0

A Guide To

MEDICAL
PARASITOLOGY
For Third year
(CNS 2)

BY

Staff members of parasitology

department
2022 - 2023
 ‫‪2‬‬

‫رقم اإليداع‬
‫‪/ ۲۱٦۳٦‬‬
‫‪۲۰۱۱‬‬

‫حقوق الطبع محفوظة لدى المؤلفين‬

‫‪2022 - 2023‬‬
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Table of Contents
❖ Preface ...............................................................................................................................................6
❖ Course Specification ....................................................................................................................7
❖ References:-.....................................................................................................................................8
❖ Parasites affected CNS and different organs ...................................................................9
Parasites in the eye:-........................................................................................... 9
Parasites in the skin and subcutaneous tissue:-................................................... 9
1. Coenurosis .................................................................................................... 10
Multiceps multiceps…………………. ....................................................................... 10
Pathogenesis and symptomatology:- ................................................................ 11
❖ Control: Similar to hydatid disease………………... ............................................................ 11
2 Loa loa………………… ......................................................................................... 12
Pathogenesis and symptomatology:- ................................................................ 13
❖ Plate 1: Loa loa microfilaria and Onchocercus life cycle .......................................... 14
3) Onchocercus volvulus .................................................................................... 15
Morphological characters:- ............................................................................... 16
Diagnosis:- ......................................................................................................... 17
Treatment:- ....................................................................................................... 18
❖ ❖ Table 1: Differences between calabar swelling and onchocercoma:-.......... 18
❖ ❖ Table 2: Differences between filariae:- ...................................................................... 19
❖ Tissue Nematodes ..................................................................................................................... 20
❖ Extra- intestinal adult nematodes...................................................................................... 20
❖ Dracunculus medinensis ......................................................................................................... 20
Life cycle Fig.(P: 2):- .......................................................................................... 22
Pathogenesis and symptomatology:- ................................................................ 22
Diagnosis:- ........................................................................................................ 23
❖ Plate 2: Dracunculus medinensis life cycle ..................................................................... 24
❖ Class: Crustacea .......................................................................................................................... 26
❖ Cyclop (TBL) .................................................................................................................................. 26
❖ Plate3: Male and female cyclop .......................................................................................... 26
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❖ Pathogenic Free-Living Amoebae ....................................................................................... 27

❖ ❖ Table 3: Morphology of free living amoebae .......................................................... 28
❖ 1) Naegleria fowleri…………………......................................................................................... 29
Diagnosis:- ........................................................................................................ 30
❖ 2) Acanthamoebae………………… ........................................................................................... 31
I) Granulomatous amoebic encephalitis:- .......................................................... 31
❖ Pathogenesis:- .............................................................................................. 32
Medical:-........................................................................................................... 33
II) Acanthamoebic keratitis: .............................................................................. 33
Prevention and control:- ................................................................................... 34
❖ Plate4: Acanthamoeba and Naegleria life cycle.......................................................... 35
❖ Genus: Trypanosoma ............................................................................................................... 36
I- African Trypanosomes ................................................................................... 36
(1) Trypanosoma gambiense ............................................................................. 36
❖ ❖ Table 4: Developmental forms in African trypanosomes:-................................ 37
❖ Life cycle (P. 5):- ............................................................................................ 38
❖ Mode of transmission:- ................................................................................. 39
❖ Plate 5: Polymorphic trypanosomes life cycle .............................................................. 40
Pathogenesis and symptomatology:- ................................................................ 41
❖Diagnosis: ...................................................................................................... 42
(2)Trypanosoma rhodesiense ............................................................................ 43
❖ II- American Trypanosoma .................................................................................................... 44
❖ Trypanosoma cruzi .................................................................................................................... 44
❖ ❖ Table 5: Developmental forms in American trypanosomes:-........................... 45
❖ Plate 6: Monomorphic trypanosomes life cycle .......................................................... 49
Diagnosis:-………………………… .............................................................................. 50
Treatment:-……………………………………………… ........................................................ 51
❖ Family: Reduviidae .................................................................................................................... 52
❖ Triatoma (TBL)............................................................................................................................. 52
❖ Myiasis ............................................................................................................................................ 53
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1)Specific myiasis…………………….. ....................................................................... 53

2)Semispecific myiasis……………………. ................................................................. 54
3)Accidental myiasis:……………….. ....................................................................... 54
Diagnosis:-……………………………… ........................................................................ 56
Treatment:-……………………………… ...................................................................... 56
❖ ❖ Table 6: Morphological differences between members of family
Muscidae:-..................................................................................................................................... 57
❖ Plate 7: Muscidae members and life cycle ..................................................................... 58
❖ Plate 8: life cycle of unhuman schistosomiasis ............................................................ 62
❖ Larva migrans............................................................................................................................... 63
❖ Family: Demodicidae ................................................................................................................ 66
❖ Demodex folliculorum.............................................................................................................. 66
❖ Chigger’s (Jigger’s) disease (TBL) ........................................................................................ 67
❖ Plate 9: life cycle of fleas ........................................................................................................ 70
Medical importance of fleas:- ........................................................................... 71
Prevention and control of fleas:- ....................................................................... 72
Activity …………………………………..……………………………………………………………………..73
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Preface
The staff members involved in teaching parasitology science welcome the
3rd year medical students to this parasitology course.

Parasitology is an important science combining the activities of physicians,

pharmacists and veterinarians.

This book (A Guide to Medical Parasitology 3) contains introduction and

information that medical students of 1st year will need during studying course of
Central nervous system 2 and Special senses module.

Simple examples of parasitic life cycle for the most famous helminthic
infections were illustrated.

Also, the infective and diagnostic stages, different procedures and

techniques for diagnosis, specific prescribed chemotherapeutic drugs and
principles of control were presented.

We would like our colleagues and students to offer their comments.

Such feedback will really enrich the subsequent editions.

