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Intestinal-Tissue - Blood Nematodes-5

The document provides an overview of various intestinal, tissue, and blood nematodes affecting humans, detailing their transmission, clinical features, diagnosis, and treatment. It highlights common infections such as Ascaris lumbricoides, Trichuris trichura, Enterobius vermicularis, and others, emphasizing their global prevalence and impact on health. Preventive measures include good hygiene practices and regular deworming, while treatments often involve medications like Mebendazole and Albendazole.

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0% found this document useful (0 votes)
25 views51 pages

Intestinal-Tissue - Blood Nematodes-5

The document provides an overview of various intestinal, tissue, and blood nematodes affecting humans, detailing their transmission, clinical features, diagnosis, and treatment. It highlights common infections such as Ascaris lumbricoides, Trichuris trichura, Enterobius vermicularis, and others, emphasizing their global prevalence and impact on health. Preventive measures include good hygiene practices and regular deworming, while treatments often involve medications like Mebendazole and Albendazole.

Uploaded by

mayaaljoayd
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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You are on page 1/ 51

INTESTINAL, TISSUE AND BLOOD

NEMATODES

Dr. Cemile Bagkur


[email protected]
2

INTESTINAL NEMATODES
Ascaris lumbricoides
• The most common human helminthic infection.

• Worldwide distribution.

• ~ 732 million people harboured Ascaris worldwide in 2021.

• Highest prevalence in tropical and subtropical regions, and areas with


inadequate sanitation.
• More prevalent in children (mostly 5-9 years old).

• Soil-transmitted infection.

• Transmission depends on the dissemination of eggs in environmental


conditions suitable for their maturation.
3

Transmission
• Unfertilized eggs are not infective.

• Fertile eggs embryonate and become infective after several weeks,

depending on the environmental conditions (moist, warm).

• After infective eggs are swallowed, the larvae hatch, invade the intestinal

mucosa, and are carried via circulation to the lungs.

• The larvae mature further in the lungs, penetrate the alveolar walls,

ascend the bronchial tree to the throat, and are swallowed.


4

Transmission
• Upon reaching the
small intestine, they
develop into adult
worms.
• Adult worms live in
the lumen of the
small intestine up to
2 years
• They reach a size of
40 cm.
• A female may
produce ~ 200,000
eggs/day.
• Definitive host is
human, no
intermediate host.
5

Clinical Features
Intestinal phase of adult worms
• Usually cause no acute symptoms.

• High worm burdens may cause abdominal pain and


intestinal obstruction, constipation.
• May migrate other parts of the body cavities.

Lung phase of larval migration


• Pulmonary symptoms can occur (cough, dyspnea,
hemoptysis, eosinophilic pneumonitis) Löeffler
Syndrome.
• Wheeze and bronchospasm due to allergic reactions.

• Eosinophilia.
6

Diagnosis

• Diagnosis based on microscopy.

• Finding eggs (fertilized/unfertilized) or adults in feces.

• Concentration method can be used.

• Rarely larvae can be found in sputum.


7

Treatment & Prevention

• Pyrantel pamoate (can be used in pregnancy), Mebendazole or

Albendazole

• Sanitary practice in fecal disposal.

• Good hygienic practices with food.

• Regular hand washing.


8

Trichuris trichura

• Also known as “whipworm”.

• The non-embryonated eggs are passed with the stool.

• In the soil, eggs embryonate and become infective in 15-30 days.

• After ingestion (soil-contaminated hands or food), the eggs hatch in


the small intestine, and release larvae that mature and establish
themselves as adults in the colon.
• Can be found together with Ascaris (because of soil transmision)

• The adult worms (~ 4 cm) live in the colon.

• Female worms shed 3,000-20,000 eggs/day.


9

Trichuris trichura
10

Clinical Features

• Most frequently asymptomatic.

• Heavy infestations cause symptoms especially in small children.

• GIS problems (tenderness, abdominal pain, chronic mucoid & bloody

diarrhea).

• Weight loss, weakness, growth retardation.

• Anemia and iron deficiency from blood loss.

• Rectal prolapse
11

Diagnosis & Treatment & Prevention

• Diagnosis based on microscopy.

• Concentration method.

• Finding eggs (lemon shaped) or adults (whipworms) in feces.


12

Enterobius vermicularis
• Following ingestion of infective eggs, the

larvae hatch in the small intestine.

• Adults establish themselves in the colon.

• The life span of the adults is ~2 months.

