NEMATODES

NEMATODES – GENERAL CHARACTERS

• Non-segmented cylindrical worms tapering at both ends

• Possess cuticle

• Sexes are separate (dieoecious), male is smaller than female & its posterior end is curved ventrally

- Parthenogenic (independent)……strongyloides stercoralis

- Male- smaller, curved posterior end, has spicule

- Female- larger, tapering posterior end, no spicule.

• Females are either

• Viviparous (produce larvae/ embryos)

• Oviparous (lay eggs) or

• Ovo-viviparous (lay eggs which hatch immediately)

• Live in intestinal tract or tissues

CLASSIFICATION – INTESTINAL NEMATODES

Small Intestine only

• Ascaris lumbricoides (round worm)

• Necator americanus (american hook worm)

• Ancylostoma duodenale (hook worm)

• Strongyloides stercoralisTrichinella spiralis (trichina worm)

• Capillaria philippinensis

Caecum and Vermiform appendix

• Enterobius vermicularis (pin worm)

• Trichuris trichiura (whip worm)

CLASSIFICATION – TISSUE NEMATODES

Lymphatic

• Wuchereria bancrofti

• Brugia malayi

• Brugia timori

Subcutaneous

• Loa loa (african eye worm)

• Onchocerca volvulus (blinding filaria)

• Dracunculus medinensis (thread worm)

Conjunctiva

• Loa loa

MODES OF INFECTION OF NEMATODES

1. Ingestion of -

• Embryonated eggs contaminating food & drinks,

e.g. A.lumbricoides, E. vermicularis & T. trichiura

• Growing embryos in an intermediate host (infected cyclops)

e.g. D.medinensis

• Encysted embryos in infected pig’s flesh

e.g. Trichinella spiralis

2. Penetration of skin - filariform larvae bores through the skin

e.g. A.duodenale, S.stercoralis, N.americanus

3. By blood sucking insects

e.g. filarial worms

4. Inhalation of infected dust containing embryonated eggs

5. e.g. A.lumbricoides, E.vermicularis

INTESTINAL NEMATODES

ASCARIS LUMBRICOIDES (ROUNDWORM) Common name: Giant intestinal roundworm

- Ascaris lumbricoides most common helminth infection in the Philippines.

- Ascariasis is very common to kids/children.

3layers of ascaris

Glycogen

Lecithin layer

Mammiliation

Adult worms

• Male 15 to 30 cms

• Female 20 to 40 cms, oviparous

Eggs

• 60 µ, bile stained

• Albuminous coat with unsegmented ovum

Infective form

• Embryonated eggs

• Mature female worm produces two lakh eggs per day, which passes with the feces.

Mode of transmission

• Ingestion

Site of localization

• Small intestine

PATHOGENICITY & CLINICAL FEATURES

• Ascariasis – infection of A.lumbricoides

• Majority of infections are asymptomatic

• Clinical disease is largely restricted to individuals with a high worm load

• Symptoms divided into two groups: those produced by

• Migrating larvae

• Adult worms

SYMPTOMS & COMPLICATIONS

• Symptoms produced by Migrating larvae

1. Pneumonia (loeffler’s syndrome)

• fever, cough, dyspnoea, blood tinged sputum that may contain larva, urticarial rash & eosinophilia

2. Visceral larva migrans

• if larvae enter systemic circulation (from pulmonary capillaries) to reach other organs like brain, spinal cord, heart, kidney.

• Symptoms produced by Adult worms

1. Abdominal discomfort, anorexia, nausea & diarrhoea.

2. PEM, Vit. A deficiency (night blindness)

3. Intestinal obstruction (particularly in children 1-5 years), intussusception & volvulus

4. Penetration through intestinal ulcer (perforation) – peritonitis

5. Hypersensitivity reactions to worm Ags (toxic body fluids) – urticaria, edema of face, conjunctivitis, irritation of URT

6. Ectopic Ascariasis – due to migration of worm up into the stomach. It maybe:

• vomited out,

• pass up through the oesophagus at night & comes out through mouth or nose,

• enter larynx to cause asphyxia.

• migrate to other organs and cause appendicitis, cholecystitis, biliary colic, cholangitis, pancreatitis

LABORATORY DIAGNOSIS

• Macroscopic - Direct detection of worm/s in stool or vomit

• Microscopic – direct examination of feces following floatation method: bile stained eggs. (eggs may not be seen at least 40 days after infection)

• Blood examination – eosinophilia.

Other modes of diagnosis

• Imaging – large collections of worms in abdomen

• USG - to diagnose hepatobiliary or pancreatic ascariasis

• Serology (Ab detection) – mainly reserved for epidemiological studies.

TREATMENT

• Mebendazole/ Albendazole – drug of choice but contraindicated in pregnancy & heavy infection

• Pyrantel pamoate – single dose

• Piperazine citrate - suspected intestinal or biliary obstruction since this drug paralyzes worms to aid expulsion.