The authors
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Course Specification
University: Menoufia
Faculty of Medicine
Department offering the courses: Medical Parasitology
1- Data of the course:
Title of the course: Medical Parasitology
Year: 1st year of M.B. & B.Ch. program of Integrated Program Central nervous system
and Special Senses module.
Code: III 04
Specialty: Medical Parasitology
Teaching and learning methods: Credit hour system
Central nervous system (Total: 19.8 hours and 15 marks)
• Lectures: 3.6 hours
• Practical sessions: 5.4 hours
• Self-learning, tutorial and presentation ( 10.8 hours)
Marks distribution:
• Theoretical: 6 marks
• Practical: 4.5 marks
• Activity: 4.5 marks
2- Objectives of the course:
- To provide students with introduction of parasites, biological, epidemiological and mode of
transmission of some parasites causing diseases to humans.
- To enable students to understand the pathogenesis, clinical presentations and complications of
parasitic diseases.
- To enable students to reach diagnosis and know the general outline of treatment, prevention and
control of parasitic infections
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3- lntended learning outcomes (ILOs): By the end of the course, students should be able to
perform:
a- Knowledge and understanding:
a1. Describe the common parasitic diseases caused by helminthes and protozoa as regards life cycle,
pathogenesis, clinical features, differential diagnosis and complications
a2. Describe the pathogenesis, clinical features differential diagnosis and complications of some
parasites of medical importance.
a3. Point out the methods of recovery of parasites and their culture methods as well as
immunological and molecular methods used for diagnosis of parasitic infections.
a4. Define the principles of management for common parasitic diseases.
b- Intellectual Skills:
b1. Assess the differentiation between the behavior and ecology of different parasite species and
stages in the environment.
b2. Diagnose different helminthes.
b3. Carry out a protection to their society and environment from pollution with parasites.
c- Professional and practical skills (p.p.s):
c1. Collect different samples for different techniques.
c2. Methods of isolation and identification of parasites.
c3. Diagnose some parasitic infection in different hosts.
c4. Use advanced techniques in diagnosis.
❖ Attendance criteria:
- Students should be according to the Faculty by attending laws.

References:-
1. Department course books
2. Diagnostic medical parasitology: Garcia LS and Bruckner, 2008
3. Clinical parasitology: Beaver PC, Jung RC and Cupp EW 9th ed 1984 Leaand Febiger,
Philadelphia.
4. Medical parasitology: Satoskar AR, Simon GL, Hotez PJ and Tsuji M, 2009, Landes Bioscience,
Austin, Taxas, USA.
5. Manson’s Tropical Diseases: Cook GC and Zumla AI, 22nd ed 2009, Saunders Elsevier, China.
6. Journal of Parasitology, Journal of Helminthology and www.Pubmed.com
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CNS 2

Parasites affected CNS and different organs

❖Parasites in the brain:-

Trematoda: Eggs of H. hetrophyes, Schistosoma & P. westermani.

Cestoda: Sparganum, Cysticercus cellulose, Hydatid cyst, Coenurus cyst.
Nematoda: Visceral larva migrans, Ascaris larva, Disseminated larva of S.
stercoralis, T.spiralis & Loa loa.
Protozoa: E. histolytica, pathogenic free living amoebae, African trypanosomes,
Trypanosoma cruzi, Plasmodium falciparum, Toxoplasma.
Arthropoda: Larvae of Sarcophaga & Wohlfahrtia  aural myiasis.

❖Parasites in the eye:-

Cestoda: Sparganum & Cysticercus cellulose.
Nematoda: Visceral larva migrans, T. spiralis (in ocular muscle), Loa loa &
Onchocerca volvulus.
Protoza: Acanthamoeba (keratitis), Trypanosoma cruzi (Romana's sign), T. gondii.
Arthropoda: Ocular myasis & Phthirus pubis in the eye lashes.

Parasites in the skin and subcutaneous tissue:-

Trematoda: Schistosoma, swimmer’s itch.
Cestoda: Sparganum & Cysticercus cellulose.
Nematoda: Filariform larvae of hookworms and S. stercoralis, Cutaneous larva
migrans, D. medinensis, Loa loa, Onchocerca volvulus.
Protozoa: E. histolytica, African trypanosome, T. cruzi and Leishmania.
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CNS 2

Arthropoda: Cutaneous myiasis, Sarcoptes scabiei, Tunga penetrans & Demodex

folliculorum.

1. Coenurosis
❖ Definition: It is a parasitic infection of humans and mammals such as
sheep, cattle and goats with coenurus cerebralis, the larval stage of
Multiceps multiceps (blind cycle).

1) Multiceps multiceps
❖ Geographical distribution: Cosmopolitan.
❖ D.H: Dogs and other canines.
❖ I.H: Herbivorous animals (sheep, cattle, goats) and occasionally man.
❖ Habitat: Small intestine of D.H.
❖ Egg (I.S to I.H): Similar to egg of Taenia.
❖ Coenurus cerebralis (I.S to D.H):
- Size: Hen' eggs to fist of hand (3-5 cm).
- Site: Mainly in brain & spinal cord.
- Its wall forms of a germinal layer only from which only scolices
develop.
- Color: Translucent.
- Contents: Watery fluid with only scolices.
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CNS 2

❖ Life cycle:-
➢ The adult worm lives in the small intestine of dogs and other canines 
eggs pass with stool.
➢ The egg is ingested with contaminated foods & water by herbivorous
animals and occasionally man (I.H) onchosphere hatches in the small
intestine  carried by blood stream to the brain & spinal cord where it
develops into coenurus cerebralis cyst.
➢ The D.H is infected by eating the cyst scolex attaches to the intestinal
wall  adult worm.

Pathogenesis and symptomatology:-

❖ In man: Symptoms of increased intra cranial pressure and space
occupying lesions  epileptic fits, vomiting, headache, hemiplegia,
paraplegia & coma.
❖ In sheep: disturbed gait (a disease called Gid).
❖ Diagnosis:-
1) Clinical.
2) Laboratory: X-ray, CT scan, Serological tests & PCR.
3) Surgical removal of the cyst if possible and microscopic examination.
4) Post mortem identification.
❖ Treatment: Surgically as brain tumour.
❖ Control: Similar to hydatid disease.
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CNS 2

2) Loa loa
(Eye worm or calabar swelling worm)

❖ Geographical distribution: West Africa especially in Cameroon.