• Gravid females migrate nocturnally outside

the anus and oviposit on the skin of the


perianal area.

• The larvae develops inside of the eggs in 4-6

hours and may remain viable for 20 days.

• Small white worms, ~1 cm.


13

Epidemiology
• Infective eggs usually carried on fingernails, clothing, bedding or house-dust.

• Autoinfection*, or the migration of newly hatched larvae from the anal skin back
into the rectum (retroinfection).
• Person-to-person transmission can also occur through handling of contaminated
clothes or bed linens.
• Some small number of eggs may become airborne and inhaled. These would be
swallowed and follow the same development as ingested eggs.
• Humans are the only hosts.

• Worldwide distribution, with infections more frequent in school- or preschool-


children and in crowded conditions
• Enterobiasis appears to be more common in temperate than tropical countries.
14

Clinical Features

• Most frequently asymptomatic.

• Heavy infestations cause symptoms especially in small children.

• Perianal itching with loss of sleep.

• Apendicitis like pain.

• Peritonitis
15

Diagnosis, Treatment and Prevention


• Eggs are asymmetric “D” like shaped.

• Diagnosis based on microscopy but by “Scotch test”, cellulose-

tape slide test on the perianal skin.

• Eggs less frequently can be found in the stool.

• Adult worms are also diagnostic, when found in the perianal

area.

• Pyrantel pamoate, Mebendazole, Albendazole

• All family members should be treated together with two weeks

intervals

• Finger nail cutting

• Hand hygiene
16

Hook Worms
• Two types: Necator americanus and Ancylostoma duedonale

• Eggs are passed in feces and develop rapidly, depending environmental conditions.

• Rhabditiform larvae are released and develop into the infective filariform stage in
about 7 days.
• On contact with an appropriate host, the filariform larvae penetrate the skin, gain access
to the host’s circulation, travel to the lungs, and move up the tracheobronchial tree to be
swallowed.
• Human is the definitive host, no intermediate host.

• Infection occurs with skin penetration / ingestion of contaminated food

• Adults (~12 mm) live in small intestine.

• Both sexes attach to the mucosa of the small intestine.

• They may reside for up to 18 years.


17

Transmission and Epidemiology


• An estimated 576-740 million people in the world are infected with

hookworm. Especially in rural poverty / urban slums.

• Women and children are at risk.

• Significant cause of iron-deficiency anemia & protein malnutrition.

 A.duodenale  N. americanus
◦ Dryer& colder areas ◦ Moist tropical regions
◦ Teeths in mouth ◦ Sharp plates in mouth
◦ 10-18 mm ◦ 10-14 mm
◦ 25-30,000 eggs/day ◦ 9,000 eggs/day
◦ 1 year life span ◦ 3-5 year life span
18

Clinical Features
Penetration stage   Itching & dermatitis at the entry site
(ground itching) inflammation, redness,
and blister formation.

Migration through lungs   Pneumonia & bronchitis. Dry cough,


wheezing 1-2 weeks later in primary
infection, intra-alveolar haemorhagie
(Löffler syndrome like Ascaris).

Attachment to intestine   Haemorrhage, sometimes diarrhea


with abdominal pain, anemia, blood
loss (as a result of sucking blood).
19

Clinical Features

• Inappearent infection  Blood loss = food intake

• Appearent infection  Blood loss > malnutrition

Chronic infection
• GIS discomfort (abdominal pain, nausea, vomiting, diarhaea)

• Progressive iron-deficiency anemia (40 – 160 worms associated with


Hemoglobin < 11 g/dL).
• Failure to grow, extreme fatigue.

• IQ loss and malnutrition.


20

Diagnosis
• Diagnosis based on microscopy.

• Finding thin-shelled eggs in feces but eggs are indistinguishable!

• Embryonated eggs or free rhabditiform larvae may be found in

unpreserved specimens that are not examined promptly.


21

Treatment and Prevention

• Pyrantel pamoate, Mebendazole, Albendazole

• Treatment of anemia!!

• Sanitary practice in fecal disposal.

• Good hygienic practices with food.

• Regular hand washing.

• Wearing boats and gloves while dealing with soil.

• Mass deworming programmes!


22

TISSUE NEMATODES
Strongyloides stercoralis
23

Transmission and Epidemiology


• Very complicated life cycle, there are some free living forms in the soil.

• Rhabditiform larvae are passed out in feces.

• They become infective filariform larvae.

