Trichuriasis

Definition
 The disease caused by the infestation of the cecum by
whipworms.
• Most infections with the whipworm are asymptomatic

• Heavy infections may cause gastrointestinal symptoms

Epidemiology
 Occurs world wide

 Infecting 1 billion people throughout the world

1
 More frequent in areas with

• warm moist tropical weather

• poor sanitation practice.

 Co-infection occurs commonly with A.lumbricoides

 In Ethiopia the mean prevalence reach up 49%
Infectious agent-
Trichuris trichiura (Common name whipworm)

2
 Adult morphology
Color- white
Shape
Anterior - long & slender thread like help to

attach colonic mucosa.

Posterior - Thicker & curved ventrally in male but

straight in female.

3
Size – male - 30-45 mm( coiled tail)
Female - 35-50mm( straight tail )
– Each female produces up to 20,000 eggs per day
• The life expectancy of a worm estimated at 1 to 3
years

4
Egg
Color - Yellow brown
Size -50-54 mm x 25mm
Shape – Barrel shape
- Boat shaped
Embryo - central granular
mass (un-segmented
ovum )

Special feature:-colorless
protruding mucoid plug at
each end
5
Mode of Transmission
– By ingesting worm eggs in food or water contaminated
with human feces

6
Host Defenses
 Little information is available on resistance &
immune responses to T trichiura infection
 Epidemiological data combined with serology
indicate
• An increase in immunity with age

• IgE antibodies are mediators of this

7
PATHOGENESIS

Colonic features
 In heavy infections, adult worms found

• In the distal colon and rectum

• In the terminal ileum

 Mucosal local hypersensitivity reaction occurs to T.

trichiura

 In the inflamed areas, especially the rectum, the

8
 Heavy infections can cause rectal prolapse

• Shear force of the fecal stream on the bodies of

worms
• Straining at defecation or during childbirth

9
 Systemic features
 Systemic consequences are anemia & impaired
growth.
Anemia
• Adult worms do not feed directly on blood or other
host tissues.
• Mechanism of anemia still unknown
• Small amounts of blood (0.005 ml per worm) are lost
each day by seepage at the attachment site
• Direct loss from the gut of RBC followed by iron
10
Impaired growth
 The mechanism for the impaired growth is not clear

 The finding of protein losing enteropathy

proportional to the worm burden
 Increased circulating TNF-α, which may inhibit
appetite as well as having direct effects on cell
division

11
Clinical Features
Light infections :- Asymptomatic
Moderate worm loads
Damage to the intestinal mucosa may induce

• Nausea & Abdominal pain

• Trichruis dysentery syndrome

• Physical Weakness, Anemia

• Stunted Growth, Cognitive Deficits

• Trichuris colitis
• Rectal prolapse 12
Laboratory diagnosis
A. Microscopic Method – stool examination
Specimen:- stool
Microscopic using:
• Wet mount
• Concentration in light infection
• Kato - katz to estimate intensity of parasite
• Stool for the ova of Trichuris trichuria

13
 Treatment
 Choice of drug for mass campaigns & clinical
treatment
• Mebendazole & Albendazole
Prevention & control
 Preventing soil becoming faecally polluted

 Providing and using adequate latrines

 Avoiding the use of untreated human faces as fertilize

 Treating individuals as part of control program

14
 Enterobiasis
Definition
 Enterobiasis is an intestinal nematode infection
caused by Enterobius vermicularis
 Most pinworm infections are asymptomatic.

 Perianal pruritus is the cardinal symptom.

15
Epidemiology
 Infect at least 200 million people, particularly children,
worldwide
 Well-recognized cofactors for increased risk of
Enterobius infection
• Overcrowding & poor sanitation
• lack of water for bathing & washing of hands & clothes
 Eggs are resistant to desiccation & may remain viable
for several days.
• Linens & Bedclothes
• house dust
16
Infectious agent - E. vermicularis (Oxyuris
vermicularis)
(Common name- pinworm)
• Phylum of nematode
• Member of the Oxyuridae class of nematodes.
• Genus Enterobius
Morphology
Adults
• Colour - yellow white
• Size – male- 2-5 mm coiled tailed
- Female 8-13mm, thin pointed Tail
17
Eggs
Size- 55x30μm

Colour- colourless (transparent)

& has a clear shell

Shape- oval & flattened on one

side (Plano convex)

Shell- smooth & thin, but a

double line is visible 18
Mode of Transmission
• Faecal- oral
• Autoinfection
• Retroinfection
• Airborne transmission
• Fomites and sexual transmission
 cofactors for increased risk of Enterobius infection
include
• overcrowding
• poor sanitation
• lack of water for bathing , washing of hands &clothes
19
Life Cycle

 The parasites mature in the large intestine.

 When gravid, female worms migrate out of anus at night

• When the anal sphincter is relaxed

• Lay as many as 10,000 eggs that adhere to the perianal skin.