❖ Habitat:-
• Adults inhabit loose subcutaneous tissue, including conjunctiva, eyelid,
back, chest, axilla, groin, penis and scrotum.
• Microfilaria appears in peripheral blood.
❖ D.H: Man.
❖ I.H (vector): Chrysops fly (deer fly, mango fly or golden eye fly).
❖ Reservoir host: may be monkeys, rodents.
❖ Morphological characters:-
1) Adult: Similar to W. bancrofti but smaller (3-6 cm), simple head with no lips.
The cuticle is covered with irregular, small bosses (high antigenic) except at
head and tail.

2) Microfilaria
• size : 250 × 8 µm
• Tight sheath.
• Angular curves.
• Tail full of nuclei
• Appears in blood in day time i.e. diurnal periodicity.
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Pathogenesis and symptomatology:-

- Disease: Loiasis or calabar swelling.
1) Adult worms migrate through the conjunctive, cornea & subcutaneous
connective tissues provoking allergic reaction  irritation, itching and creeping
sensation.
2) Localized calabar swelling (fugitive swelling):-
• It is due to allergic reaction to the worm metabolites.
• Transient rapidly developed swelling appears for 2-3 days then disappear.
• About 2-3 cm in size (hen’s egg).
• Localized, hard, non pitting, painful swelling observed on the wrists and
ankles.
3) Invasion of CNS: Encephalitis.
4) Arthritis.

❖ Diagnosis:-
a) Clinical:
Observation of the adult worm, under conjunctiva or over the nose bridge.
 History of calabar swellings.
b) Laboratory:
Demonstration of microfilariae in blood at day time (diurnal).
Serological tests.
Eosinophilia.
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Plate 1: Loa loa microfilaria and Onchocercus life cycle

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CNS 2

❖ Treatment:-
1) Antihistaminic, antibiotics and corticosteroids.
2) Di-ethyl-carbamazin citrate (DEC).
3) Ivermectin.
4) Surgical removal of adult worms from the conjunctiva (see practical book).
❖ Prevention and control:-
1) Mass treatment of patients.
2) Control of Chrysops.
3) Heath education.

3) Onchocercus volvulus
(Convoluted worm, river blindness worm)

❖ Geographical distribution: Tropical Africa (where 30 million are infected),

Sudan, Saudi Arabia, Yemen and Central America.
❖ Habitat:-
• Adults inhabit subcutaneous tissues over boney prominences.
• Microfilariae does not reach the circulation, they are present in the dermis,
subcutaneous nodules, subcutaneous tissues, all chambers of the eye and
they are non periodic.
❖ D.H: Man.
❖ I.H (vector): Black flies or Simulium.
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CNS 2

Morphological characters:-
1) Adults:-
• Male: 4cm, curved ventrally with post-anal papillae.
• Female: 50cm, vulva opens just behind the oesophageal region. Fig.(2 - 2)
2) Microfilaria
• 300 × 8 µm
• Smooth curves.
• Non sheathed.
• Anterior end &tail free of nuclei.
• Not found in blood
❖ Life cycle: (P: 1)
❖ Pathogenesis and symptomatology:-
- Disease: Onchocerciasis or onchocercosis or river blindness.
1) Cutaneous lesions:-
A. Onchocerca nodule or tumour (onchocerchoma).
• Slowly growing fibrous subcutaneous nodules over bony prominences as
scalp, elbow, knee, ribs, iliac crest& scapula.
• Nodules are firm rounded or oval, well localized, mobile and about 1-
2.5cm in diameter containing adults and microfilariae.

• The location of nodules differs according to geographical area. In Africa,

most infections found in pelvic girdle; in Central America, they are in
shoulder girdle.
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CNS 2

B. The skin over and near nodules shows sever dermatitis, an intense itching
and may lead to 2ry infection. It may be depigmented (Leopard) or hyper
pigmented (Sowda) and elephantoid (oedemateous).
The lymph nodes in femoral triangle are enlarged (in males and females) 
adeno-lymphocele (hanging groin) with loss of skin elasticity (sagging of
the skin).
2) Eye lesion:-
• Due to immunologic response to microfilaria (especially the dead).
• River blindness or Sudan blindness.
- Microfilaria invades many parts of the eye  keratitis with corneal opacity
 iridocyclitis, chorioretinitis with degenerative changes and optic neuritis
 blindness.
Diagnosis:-
1) Clinical: Onchocercoma and eye lesions.
2) Laboratory:-
• Direct:-
a. Detection of microfilariae in aspirate of nodules and skin-snips.
b. Eye examination: presence of microfilariae in cornea and eye chambers.
c. Histopathological examination of excised nodule to demonstrate adults.
d. Mazzotti test: 50 mg - 100 mg of DEC (hetrazan) is given orally 
appearance of skin rash, itching within 24 hours (due to death of
microfilaria in subcutaneous tissue and liberation of high amount of antigen
and toxins).
• Indirect:-
a. Eosinophilia (20%).
b. Intradermal test (using Dirofilaria antigen).
c. Serological tests and PCR.
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Treatment:-
• Excision of the nodule (nodulectomy).
• Hetrazan
• Ivermectin.
❖ Prevention and control:-
1) Mass nodulectomy in endemic areas.
2) Elimination of the vectors by application of insecticides (DDT) over running
streams of water.
3) Mass treatment with Ivermectin.