• This transformation takes place either sexually with male and female in the soil or
asexually in the intestine (autoinfection).
• They reach to small intestine via bloodstream.

• Only adult females live embedded in the small intestinal mucosa and reproduces in
a “Parthenogenetic manner”.
• Called as threadworm

• Soil-transmitted diseases.

• Worldwide prevalence: ~100 million


24

Clinical Features
• Skin penetration may cause local irritations: rash, pruritus

• Larva currens is seen on the trunk and buttocks.

• Migrating larvae can cause mild respiratory symptoms in a few week

with asymptomatic eosinophilia (Löffler pneumonitis).

• Sometimes ectopic larvae can be found in the brain or other viscera.


25

Clinical Features
• Established infection may have no sign.

• In severe infection manifestations include intestinal symptoms: epigastric

pain, abdominal distension, vomiting, diarrhea with voliminous stools and


malabsorbtion with dehyration and electolite disturbance, anemia.

• Hyper-infection results from massive autoinfection in the presence of

immunsupression.

• Hemorrhagic diarrhea, intestinal perforation

• hemorrhagic pneumonia, gram-negative meningitis, shock, sepsis with high

mortality.
26

Diagnosis and Treatment

• Rhabditiform larvae in feces,

• Duodenale aspiration,

• Sputum

• Mebendazole or Thiabendazole
27

Trichinella spiralis

• Zoonotic infection

• Usually human infection is from the domestic pigs.

• Larvae penetrate the intestinal wall and are carried into the muscle
cells where they coil up.
• Become infective within 3 weeks.

• If the larvae are ingested by a new host in undercooked meat, they are
released and develop into adults around a day.
• Adults live in the intestine, larvae in the muscle!

• Infected pork ingestion is the main source.


28

Trichinella spiralis
29

Clinical Features
• Intestinal inflammation leading to diarrhea.

• Migration of larvae provoke inflamatory response leading to periorbital

oedema, haemorrhages under nails, muscle pains and myocarditis.

• Especially muscles of respiration and tongue are involved.

• Eosinophilia is high.

• In long term eventual fibrosis and degeneration, resulting in calcification.


30

Diagnosis and Treatment

• Clinical features

• Serology

• Muscle biopsy

• Mebendazole or Thiabendazole

• Steroid
31

Dracunculus medinensis
32

Transmission and Epidemiology

• Humans become infected by drinking unfiltered water containing

copepods (small crustaceans) which are infected with larvae of D.


medinensis.

• Releasing larvae penetrate the host stomach or intestinal wall and

enter the abdominal cavity.

• After copulation, the male worms die and the females (length: 70 to

120 cm) migrate in the subcutaneous tissues towards the skin surface.

• ~1 year after infection, the female worm induces a blister on the skin,

generally on the distal lower extremity.


33

Clinical Features, Diagnosis and Treatment


• The clinical manifestations are localized.

• The worm emerges as a whitish filament (duration of emergence: 1 to 3 weeks) in

the center of a painful ulcer, accompanied by inflammation and frequently by


secondary bacterial infection.

• Local cleansing of the lesion.

• Local application of antibiotics, if indicated because of bacterial superinfection.

• Mechanical, progressive extraction of the worm over a period of several days.

• No specific drug is used to treat dracunculiasis.


34

Toxocara spp.
35

Transmission and Epidemiology


• Cat/dog ascarids (Toxocara cati & Toxocara canis).

• Humans acquire the infection as accidental hosts.

• After ingestion, the eggs hatch and larvae penetrate the intestinal wall and are
carried by the circulation to a wide variety of tissues (liver, heart, lungs, brain,
muscle, eyes).
• While the larvae do not undergo any further development in these sites, they
can cause severe local reactions.
• Cosmopolitan especially where large populations of dogs are present including
urban as well as rural area
• Most prevalent in children.

• Puppies are the major source of infection!


36

Clinical Features

• Pathology and symptoms depends on number of migration larvae and

location.

• Many human infections are asymptomatic, with only eosinophilia and

positive serology.

• The two main clinical presentations

• Visceral larva migrans (VLM)

• Ocular larva migrans (OLM)


37

Clinical Features
VLM
• Mostly in preschool children.

• Larvae invade multiple tissues (liver, heart, lungs, brain, muscle) and cause
granulomata.
• As well as fever, anorexia, weight loss, cough, wheezing, rashes,
hepatosplenomegaly and eosinophilia.