 The eggs embryonate & become infective within a few hours

20
21
IMMUNITY
 Little is known about immune responses to pinworm
infection.
 Infections are more common in children than in
adults
• Suggesting that acquired immunity

• Some other type of age-related resistance

develops
22
PATHOGENESIS
 The adult worms produce no significant intestinal
pathology
 Pinworms can make extraintestinal locations &
cause complications.
• Parasites may carry bacteria into other organs

• Resulting in abscess formation.

23
CLINICAL MANIFESTATIONS
 Most pinworm infections are asymptomatic.
 The most frequent symptom is pruritus ani (anal
itching).

Adult Enterobius vermicularis worms in the perianal region.

24
 In severe infections, the intense itching may lead to
• Scratching & secondary bacterial infection.

 Recurrent UTI have been attributed to ectopic

pinworm infections
• Worms might carry enteric bacteria into the urinary
bladder
• Inducing an acute bacterial infection of the urinary
tract
25
 Gravid female worms migrate up
• the vagina

• fallopian tubes

• peritoneal cavity

i.e. encapsulated with granulomatous tissue.

26
Diagnosis
 The diagnosis is suggested by the clinical
manifestations
A. Macroscopic method
• The small, whitish adult worms can be found in the
stools or near the anus of diapered children

27
B. Microscopic method
Specimen: - anal mucosa, perianal skin, Rectal Swabbing
Method: -cellophane tape procedure (Scotch tape
technique)

Result: Recovery of the characteristic eggs 28

29
Treatment
 Choice of drug for Enterobius infection
• Mebendazole

• Albendazole

• Ivermectin
 All individuals sharing a household should be given
empiric treatment (Treat the whole family)

30
Prevention
 Hand hygiene

Trimming of fingernails

Washing of bedclothes and underwear

Treating the cases & education

31
 Hookworm Infections
Introduction
 The first description was made by Dubini in 1843.

 Looss in 1898 described

• Percutaneous transmission of hookworm

• Elucidated the entire life-cycle of Ancylostoma

duodenale.
 Stiles in 1902 described
• A second major hookworm species
• Later re-named Necator americanus.
32
 Hookworm Infections

Definition
 Infection by nematode endoparasites of the genus
Ancylostoma or by Necator americanus.
 Cause intestinal blood loss during a part of their life
cycle
 Results in iron-deficiency anemia
33
Epidemiology
 Hookworm infection is found worldwide
 N. americanus is found
• Tropical areas of South Asia, Africa, and America
• Southern United States
 A. duodenale is seen
• Mediterranean basin, Middle East
• Northern India, China, and Japan
In Ethiopia
• Both A. duodenale & N. americanus are found.
• A. duodenale Less common than N. americanus 34
Infectious agent
 Ancylostoma duodenale (old world hook worm)

 Necator americanus (new world hook worms)

35
Adult of hookworm
 Small nematodes (1-1.5 cm)

 Head is slightly bend (hook)

 The ‘mouth’ carries characteristic teeth

(Ancylostoma) or plates (Necator)
 The two species can be differentiated by the
morphology of their oral cavity

36
Ancylostoma duodenale
• Mouth capsule has 4
"teeth"
• Two on each side

Necator americanus
• Mouth capsule has two
cutting "teeth“.

Necator americanus
37
Properties of the Major Species of Hookworm

38
Egg
Color - colorless with a tin shell, which appears as a black
line around the ovum
Shape - oval, poles more flattened
Size - 65x40mm
Embryo - always contain at least 8 cells (N americnaus)
&4
cells (A. duodenale) in fresh stool
Other- Clear space b/n egg shell & embryo

Note-The two species can not be differentiated by the

morphology of egg. 39
40
Mode of transmission
 Skin penetration by filariform larva (walking
barefoot)
 Ingesting infective larvae (A. duodenal)

 Transmammary - from mother to infant when larva

are present in breast milk (A. duodenal)

41
42
Immunology
 Human immune responses to hookworms are not
well characterized
Spontaneous reduction of worms
 Immediate hypersensitivity reactions in the
intestinal wall
 Necessary ingredients for the reaction
• Worm allergens
• IgE antibody
• Mast cells
43
Pathogenesis
Invading L3 larvae
 A local reaction occur at the invasion site ( Ground
itch)
• usually the feet or hands

• particularly in sensitized individuals

• Causes an allergic dermatitis

44
Migrating larvae
 Causes Lung pathology

• Large numbers of larvae migrating through the

lungs
• Focal haemorrhages

• Cause pneumonitis.

45
Blood-feeding adults
 Hookworm-induced blood loss

• Occurs at the site of adult parasite intestinal attachment

• Use their teeth to fasten onto the mucosa & submucosa

• Secrete a battery of pharmacologically active polypeptides

prevent blood from clotting

 down regulate the host inflammatory response

• Adult hookworms also release hydrolytic enzymes

46
 Hookworm-associated blood loss due to
• The destruction of mucosal capillaries

• The worm ingests mucosal tissue with blood

• Blood is also lost by seepage around the

attachment site.