❖ Table 1: Differences between calabar swelling and onchocercoma:-

Items Calabar swelling Onchocercoma

Parasite Loa loa Onchocercus volvulus
Vector Chrysops (deer fly) Simulium (black fly)
Mazzotti test Negative Positive
- Present in blood (diurnal) - Present in skin and sub-
Microfilaria cutaneous tissue (not in blood)
- Sheathed - Unsheathed
Size 2 - 3 cm 1 - 2.5 cm
Nodule

Duration Transient (2 - 3days) Permanent (adults)

- Painful - Painless
- Soft - Hard
- Allergic reaction to adult - Inflammatory reaction to adults
Characters with itching and urticaria and microfilaria
of nodule - In loose connective tissues - Over bony prominences
- Depigmented or hyperpigmented
skin
- Adults under conjunctiva - Keratitis, iridocyclitis & retinitis
- Itching, conjunctivitis - degenerative changes with optic
Ocular lesion
neuritis
- No blindness - Blindness
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❖ Table 2: Differences between filariae:-

Parasite Name Disease Distribution Microfilaria Habitat Periodicity Vector Diagnosis
W. bancrofti ■Elephantiasis in ■Tropical & ■250×8µm ■Lymph nodes ■Nocturnal ■ Blood
lower limbs and subtropical ■Loose and lymph (10 p.m – 2 a.m) examination
♂ 4 cm external genitalia sheath vessels of ■Culex at night &
■Lymphangitis ■Egypt ■Smooth lower limbs ■Present in pipiens urine
♀ 8 cm and curves blood ■ Hetrazan
■Anopheles
lymphadenitis ■Tail free Aedes provocation
■Varices & of nuclei test
oedema ■ Examination
B. malayi ■Elephantiasis in ■Malayi ■250×8µm ■Lymph nodes ■Nocturnal of chylous
upper limbs and ■Loose and lymph (10 p.m – 2 a.m) effusion
♂ 2 cm ■India ■ I.D. &
mammary glands sheath vessels of ■Mansonia
■Smooth upper limbs ■Present in serological
♀ 5 cm ■China curves blood ■Anopheles tests
■Tail with ■ Eosinophilia
2 nuclei
Loa loa ■Calabar swelling ■West and ■250×8µm ■Subcutaneous ■Diurnal ■ Blood
Central ■Tight tissues periodicity examination
♂ 3 cm ■Eye worm, Africa sheath at day time
irritation & ■Angular ■Free ■Present in ■ Adult under
♀ 6 cm itching curves migrating blood conjunctiva
■Chrysops
■Tail end ■Eosinophilia &
full of Serological
nuclei tests
■ Calabar s.
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O. volvulus ■Onchocercoma ■West and ■250×8µm ■Subcutaneous ■Non-periodic ■ Microfiliria

tumour central tissues in the nodule
♂ 3 cm Africa ■No sheath ■In skin and and skin
■Sudan blindness ■Bony subcutaneous ■ Positive
♀ 50 cm ■South ■Tail free prominences, tissues Mazzotti
■Dermatitis, hyper America of nuclei ■Simulium
scalp, iliac test
or depigmented
crest & costal ■ Eosinophilia,
skin
ribs I.D. &
serological
tests
M. perstans ■Non pathogenic ■Tropical ■100×5µm Serous cavities ■Non periodic ■Blood
Africa e.g.
exanimate for
♂ 4 cm ■No sheath ■Pericardium ■In blood
■South microfilaria at
■Culicoides
♀ 7 cm America ■Rounded ■Pleural cavity
any time
tail & full
of nuclei ■Peritoneal
cavity
M. ozzardi ■Non pathogenic ■South ■200×5µm Serous cavities ■Non periodic ■Blood
America e.g.
exanimate for
♂ 4 cm ■No sheath ■Pericardium ■In blood
microfilaria at
■Culicoides
♀ 7 cm ■Tapering ■Pleural cavity
any time
tail & free
of nuclei ■Peritoneal
cavity
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CNS 2

Tissue Nematodes
1) Extra-intestinal adult nematodes: Dracunculus medinensis and filariae.
2) Extra–intestinal larval nematodes: Larvae of Trichinella spiralis,
Larvae of Toxocara canis & cati, Larvae of Ancylostoma caninum &
Ancylostoma braziliense and larvae of some filariae.
❖ General characters:-
1) Adults or larvae live in the extraintestinal tissues.
2) Adult worms are slender and thread like.
3) Cylindrical (filariform) oesophagus.
4) Females are larviparous (T. spiralis, D. medinensis & filariae).
5) Require an arthropod as intermediate host for their life cycle (D. medinensis
& filariae).

Extra- intestinal adult nematodes

Dracunculus medinensis
❖ Distribution: Tropics of Asia and Africa (especially Sudan, Ghana, Mali,
Nigeria and Niger), Yemen, Iran, Saudi Arabia. Areas depend on wells for water
supply and not recorded in Egypt.
❖ Habitat: Subcutanous tissues, most commonly in feet, leg, hand & shoulders.
❖ D.H: Man
❖ R.H: Dog & cat.
❖ I.H: Cyclop.
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CNS 2

❖ Morphological characters:-
1) Adults:-
• Elongated, cylindrical.
• Mouth lipless.
• Male:-
- 3 - 4cm ×0.2mm.
- Posterior end coiled
- One set of genital organs.
- Two spicules.
• Female:-
- 80-120cm × 2cm.
- Posterior end with hook for fixation to the host tissue.
- Two sets of genital organs, gravid female have a distended uterus filled
by coiled larvae. Vulva opens 1cm from anterior end.
2) Larva:-
• Comma shaped 600 × 20µm.
• Blunt rounded anteriorly and with long tapering tail
posteriorly (1/3 body length).
• Striated cuticle.
• Rhabditiform esophagus.
 22

Life cycle Fig.(P: 2):-

➢ Adult worms live in subcutaneous tissues of man (D.H)&reservoir hosts
(dogs, cats, cattle & horse). The gravid female migrates in the subcutaneous
tissues in parts that become in contact with water (+ hygrotropism).
➢ The female worm irritates the skin through its secretion producing blister and
ulcer.
➢ When the ulcer becomes in contact with water, a loop of uterus prolapses and
discharges larvae in water.
➢ In water, larvae are swallowed by Cyclops (I.H) and when reach the body
cavity they moults twice and become infective larvae within 3 weeks.
➢ Infection occurs if Cyclop is swallowed by D.H or R.H larvae are liberated
by digestive juices and migrate through the intestinal wall to the
retroperitoneal space  subcutaneous tissues to mature to adult worm.
➢ Adult worms appear under skin after one year.

Pathogenesis and symptomatology:-

- Disease: Dracunculiasis, dracunculosis.
1) Blisters are formed due to local inflammatory reaction and toxin products by
female.
2) Pain, pruritis and 2nd bacterial infection  abscess formation and cellulitis.
3) Nausea, vomiting, diarrhea& headache due toxicity.
4) Rupture of the worm  severe allergic reaction.
5) Worms that not reach skin  died and calcified.
 23

Diagnosis:-
1) Clinical.
2) Laboratory:-
• Detection of larvae released from ulcer, when the limb is immersed in
water.
• X-ray to show calcified female.
• Intradermal test.
• Serological tests.
• Eosinophilia (10%).

