephants

Dead and decalcifying adult worms illicit immune

responses
- Lymphatic blockage and lesions

ACUTE DERMATOLYMPHANGIOADENITIS
(ADLA)
 Most common acute manifestation of
LF
 Localized pain
 Lymphadenitis or lymphangitis

INTERMEDIATE HOSTS: LYMPHEDEMA

 Mansonia  Most common chronic manifestation of
LF
DEFINITIVE HOSTS:  Most common affected: LOWER LIMBS
 Humans (but upper limb and male genitalia can be
affected also)
MODE OF TRANSMISSION:  Progression to ELEPHANTIASIS
 Mosquito bite  Formation of HYDROCELE (CHYLOCELE)
– obstructions of the lymphatic in the
PERIODICITY: tunica vaginalis
 NOCTURNAL and SUBPERIODIC  HYDROCELE – accumulation of fluid or
(microfilaria present in blood at all time hydrocele fluid (clear or straw colored)
and the max. level is during afternoon)  CHYLOCELE – milky fluid (presence of
lymph fluid)
DISEASE ASSOCIATION - Accumulates in the sac of the testes of the
LYMPHATIC FILARIASIS male patients
 Can be acquired during childhood  GENITALS – BANCROFTIAN
 May take years to manifest itself FILIARISIS (common and more severe)
 Can be asymptomatic, acute stage or  GROIN - MALAYAN FILIARIASIS (less
chronic stage common and severe)
 Lymphatic localization (important for
parasite survival) EXPATRIATE SYNDROME
 Lymph is less aggressive than blood  Immunologic hyper-responsiveness to
because there is no platelets, no mature/maturing worms
complement system, no coagulation, no  Typically occurs from foreigners infected
granulocytes and less violent by LF from endemic areas
 LYMPHADENITIS (enlargement of lymph
CARDINAL FEATURES: nodes) or LYMPHANGITIS (inflammation
 LYMPHANGIECTASIA of lymphatic channels)
- parasite induced lymphatic dilatation,
common feature of patent infection TROPICAL PULMONARY EOSINOPHILIA
(parasitic org. can be demonstrated in the  Clinical manifestation is not present and
body) microfilaria is not seen in the blood but
- Lymph node/system dilates

PREFINAL DESO-ACIDO, G.
THE FILARIAE CLIN.PARA.
microfilaria hides in tissues specifically Wuchereria Brugia malayi
LUNG TISSUE bancrofti
 Occult form of FILIARIASIS Mean length 290 222
 May progress to CHRONIC PULMONARY (um)
FIBROSIS and RESPIRATORY FAILURE Cephalic 1:1 2:1
if untreated space:
 High titers of IgE (Ig of parasite) breadth
Sheath in Unstained Pink
DIAGNOSIS Giemsa
 URINE Nuclei Regularly Irregularly
o Milky – chyle/lymph fluid leakage spaced, spaced, and
 MICROSCOPIC FINDINGS of separately overlapping
MICROFILARIA IN THE BLOOD situated
o Traditionally accepted procedure Tail Single row of Single row of
for diagnosis nuclei that nuclei that
 BLOOD does not reach reaches the
o Microfilariae in wet/thick blood the tail’s end tail’s end
smears (8pm-4am due to Terminal none 2 nuclei, which
NOCTURNAL) nuclei bulge the
o Knott’s Concentration Method cuticle,
/Nucleopore Filter – for low conspicuously
infections placed
o Chronic Infections may not be Appearance Smoothly Kinky
demonstrable in the peripheral in blood film curved
blood cause by low intensity of Innenkorper 34 30.7
infection, dead worms or length (um)
obstructive lymphatics due to
increased no. of parasites TREATMENT
 DEC (DIETHYLCARBAMAZINE)
 DEC/ DIETHYLCARBAMAZINE
- Drug of Choice
PROVOCATIVE TEST - 6mg/kg for 12 CONSECUTIVE DAYS
o 3 mg/kg DEC SINGLE DOSE
- Discover in 1948
o Allows collection during daytime
o Stimulate the microfilaria to migrate
in the peripheral circulation and collect SUBCUTANEOUS (under the skin) FILARIAE
blood through blood smears
Loa loa
 “AFRICAN EYE WORM”
 CIRCULATING FILARIAL ANTIGENS
(CFA)
FORMS:
o PREFERRED
 ADULT WORMS:
o Antigens from microfilaria
- Typically white in color and Threadlike
o Latent infections (infections that are appearance
delayed/natutulog na parasite)
 MALE: 28-35 mm
o Mainly done using
 FEMALE: 38-72 mm
IMMUNOCHROMATOGRAPHIC CARD TEST
o ANTIGEN DETECTION STRIP (card) TESTS MICROFILARIA
– RDTs (sensitive and specific)
 248-300 um
 Sheathed
 XENOMONITORING OF MOSQUITOES  When stained, shows tail with continuous
o Growth of mosquito inside the laboratory
end of nuclei (1 nuclei)
 ANTIBODY DETECTION
LIFE CYCLE
MICROSCOPIC COMPARISON using STAINED
 Genus Chrysops fly (DAY BITING FLY)
THICK BLOOD FILMS