47
48
Clinical features
 If the worm burden is small , infection is
asymptomatic
1. Clinical features attributable to larval worms
1.1. Ground itch
 The larvae penetrating the skin cause

• Allergic reaction

• Petechiae 0r papule with itching burning

sensation.
49
1.2. pneumonitis , Loeffier's syndrome:
• Cough & asthma
• Low fever
• Blood-tinged sputum or hemoptysis,
• Chest-pain, inflammation shadows in lungs under
X-ray.

50
2. Clinical features attributable to adult worms
Heavy infection
 Causes iron deficiency & IDA

 Protein lost enteropathy

 Abdominal pain & diarrhea

 Weight loss
 Stunted growth & mental development
 Sexual retardation.
 Anemia in children can impair their educational
performance 51
Anemia in pregnant women
 Increased risk of having premature & low birth
weight
 Risk of having impaired lactation after delivery

52
Diagnosis
 Hookworm infection is difficult to differentiate
clinically from other parasitc infections
A. Microscopic method
Specimen: - Stool
Method: - direct stool exam or concentration method
Result: - ova of Hookworm

53
 Treatment
 Choice of drug for Hookworm infection for both clinical
case & mass treatment programs
• Mebendazole

• Albendazole
Prevention and control
Sanitary disposal of faeces

Avoid the use of night as fertilizer

Wearing adequate protective foot ware

54
 Strongyloidiasis
Definition
 Intestinal nematode infection caused by
Strongyloides stercoralis
Epidemiology
 World wide distribution

 Warm moist climates of tropical & subtropical countries.

 It infects 90 million individuals worldwide

 The distribution of S. stercoralis parallels that of the

55
Infectious agent -Strongyloides stercoralis
(Common name dwarf thread worm)
i.e. Free-living & parasitic generations
Morphology
Adult
 Male (free living - Size- 1.7mm - )
 Female (parasitic) - Size – 2.2mm in length
 Female (free living) - Size- 1mm in length

Rhabditiform Larvae- Diagnostic stage

Filariform larvae - Infective stage 56

57
Mode of transmission
 Skin penetration (filariform)

 Autoinfection

• Internal auto infection- penetration of the gut wall

• External auto infection- penetration of perianal skin

 Transmammary – mother to infant in breast milk

58
Life cycle
 The Strongyloides life cycle is more complex than that
of most nematodes
• Alternation between free-living & parasitic cycles

• Its potential for autoinfection

• Multiplication within the host.

• Infection persist indefinitely

• Without the need for reinfection from the

environment 59
60
61
PATHOGENESIS AND IMMUNITY
 Immunity in strongyloidiasis is not well understood

 Chronic strongyloidiasis is probably sustained by

• Adult worms reside in harmony within their host’s
intestine
• survive by means of well-regulated autoinfection

• Autoinfection is believed to be regulated by host cell–

mediated immunity
62
 parasites may play role in their own
regulation
 Reserchaer propose that S. stercoralis may have the
ability to reach an optimal population in size
A.when initial infective dose of larvae is low
• A higher rate of intraluminal molting
( autoinfection) occurs
• until the “optimal” size of the adult population is
reached
63
B. Replace the dying adults
 Strongyloides transmits its molting signal by molting

hormones (ecdysteroids)
 Adult females adjust their production of
ecdysteroids
 To levels sufficient to replace the dying adults

64
In certain study
 Immune suppression is not the major cause of
hyperinfection
 The direct effect of steroid on the parasite that
causes the hyperinfection.

65
66
67
Clinical Manifestations

In light infections
 Most patient are asymptomatic

Ground itch
 infective larvae penetrate the skin in large numbers.

Pneumonitis
 Result from larval invasion in the lung.
68
In heavy worm loads
 The patient may complain
• Epigastric pain & tenderness

• Peptic ulcer-like pain associated with peripheral

eosinophilia

• With widespread involvement

the intestinal mucosa,

vomiting, diarrhea,
69

 Massive hyperinfection may occur
• Immunosuppressed patients

• in those receiving glucocorticoid therapy

• producing severe enterocolitis

 Widespread dissemination of the larvae to
extraintestinal organs
• Heart
• Lungs
• Central nervous system.

70
 The larvae may carry enteric bacteria with them,
• Producing Gram-negative bacteremia

• Occasionally Gram-negative meningitis that may result

in death

71
Reading Assignment
• Is strongyloidiasis under the list of AIDS-
defining illnesses ??

72
Laboratory diagnosis

A. Microscopic method

Specimen: - Stool, duodenal aspirates or jejunal

biopsy, sputum

Method: - direct wet smear

Result:- to look for rhabditiform larvae in the stool

73
Serological-.
– Enzyme-linked immunosorbent assays

– for antibodies to somatic antigens are now available

Treatment
 Choice of drug
A.Ivermectin
B.Thiabendazole
C. Albendazole

74
 Prevention and control
 Preventing soil becoming faecally polluted by:

 Providing and using adequate latrines

 Avoiding the use of untreated human faeces as

fertilizer
 Preventing the entry of larval by wearing protective
foot ware
•
75