❖ Treatment:-
• Antihistaminic and corticosteroids for allergic reaction.
• Antibiotics for 2ry infection.
• Female-traction when the worm protrudes, tie a piece of thread around it
and fix the thread around piece of wood. Gradual traction by rolling the
wood to avoid worm rupture (if rupture  liberation of toxins  cellulitis
due 2ry infection).
• Drugs:-
a. Thiabendazole (Mintezol): 25 mg / kg twice daily for 4 days.
b. Diethylcarbamazine citrate (hetrazan): 2mg / kg t.d.s orally for 2-3
weeks.
c. Metronidazole (Flagyl): 250 mg / t.d.s for one week.
d. Surgical removal of worms.
 24

Plate 2: Dracunculus medinensis life cycle

 25

CNS 2

❖ Prevention and control:-

1) Patients:-
• Treatment of patients.
• Pure water supply.
• Avoid washing skin ulcers in wells water.
• Elimination of step wells and using wells with pumps.
• Health education especially in endemic areas & step wells should be
covered to prevent larvae from reaching water.
2) Destruction of Cyclops:-
• Wells water should be boiling or filtrated to remove cyclop.
• Addition of copper sulphate, chlorine or quick lime (1:1000).
• Natural enemy e.g. fishes that feed on Cyclops (Barbus).
 26

Class: Crustacea
Cyclop (TBL)
(Water flea)
❖ Geographical distribution: Cosmopolitan, living in fresh water such as
lakes and ponds.
❖ General characters fig.(16 - 6, 7):-
• Body is divided into cephalothorax and abdomen.
• 2 pairs of antennae (one pair is long and the other pair is short).
• Wingless.
• 4 pairs of legs.
• Aquatic and breathing by gills.
• Incomplete metamorphosis (adult  eggs  larvae  adult).

Plate3: Male and female cyclop

 27

CNS 2

❖ Life cycle:-
➢ Fertilized female carries her eggs in egg sacs on the sides of its abdomen.
➢ Eggs hatch  larvae that moult several times to mature to adults.

❖ Medical importance: Cyclop acts as intermediate host for (3D):-

1- Diphyllobothrium latum.
2- Diphyllobothrium mansoni.
3- Dracunculus medinensis.
❖ Prevention and control: The same as in Dracunculus medinensis.

Pathogenic Free-Living Amoebae

❖ Geographical distribution: Worldwide.
❖ Medically importance free living amoebae are:
1) Naegleria fowleri  causative organism of primary amoebic meningo-
encephalitis.
2) Acanthamoeba castellani & culbertsoni  causative organism of
granulomatous amoebic encephalitis, keratitis and chronic granulomatous
infection of the skin.
3) Balamuthia mandrillans  causative organism of granulomatous amoebic
encephalitis.
❖Habitat:-
1) Commensals: In the upper respiratory tract (nostril and throat).
2) Pathogenic: In the CNS, cornea and skin.
3) Free living forms: In stagnant warm fresh water and in soil.
 28

❖ Table 3: Morphology of free living amoebae

Items Naegleria fowleri Acanthamoeba species
Trophozoite stage -Amoeboid in shape with -Amoeboid in shape with
broad pseudopodia spiky pseudopodia
-Found in brain tissues -Found in brain & cornea
-Found in CSF -Not found in CSF
Cyst stage -Rounded -Rounded with wrinkled wall
-Not found in brain tissue -Found in brain & cornea

Flagellate stage -Present & detected in -No flagellate stage

CSF only
Infective stage -Trophozoite in water -Trophozoite in water
-Cyst inhaled with dust -Cyst inhaled with dust

Diagnostic stage -Trophozoite in CSF -Trophozoite & cyst in brain

&brain tissue tissues & cornea
-Flagellate form in CSF
 29

CNS 2

1) Naegleria fowleri
It is a pathogenic free- living amoeba that infects central nervous system causing
primary amoebic meningoencephalitis.
❖ Sources of infection:-
1) Water particularly stagnant fresh water (lakes, ponds and swimming pools)
in summer months and warmer climates.
2) Soil.
❖ Life cycle (P. 3):-
➢ Infection with Naegleria fowleri occurs during swimming, diving or bathing
in warm stagnant fresh water. They enter the nose  nasal mucosa 
olfactory nerve  penetrate cribriform plate  to reach the cranial cavity 
to the brain. Also, infection occurs due to inhalation of cysts in dust.
❖ Pathogenesis:-
1) Naegleria fowleri multiplies in the brain causing intense inflammation with
infiltration of polymorphonuclear leukocytes  haemorrhage, and necrosis
typical of acute meningitis.
2) The disease has rapid acute course which ends by death within 4 - 5 days.
3) Commonly affects healthy children and adults.
 30

CNS 2

Clinical pictures:-
1) General: High fever, headache, blocked nose due to upper respiratory tract
infection and photophobia.
2) CNS involvement: Altered taste or smell, stiff neck, seizures, confusion and
coma  death.

Diagnosis:-
1) Clinical: Clinical pictures with history of swimming in fresh water.
2) Laboratory:-
- Lumbar puncture for CSF analysis is the primary diagnostic tool:-
- By direct film: CSF is purulent (but there is no bacteria) with abundant
neutrophils, RBCs, elevated protein levels and decreased glucose levels.
- Centrifugation of CSF and examination of the sediment: For motile
trophozoite and flagellate form.
1. Head CT scanning or MRI should precede lumbar puncture if evidence of
focal CNS involvement or elevated intracranial pressure is present.
2. Culture of CSF on non nutrient agar plate enriched with Escherichia coli.
3. Animal inoculation: Intrathecal injection of mice with CSF.
4. Fluorescent antibodies help in detection of the numerous trophozoites.
5. PCR: A recently sensitive diagnostic test.
 31

CNS 2

❖ Treatment:-
1) Medical:-
- Amphotericin B (1 mg /kg/ day IV for 10 days or intrathecally in severe
cases) +
- Miconazole (IV injection of 117 mg / m2 surface area t.d.s. for 9 days) +
- Rifampicin (3.3 mg /kg t.d.s. orally for 9 days).
1- Surgical: Hydrocephalus may necessitate shunting.