• Levamisole

PREVENTION

• Good sanitation and personal hygiene

• Mass treatments with single dose mebendazole or albendazole for all school-age children every three to four months - serves dual function:

• treats the children and

• reduces the overall worm burden in the community

Appearance of the eggs hookworm mudolable (d ko maintindihan maigi kung mudolable)

ANCYLOSTOMA DUODENALE (HOOK WORM) Common name is old world hookworm

- Second most common helminthic infection among humans is caused by hookworms

Two types of Hookworms:

1. Ancylostoma duodenale

2. Necator americanus (Common name: American murderer)

Additional hookworms associated with animals:

1. Ancylostoma braziliense

2. Ancylostoma caninum

* A. lumbricoides - human infection

* Toxocara canis - dog infection (Common name: Dog ascarid)

* Toxocara cati - cat infection (Common name: Cat ascarid)

* A. lum host is humans

* Final / Definitive host is dog to canis and cat to cati

* Intermediate host of toxocara canis and cati - humans.

* Their mode of Transmission is ingestion

- Habitat of Toxocara canis and cati is through tissues and organs. Their laboratory diagnosis is through tissue biopsy.

- They can also exhibit visceral larva migrants. They can travel through different organs.

* A. duodenale (Common name: Old World Hookworm)

* N. americanus (Common name: New World Hookworm)

* Ancylostoma caninum - Dog infection

* Ancylostoma braziliense - Cat infection

They can be differentiated through their appearance or morphology.

Adult stage is where we can identify / differentiate parasite hookworm infection. (Buccal cavity).

Egg - larvae - adult > Life stages of Nematodes

* Habitat for hookworm -> Small intestine

* Mnemonic for small intestine -> CASHT

* Hookworm's final stage is man

* Hookworms infective stage is 3rd stage filariform larva

Characteristic for hookworm's egg:

* Oval, thin- shelled , colorless

* Germ cell in fragmentation (2-8 Blastomeres)

* "Morula Ball' formation

SITES OF SKIN PENETRATION

• Most common sites are:

1. Thin skin between toes

2. Dorsum of the feet

3. Inner side of the soles

• Gardeners & miners – skin of hands

Note: Ancylostoma duodenale can do vertical transmission that can cause Congenital infection. (e.g: Mother to baby). However, Necator americanus can't do it.

Further Difference between Ancylostoma duodenale and Necator americanus in terms of Eosinophilia

Ancylostoma duodenale - eosinophilia count will peak after 1 month of infection.

Necator americanus - eosinophilia count will peak after 2 months.

*Eosinophil count increases because eosinophils are responsible for parasitic infection.

PATHOGENICITY & CLINICAL FEATURES

• Ancylostomiasis or hookworm disease, characterised by iron deficiency anaemia

• Majority of infections are asymptomatic

• Symptoms develop in heavy infections and divided into two groups: those produced by

• Migrating larvae

• Adult worms

SYMPTOMS PRODUCED BY LARVAE

• Lesions in the skin:

1. Ancylostome dermatitis or Ground itch – occurs at the site of entry (more common in necator), lasts for 2 to 4 weeks

2. Creeping eruption – reddish itchy papule along the path traversed by filariform larvae (larva migrans)

• Lesions in the lungs – bronchitis & bronchopneumonia.

SYMPTOMS PRODUCED BY ADULT WORM

• Epigastric pain, diarrhoea & vomiting during early phase of infection.

• Microcytic hypochromic (Iron deficiency) anaemia – due to chronic blood loss:

• a single adult hookworm sucks 0.2ml of blood/ day

• Hemorrhages from punctured sites

CLINICAL FEATURES OF HOOKWORM ANEMIA

• Extreme pallor

• Abnormal appetite showing Pica or Geophagy – perverted taste for earth, mud or lime

• Epigastric tenderness with dyspepsia

• Constipation

• Puffy face with swelling of lower eyelids

• Pedal edema

• Growth retardation

• General appearance – pale plumpy with protuberant abdomen & dry lustreless hair.