OLM
• Often occurs in older children or young adults.

• Only rare eosinophilia or visceral manifestations.


38

Clinical Features
Cutaneous Larva Migrans
• Definitive host is not human.

• Ancylostoma braziliense & Ancylostoma


caninum
• Filariform larvae penetrates into skin, but does
not migrate to intestines. May cause dermatitis,
wound becomes infected.
• Also called as “creeping eruption”.

• Cause significant inflammation and painful


swelling.
39

Diagnosis and Treatment

• Since the larvae do not develop into adults, stool examination would

not detect any Toxocara eggs.

• Antibody detection tests are the only means of confirmation of a

clinical diagnosis.

• For all type larva migrans;

• Mebendazole or thiabendazole

• Steroid
40

Blood Nematodes
41

Transmission and Epidemiology

• Filariasis (threadworms) is caused by blood nematodes.

• Arthropod-borne diseases (by mosquito).

• Eight main species infect humans.

• Three of these are responsible for most of the morbidity due to

filariasis:

• Wuchereria bancrofti and Brugia malayi cause lymphatic filariasis,

• Onchocerca volvulus causes onchocerciasis (river blindness).


42

Transmission and Epidemiology


• Infective larvae are transmitted by mosquitoes (Culex and Anopheles).

• The larvae migrate to the lymph nodes of the host's body, where they develop into adults.

• The female worms produce microfilariae which circulate in the blood (larviparous).

• The microfilariae infect biting insects (mosquitoes).

• Inside the insect (thoracic muscles), the microfilariae develop in 1 to 2 weeks into infective

larvae.

• During a subsequent blood meal by the insect, the larvae actively infect the vertebrate host.

• Inhabit a variety of tissues, including subcutaneous tissues, lymphatics, blood vessels, peritoneal

and pleural cavities, heart, and brain.

• All species produce larvae (microfilariae), which may be recovered from blood or skin,

depending on the species.

• The microfilariae of some species circulate in the blood with a well-defined periodicity (diurnal

or nocturnal), whereas others do not.


43

Clinical Features
• Lymphatic filariasis most often consists of asymptomatic microfilaremia.

• Some patients develop lymphatic dysfunction causing elephantiasis


(frequently in the lower extremities and scrotum in men and breasts and
vulva in women).
• 120 million people infected in >80
countries in Africa, Asia, the Pacific
islands and South and Central
America.
• 40 million of those infected are
disfigured.
• 95% cases due to Wuchereria
bancrofti, other species include
Brugia malayi and B.timori.
44

Clinical Features
Wuchereria bancrofti
• Responsible for bancroftian filariasis.

• Most common filarial species that infect humans.

• Microfilariae circulate in peripheral blood with a nocturnal periodicity


that corresponds with feeding activities of the usual vectors—Culex,
Aedes and Anopheles mosquitoes.
• Adult worms reside in the lymphatic system, where chronic infection and
reinfection result in lymphadenopathy and lymphangitis, which may
progress to lymphedema and obstructive fibrosis.
• Severe involvement of the lower extremities and genitalia may result in
elephantiasis.
45

Clinical Features
Wuchereria bancrofti
46

Clinical Features
Brugia malayi

• Produces disease similar to that of W. bancrofti.

• Often milder and more frequently involves the lymphatics of the

upper extremities.
47

Clinical Features
Onchocerca volvulus
• Leading cause of blindness in endemic areas, central Africa, Central &
South America.
• Vectors are black flies of the genus Simulium.

• Adult worms live in hard, fibrous nodules in subcutaneous and deeper


tissues.
• Complications arise from the migratory activities of microfilariae.

• Movement of microfilariae through the surface of the eye may result in


keratitis, corneal opacity and damage to the anterior and posterior
chambers and iris, thus leading to blindness with repeated infection over
time.
48

Diagnosis
• Clinical features and history

• Made by the finding of microfilariae in the blood or skin, because adult stages are

often sequestered in the tissues.

• Use of Giemsa or hematoxylin-stained thick smears of peripheral blood is routine.

• Microfilariae may be seen moving in direct mounts of blood or tissue fluid.

• Concentration procedures may be necessary for recovery because microfilariae

may be present in small number.

Wuchereria bancrofti diagnosis


by microfilaremia in night blood
(a case of nocturnal periodicity)
49

Diagnosis
50

Treatment

• Diethylcarbamazine

• Ivermectin (for microfilariae)


51

Thanks for listening…

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