2) Acanthamoebae
(A. castelleni & A. culbertsoni)
They are pathogenic free- living amoebae that infect central nervous system, eyes
and the skin causing granulomatous amoebic encephalitis, keratitis and
granulomatous infection of the skin.

I) Granulomatous amoebic encephalitis:-

❖ Sources of infection: As Naegleria fowleri.
❖ Life cycle (P. 4):-
Mainly the parasites enter the body via lesions in the skin or upper respiratory tract
or via inhalation of airborne cysts then reach the blood to spread into the central
nervous system. Rarely, the parasites enter the body as a result of keratitis.
 32

CNS 2

❖ Pathogenesis:-
1) Acanthamoeba species multiply in the brain  moderate granulomatous
inflammation with vascular involvement. Both trophozoites and cysts are found
in the brain tissues.
2) The disease has subacute or chronic prolonged course and ends by death within
one week to several months.
3) Commonly affects individuals of all ages (but very young or very old persons
are more susceptible) and immunodeficiency persons.
❖ Clinical pictures:-
Low- grad fever, focal neurologic signs (as cranial nerve paralysis, hemiplegia,
ataxia, aphasia, diplopia & seizures), stiff neck, signs of increasing intracranial
pressure (nausea & vomiting) and coma  death.

❖ Diagnosis: Same as Naegleria but differes in:-

1) In lumber puncture: No trophozoites appear in the CSF.
2) Biopsy specimen from brain tissue to detect trophozoites and cysts.
3) Fluorescent antibodies help in detection of less numerous trophozoites and
cysts in brain tissues.
 33

❖ Treatment:-
Medical:-
- Ketoconazole and amphotericin B (alone or in combination).
- Sulfadiazine may be indicated.
1) Surgical: Same as Naegleria.

II) Acanthamoebic keratitis:

❖ Mode of infection: Direct contact of cornea with Acanthamoeba species
which may be introduced by:-
1) Minor corneal trauma that leads to corneal ulcer.
2) Exposure to contaminated water.
3) Contaminated soft contact lenses due to contamination of lens solution.
❖ Clinical picture: Unilateral severe keratitis with severe ocular pain  ring
ulcer  blindness.
❖ Diagnosis:-
1) Corneal scraping or biopsy  to detect trophozoites and cysts.
2) Stained smear with Giemsa or Calcuflour white stain.
3) Culture of contaminated lenses on non-nutrient agar plate enriched with
Escherichia coli.
4) Fluorescent antibodies  detect trophozoites and cysts.
5) PCR.
 34

CNS 2

❖ Treatment:-
1) Medical:-
- Topical application of a combined regimen of propamidine, miconazole,
and neomycin.
2) Surgical: Keratoplasty may be required.

III) Granulomatous skin lesions: Rare. It diagnosed by skin biopsy.

Prevention and control:-
1) Avoid swimming and diving in warm stagnant water of small lakes and
ponds.
2) Swimming pools should be adequately chlorinated.
3) Excessive salinity of water of swimming pool to 0.7% to inhibit the growth
of amoebae.
4) Proper care of soft contact lenses to avoid contamination with
Acanthamoeba by using adequate sterile rinsing and storage solution.
 35

Plate4: Acanthamoeba and Naegleria life cycle

 36

Genus: Trypanosoma
❖ Trypanosomes that infect man include:
I- African trypanosomes (polymorphic trypanosomes):
1- Trypanosoma gambiense.
2-Trypanosoma rhodesiense.
II- American Trypanosoma (monomorphic Trypanosoma):
- Trypanosome cruzi.

I- African Trypanosomes
(1) Trypanosoma gambiense
❖ Geographical distribution: West and Central Africa between 15°N and

10°S of the equator.

❖ D.H: Man
❖ R.H: Domestic animals e.g. Cattle, pigs and goats.
❖ Vector: Glossina palpalis (both male and female).
 37

Morphological characters:-

❖ Table 4: Developmental forms in African trypanosomes:-

Developmental forms
Items
Epimastigote Trypomastigote
(Crithidia form) (Trypanosoma form)

1) Morphology
- Size 10 - 20 µm 15 - 30 µm

-Shape Spindle or fusiform Spindle or fusiform

-Kinetoplast Just anterior to the nucleus At the posterior end

-Free flagellum Present Present

-Undulating Present & short Present & long

membrane Slightly moved posterior Central with central

karyosome
-Nucleus

2) Habitat 1-In the salivary glands of 1-In the blood and lymphatics
vector of man
2-Culture media 2-Vector

3)Vector 1-Glossina palpalis in Trypanosoma gambiense

2- Glossina morsitans in Trypanosoma rhodesiense

4) Infective Metacyclic trypomastigotes in the saliva of the vector

stage
(Anterior station transmission)
 38

CNS 2

✓ In the blood, trypomastigote (Trypanosoma) has different shapes:-

1- Long slender form (30 µm), active and with long free flagellum.
2- Short stumpy form (15 µm), sluggish in motility and without free
flagellum.
3- Intermediate form (20 µm), with a short free flagellum.