LABORATORY DIAGNOSIS

• Stool examination – microscopy: non bile stained egg, segmented

• Occult blood in stool – positive

• Blood examination – anaemia, eosinophilia

TREATMENT

• Mebendazole / Albendazole

• Pyrantel pamoate

• Oral iron replacement – ferrous sulphate 400mg tid

• Nutritional support

• * If Hb is below 30%, then anemia should be treated first with Iron till Hb comes over 50%

PREVENTION & CONTROL

• Proper sanitation measures & sewage disposal

Personal hygiene

• Personal protection – wearing boots & gloves

• Simultaneous treatment of carriers & diseased with wholesale treatment of community

STRONGYLOIDES STERCORALIS Common name is thread worm

The smallest nematode infecting man

When we say autoinfection, Strongyloides stercoralis agad

Strongyloides stercoralis (thread worm)

Hookworm

L1 Rhabditiform larva

• buccal cavity- shorter

• genital primordium- prominent, conspicuous L1 Rhabditiform Larva

• 1st larval Stage

• Open Mouth: Feeding stage

• Long buccal cavity

• Short/small genital primordium (mode of reproduction)

L3 filariform larva

• Unsheathed

• Tail- noched L3 filariform larva

• Closed mouth : Non-feeding stage

• Sheated, pointed tail

Final host – man

Infective stage – filariform larva

Diagnostic stage- Rhabditiform larva, egg

PATHOGENICITY

1. Skin lesions (2 types) – “larva currens”

• At the site of entry – urticarial rash

• In the perianal region – linear, erythematous urticarial wheal

2. Pulmonary lesions – due to migrating larva

• Alveolar hemorrhages

• Bronchopneumonia

- When many adult worm in intestine in cause diarrhea (Cochin China diarrhea and the Vietnam diarrhea)

3. Intestinal lesions - “burrowing lesions”

• Epigastric pain

• Diarrhoea with blood & mucus

• Nausea

• Weight loss

IMPORTANT TERMS TO KNOW

• Autoinfection – filariform larva

1. In the Intestinal lumen

2. Perineal & perianal skin penetration

• Hyperinfection – can result in autoinfection

1. Steroids or Immunosuppressive Therapy

2. Malignancy

3. Malnutrition

4. Pregnancy

5. Puerperium

6. AIDS

• Persistence of infection – due to autoinfection

LABORATORY DIAGNOSIS

• Stool examination –.

- rhabditiform larva

- rarely found egg of strongy. And it usually diagnos as hookworm eggs because they are indistinguishable, the strongy, egg are almost same as the hookworm eggs. But strongy. Is smaller in size, develop larvae inside the eggs it appears as Chinese lantern appearance

• Culture –

- larva

- baermann funnel culture

- harada-mori test tube culture method

this 2 can use to hookworm and strongy.

• ELISA – to detect Abs

TREATMENT & PREVENTION

• Potentially life threatening disease – treat even if its asymptomatic

• Thiabendazole for 2 days

- Disseminated strongyloidosis – 5 to 7 days.

• Strongyloides fuelleborni – causative agent for swollen belly syndrome

- Primarily it infects primate but there is an infection of human if _____ interaction

Treatment

- Albendazole, mebendazole, Thiabendazole, and ivermectin

TRICHINELLA SPIRALIS ( common name: TRICHINA WORM or muscle worm

A great imitator

Final host – pigs and other mammals that are carnivores or omnivore in nature, so why men infected if the final host are pigs, it is because we man are considered as accidental host or the dead end host.

Diagnostic stage – encysted larvae (we use muscle biopsy instead of stool)

Infective stage - encysted larvae

In the life cycle trichinella spiralis encyst in striated muscle.

PATHOGENICITY

• Trichinelliasis / Trichinosis – clinical features depends on the stage:

1. Stage of intestinal invasion: 5-7 days, pain in abdomen, nausea, vomiting, diarrhea

2. Stage of larval migration: fever, urticarial rash, splinter hemorrhages, periorbital & facial edema

3. Stage of encystation: asymptomatic in light infections; if heavy na sa myalgia na, weakness in heavy infections

• Complications – during migration:

- myocarditis, encephalitis

Symptoms and patholgy

- increased of eosinophil count

LABORATORY DIAGNOSIS

• Muscle biopsy – encysted larva

• Blood – eosinophilia between 2nd & 4th week

• Serology – to detect specific Abs by:

- Bentonite flocculation test ( aside from trichinella spiralis it can also perform in Echinococcus granulosus )

- Latex agglutination test

- Bachmann intradermal test

- Beck's Xenodiagnosis ( use in test animals, we use albino mice or rats)

TREATMENT

• Thiabendazole & Mebendazole – adult worms

• Or removal of mucle with encysted larva

• Prednisone

• Corticosteroids – complications

PREVENTION

• Proper cooking of pork or proper storage ( why, because one of the ways in order to destroy encysted trichinella spiralis larva on mucles on pork is to freezing, because if we freeze the meat it will destroy the larva of TS. Freezing below 0, -15 degrees celcius for 20 days or -30°C for 6 days . It is grratly decrease the viability of organism.

• Avoidance of feeding bits & refuse from slaughter houses & farms to pigs – breaks life cycle.