PREFINAL DESO-ACIDO, G.
THE FILARIAE CLIN.PARA.
 Adult worm resides in the subcutaneous - Initial bite of fly, the patient will
tissue experience itchiness or localized pain in
 Adult produced sheathed microfilaria the bitten area
 Microfilaria have diurnal periodicity - Localize subcutaneous edema
 FLY STAGES: microfilariae penetrate fly’s  Adult worm can be extracted from a
midgut through the hemocele and migrate variety of location (includes eye)
to thoracic muscles  Eosinophilia
 Microfilariae developed to L1 -> L3  Presence of circulating worms show no
 L3 migrate to head and fly’s proboscis discomfort
 Adult worms migrate to:
o Conjunctiva
DIAGNOSTIC STAGE: o Under the skin
 MICROFILARIAE IN BLOOD AND o Bridge of the nose
TISSUES
 ADULT WORMS EXTRACTED DIAGNOSIS
INFECTIVE STAGE: 3RD STAGE LARVAE  BLOOD
- MICROFILARIAE IN GIEMSA STAINED IN
BLOOD (10:15 AM – 2:15 PM)
 Extraction of adult worms on body
locations
 Serologic testing

TREATMENT
 DEC (DIETHYLCARBAMAZINE)
 SURGICAL REMOVAL/EXTRACTION

Onchocerca volvulus
 “BLINDING FILARIA”

FORMS:
 ADULT WORMS:
- Thin and wirelike appearance
 MALE: 25-50 mm
 FEMALE: up to 500 mm

MICROFILARIA
 150-355 um
 Unsheathed (found in tissue only)
HOST  When stained, nuclei do not extend to
INTERMEDIATE HOST: tip of tail
 CHRYSOPS FLY (DAY BITING FLY)
DEFINITIVE HOSTS: LIFE CYCLE
 HUMANS  Blackfly (genus Simulium)
MODE OF TRANSMISSION:  Adult filariae can live to the nodules
 FLY BITE for approximately 15 years
PERIODICITY:  Female worm will produced unsheathed
 DIURNAL (they can be found during the microfilariae, the female worm of O.
day) volvulus can produced microfilarie for
approximately 9 years
DISEASE ASSOCIATION  LIFE SPAN OF MICROFILARIAE: 2 YEARS
LOIASIS
 CALABAR/FUGITIVE SWELLINGS DIAGNOSTIC STAGE:
- Transient subcutaneous swellings  MICROFILARIAE IN BLOOD AND
TISSUES

PREFINAL DESO-ACIDO, G.
THE FILARIAE CLIN.PARA.
 ADULT WORMS EXTRACTED
INFECTIVE STAGE: 3RD STAGE LARVAE

HOSTS
INTERMEDIATE HOSTS:
 SIMULIUM (BLACKFLY)
DEFINITIVE HOSTS:
 HUMANS
MODE OF TRANSMISSION:
 FLY BITE
PERIODICITY:
 NONPERIODIC (microfilaria circulate in the
blood throughout 24 hour period)

DISEASE ASSOCIATE
ONCHOCERCIASIS
 SKIN: loss of elasticity and nodules
 RIVER BLINDNESS: lesion formation in
the eye

DIAGNOSIS
ONCHOCERCIASIS
 SKIN SNIPS
- MICROFILARIAE IN GIEMSA STAINED
TISSUE
- Tissue biopsy in the infected area –
SPECIMEN OF CHOICE
- Obtained with little blood (to avoid
contamination sample)
 Extraction of adult worms on infected
nodules
 OPHTHALMOLOGIC EXAM
- Uses SLIT LAMP
 PCR AND SEROLOGIC METHODS

TREATMENT
 IVERMECTIN
 THERAPY CAN BE LONG BECAUSE OF THE
ADULT WORM LIFESPAN (15 YEARS)

PREFINAL DESO-ACIDO, G.