❖ Life cycle (P. 5):-

➢ Glossina (tsetse fly) becomes infected by feeding on human or animal blood
that contains bloodstream trypomastigotes (polymorphic).
➢ In the fly's midgut, the trypomastigotes transform into  procyclic
trypomastigotes, multiply by binary fission  then leave the midgut and
transform into epimastigotes  they reach the fly's salivary glands and
continue multiplaication by binary fission and transform into metacyclic
trypomastigotes (the cycle in fly takes approximately 3 weeks).
➢ Man is infected when the infected tsetse fly injects metacyclic
trypomastigotes (I.S) into skin tissue (anterior station transmission) 
they enter the lymphatic system and pass into bloodstream where they
transform into bloodstream trypomastigotes (polymorphic)  they are
carried to other sites through the body  reach other fluids as lymph and
spinal fluid and continue in replication by binary fission.
 39

CNS 2

❖ Mode of transmission:-
1) Bite of infected Glossina palpalis (cyclopropagative transmission).
2) Mechanical transmission of the organism by some blood sucking insects
during feeding as Stomoxys.
3) Congenital transmission: the trypanosome can sometimes cross the placenta
and infect the fetus.
4) Blood transfusion.
5) Sexual transmission may be possible.
6) Accidental infections in laboratories due to pricks from infected needle.
 40

Plate 5: Polymorphic trypanosomes life cycle

 41

CNS 2

Pathogenesis and symptomatology:-

• Disease: West African sleeping sickness (Gambian trypansomiasis).
• Incubation period: 2 weeks to several months.
• The disease has 3 stages:-
1) Chancer (primary lesion at the site of bite): Local multiplication of
trypomastigotes at the site of tsetse fly biting  inflammatory reaction 
formation of firm painful nodule (chancer) which may ulcerate with
oedema and erythema after few days of biting.
2) Haemolymphatic stage:-
a- Invasion of the blood:-
- High parasitaemia is accompanied by fever, headache, joint pains,
muscle pain, malaise and itching.
- Toxic depression of bone marrow  anaemia (hypoplastic),
leukopenia and thrombocytopenia.
b- Invasion of lymphatic system:-
- Generalized lymph nodes enlargement especially posterior cervical
lymph nodes in the posterior triangle of the neck (Winterbottom's
sign).
- Hepatomegaly and splenomegaly.
3) Neurological stage (Sleeping sickness syndrome): The parasite invades the
CNS by passing through the blood brain barrier  multiply there 
perivascular lymphatic infiltration  ischemia and petechial haemorrhage
 meningoencephalitis which manifested by:-
1. Fever, severe headache, mental dullness, apathy, reduced
coordination, fatigue and daytime sleeping.
 42

CNS 2

2. Without treatment, the disease is fatal with progressive mental

deterioration leading to coma and death from intercurrent infections as
malaria, pneumonia and dysentery.
 N.B. Damage caused in the neurological stage is irreversible.
❖Diagnosis:
1) Clinical.

2) Laboratory:-
a- Direct: Detection of trypomastigotes in blood, lymph nodes aspiration, fluid
aspirated from chancre, bone marrow puncture (sternum) and CSF by:-
1- Microscopic examination of stained and unstained smear.
2- Culture on NNN medium.
3- Animal inoculation such as rat, mouse and guinea pig.
b- Indirect:-
- Serological tests: IFAT & ELISA.
- Serum IgM: Always elevated in the blood and CSF due to antigenic
variation of the trypanosome (changing its antigenic coat) to escape from
host immune response (evasion).
- Blood examination: Anaemia, leucopenia and thrombocytopenia.

❖ Treatment:-
1) Early stage treatment (haemolymphatic stage):-
a- Suramin: 1 gm (10% solution) I.V every 3 - 7 days for 5 doses.
b- Pentamidine: 4 mg / kg I.M daily for 10 days.
 43

CNS 2

2) Late stage treatment (Cerebral stage):-

a- Melarsoprol: I.V injection of 3.6mg /kg/day for 3 days. Repeated 3 or 4
times with interval of one week between courses of treatment.
b- Tryparsamide: 2 - 4 gm I.V weekly for 10 doses.
c- Eflornithine (New drug): It is effective in the treatment of T. gambiense
only.
❖ Prevention and control:-
1) Treatment of the patients.
2) Control of vector (Glossina).
3) Elimination of reservoir animal hosts.
4) Chemoprophylaxis: Injection of pentamidine every 5 - 6 months.

(2)Trypanosoma rhodesiense
❖ Geographical distribution: Eastern parts of Tropical Africa between 10
° N and 15 °S.
❖ R.H: Wild game animals.
❖ Vector: Glossina morsitans (both male and female).
❖ Pathodenesis and symptomatology:-
• Disease: East African sleeping sickness (Rodesian trypanosomiasis).
• Incubation period: Short.
 44

• The disease in man is characterized by:-

- More acute and fatal course than Gambian sleeping sickness. The
patient dies before the cerebral stage develops.
- Fever is more frequent, severe anaemia, myocarditis and jaundice.
- Lymph nodes involvement is less and Winterbottom's sign may be
absent.
- Death occurs due to arrhythmia and congestive heart failure.
• Experimental animals:
- They are more susceptible to T. rhodesiense (easily infected) and the
short stumpy form of the parasites develop posterior nuclear shift.

❖ Diagnosis: As T. gambiense but the parasite is more plentiful in the blood.

❖ Treatment: As T. gambiense but the parasite is more resistant to treatment.
❖ Prevention and control: As T. gambiense.

II- American Trypanosoma

Trypanosoma cruzi
❖ Geographical distribution: Central and South America.
❖ D.H: Man.
❖ R.H: Domestic and wild animals (dogs, cats, rodents & armadillo).
❖ Vector: Triatoma (winged bug or kissing bug).
 45

Morphological characters:-

❖ Table 5: Developmental forms in American trypanosomes:-

Developmental forms

Trypomastigotes
Items Amastigotes Epimastigotes
(Monomorphic)

1) Morphology
-Size 10 - 20 µm
-Shape 2 - 5 µm 20 µm
Spindle-shaped
-Kinetoplast Ovoid C-shaped
Just anterior of
Beside the nucleus At the posterior
the nucleus
-Free flagellum end
Present
-Undulating Absent Present
Present & Short
membrane Absent Present & Long
-Nucleus Slightly moved
Eccentric Central with
posterior
central karyosome

2) Habitat Intracellular Blood Midgut of the

(R.E.Cs, C.N.S. vector
& Myocardium )
3) Vector Triatoma (winged bug, Kissing bug)