Enterobius vermicularis(Pin Worm, Seatworm)

Oldest known of enterobius vermicularis is oxyuris vermiculairs

IS - embryonated egg

DS- embryonated egg

MOT- additional, inhalation and sexual transmission

FH- man

Life cycle- adult male and female are in the large intestine, once they meeted, the adult female( gravid female)- eggs ay meron na ready for hatching) it will migrate to perianal region in anus, at night to lay eggs. And EV considerex as noctural. We can say or lay egg during 2-4 am. Kapagmakati pwet mo midnight it is possible that you have E.V

After lay eggs. DS- the eggs in perianal folds, the larva within the egg it will mature with in 4 to 6 hours very fast. And what will happen? It will become an embryonated egg and will be ingested by man.

CLINICAL FEATURES

• Due to migration of worm - Perianal, perineal & vaginal itching (pruritis- redness of perianal region) worsens at night.

• Insomnia and restlessness

• Nocturnal enuresis

• Adult E. V. - it is small, whitesh or brown in color, and has anterioir end with lateral wanes or cephalic alae. Distinct feature of adult worm in anterioir part we can see the cephalic alae or lateral wanes, in posterior part of adult worm we can see the esophageal bulb, it is a flask shape or bulbous

adult male- the male worm will immmediately die after population. DIE FOR SEX

Adult female- after populating it will go to perianal region and deposit egg (oviposit) and it will die right. DIE FOR CHILDREN

LABORATORY DIAGNOSIS & TREATMENT

• Detection of adult worms in

- Feces

- Perianal region

Eggs are Rarely survive when it come to detecting it in stool that why we are using NIH swab. And cellaphane tape method . Egg is elongated, it has a flattened on one side, that why it is tshaped. embryonated, it can be seen as double layer egg 1 is albuminous and the other is lipoidal layer. It has no glycogen layer.

The reason why it is not advisable to use stool examination here in EV. It is because of the survival rate of eggs in stool it is less than 5%. So we use NIH swab or cellolous tape or scatch tape swab.

• NIH swab – scrapings from perianal region

• Microscopy – non bile stained eggs

• Mebendazole, pyrantel pamoate

• It is considered as the most common helminth to infect man worldwide. But if philippines si ascaris lumbricoides.

Trichuris trichiura (Whip Worm)

Infective form/ stage - Mature embryonated eggs

Diagnostic stage – ova found in stool

Mode of transmission – Ingestion

- Fecal oral transmission

Final Host – man

Egg like a football shape

Resembles as a Japanese lantern

Key feature is bipolar mucus plug, other term prominent hyiodine polar plugs.

Life cycle

Their on the colon which will lay eggs (found on the feces) after the undeveloped eggs na sumama sa feces it will developed into embryonated. It will embryonated on the moist soil and will be ingested by man. Once ingested by man it will hatch and will penetrate and developed on the filai and finally return in the lumen and migrate to the colon to mature as adult worm

Adult worm – fresh colored / pinkish or gray slender and attenuated posterior

Anterior attenuated (resembles Whipworm)

CLINICAL FEATURES

• Infection – Trichuriasis, Trichocephaliasis, whipworm infection

• Symptoms depend on worm burden

- Less than 10 worms – asymptomatic

- Heavier infections –

1. chronic profuse mucus and bloody diarrhea with abdominal pains and edematous rectum

2. malnutrition, weight loss and anemia

LABORATORY DIAGNOSIS & TREATMENT

• Stool examination – bile stained eggs with bipolar mucus plugs

• Treatment – albendazole / mebendazole

• Prevention

- Proper disposal of night soil

- Prevention of consumption of uncooked vegetables & fruits .

Capilaria philipinensis ( Pudoc worm found in Ilocos Sur

Discovered by Nelia Salasar

Adult worm - adult males worm – Chitinized spicul

- female has egg on utero

-

Eggs – describe as having bipolar mucus plug

- It is striated and smaller compared to trichuris trichiura

- Describes as guitar shape or peanut shape

- Typical egg and Atypical egg

Typical Egg Atypical Egg

- Immature eggs

- Unembryonated

- Will go to fresh water where embryonation process occur

- Eaten by fishes - Segmented

- Embryonated

- Hatch inside the small intestine

- Responsible for autoinfection

Natural host - Migratory birds

Intermediate host – Fresh water fishes / Brackies water fish (Ipon(Hypseloths bipartite) ,Birot,Bagsang,Bagtu

Final host-man

Infective form (Larval stage) found in the infective fishes

Diagnostic stage- larva or ova found in stool

Mode of transmission – Ingestion of undercooked or raw fishes or seafoods

Site of localization – Large intestine – caecum

Disease – mystery disease or pudok disease

SYMPTOMS AND PATHOLOGY

- Malabsorption cause of Steatorrhea (fattystool )

- Borborygami : peculiar abdominal gurgling sound

- LBM alternating with constipation

LABORATORY DIAGNOSIS

- Stool examination: egg /larva found in stool

TREATMENT

Albendazole and mebendazole