4)Infective Metacyclic trypomastigotes in the faeces of the vector

stage (Posterior station transmission)
 46

CNS 2

❖ Life cycle (P. 6):-

➢ The kissing bug (Triatoma) becomes infected by feeding on human or animal
blood that contains bloodstream trypomastigotes (monomorphic).
➢ In the fly's midgut, the ingested trypomastigotes transform into
epimastigotes. The parasites multiply and differentiate in the midgut. The
epimastigotes differentiate into infective metacyclic trypomastigotes in the
hindgut that pass out with faeces near the site of bite wound.
➢ Man is infected when the metacyclic trypomastigotes (I.S) in the faeces of
the vector enter through the bite wound or mucous membrane such as
conjunctiva (posterior station transmission).
➢ Inside the human body, metacyclic trypomastigotes invade cells from a variety
of tissues (R.E.Cs, C.N.S. & heart) where they differentiate into intracellular
amastigotes. The amastigotes multiply by binary fission and differentiate
into trypomastigotes, and then are released into the circulation as bloodstream
trypomastigotes (monomorphic Trypanosoma).
➢ The bloodstream trypomastigotes do not replicate (different from the African
trypanosomes). Replication occurs only when the parasites enter another cell
or are ingested by another vector.
 47

❖ Mode of transmission:-
1) Contamination of the bite wound or mucous membrane by the faeces of the
vector (cyclopropagative transmission).
2) Congenital transmission: T. cruzi can sometimes cross the placenta and infect
the fetus.
3) Blood transfusion and organ tranplantation.
❖ Pathogenesis and symptomatology:-
• Disease: Chagas' disease (American trypanosomiasis).
• The disease has 2 stages:-
1) Acute stage:-
- Short I.P. of about 1 - 2 weeks.
- Common in children.
- Manifested with:-
1. General symptoms: Fever, fatigue, body aches, headache, diarrhea and
vomiting.
2. Hyperplasia of R.E.Cs: Hepatomegaly, splenomegaly and lymph nodes
enlargement.
3. Chagoma: Red firm nodule at the site of vector bite, usually in the face or
near the eye.
4. Romana's sign: Unilateral oedema of the conjunctiva and eye lids after
contamination with the vector's faeces which contain the parasite.
5. Death occurs from myocarditis and meningoencephalitis.
 48

2) Chronic stage:-
- Long I.P. of about many years.
- More common in adults.
- Manifestations depend on the affected organs:-
1. Heart: Myocardial damage and fibrosis  dilated cardiomyopathy 
heart failure and death.
2. Digestive system: Digestive system damage  dilatation of the digestive
tract  megaoesophagus and megacolon accompanied by dysphagia and
constipation  malnutrition and loss of weight.
3. Central nervous system: Neuritis, dementia, confusion, chronic
encephalopathy  paralysis.
 49

Plate 6: Monomorphic trypanosomes life cycle

 50

❖ Diagnosis:-
1) Clinical.

2) Laboratory:-
a- Direct:-
1. Detection of monomorphic Trypanosoma in the blood during the acute stage
by:-
• Microscopic examination of smear stained by Giemsa.
• Culture on N.N.N. medium
• Animal inoculation (Guinea pigs or mice)  blood is examined after
2 weeks for Trypanosoma.
2. Detection of amastigotes (Leishmania form) in tissue aspirate from spleen,
liver, lymph nodes or bone marrow by smear, culture or animal
inoculation.
3. Xenodiagnosis: Laboratory bred winged bug (Triatoma) is allowed to bite
the suspected patient or fed on suspected blood. If Trypanosoma cruzi
are present in the blood, metacyclic trypomastigotes appear in faeces of
the vector.
b- Indirect:
1. I.D. test (Cruzin test): Delayed reaction in +ve cases.
2. Serological tests: IHAT, ELISA & IFAT.
 51

❖ Treatment:-
1) Acute stage of Chagas' disease:-
- 8-aminoquinolines (Primaquine): 15 mg/day for 14 days  active against
blood trypanosomes only.
- Benznidazole (Radanil): 5 mg/kg/day for 2 months.
- Nifurtimox (Lampit): 15 mg/kg/day for 3 - 4 months.
N.B. Benznidazole & Nifurtimox inhibit the intracellular multiplication of the
amastigotes.
2) Chronic stage of Chagas' disease: Medications are not effective for curing the
disease. Treatment depends on the specific signs and symptoms:
a- Heart complications: Treatment may include medication, a pacemaker or
other devices to regulate heart rhythm, surgery or even a heart transplant.
b- Digestive system complications: Treatment may include diet modification,
medication, corticosteroids or in severe cases surgery for megacolon and
megaoesophagus.
❖ Prevention and control:-
1) Treatment of patients.
2) Elimination of animal reservoir host.
3) Control of winged bug.
 52

CNS 2

Family: Reduviidae
Triatoma (TBL)
(Winged bug, kissing bug, Cone-nosed bug)

❖ Geographical distribution: North &

South America.
❖ Life cycle (4 - 48 months):-
➢ Female lays eggs in cracks of wall or
roof of houses that build with palm
leaves or other vegetations (huts).
➢ Eggs hatch in 7 - 14 days  nymphs
feed on blood and moult five times to
develop into adults.
❖ Habits:-
• Obligatory temporary ectoparasites.
• Adult and nymph are blood suckers.
• They bite at night and hide during the day in cracks.
• Attack the face (Kissing bug).
• They show cannibalism  spread of infection among winged bugs.
❖ Medical importance: It transmits Trypanosoma cruzi, the causative protozoa
of Chagas disease. The infection occurs by contamination of the bite wound with
infected feaces of the winged bug (posterior station transmission).
 53

❖ Control:-
1) Physical: Repair of cracks.
2) Chemical: Application of insecticides (as bed bugs).

Myiasis
❖ Definition: Parasitic infection of human or animals tissues with larvae of
dipterous flies.
❖ Geographical distribution: Tropical and subtropical regions.
❖ Classification:
I. According to the biology (habit) of the fly:-
1) Specific myiasis (obligatory sarcobiots): Caused by larvae of
certain flies which bread normally in living tissues of man or animals e.g.:
➢ Dermatobia (human botfly): Female deposits eggs on other blood
sucking insects like mosquitoes or flies (Stomoxys). When such insects
bite man or animals for blood meal, the eggs hatch and larvae penetrate
intact skin  nodular cutaneous myiasis.
➢ Cordylobia: Female deposits eggs on skin or clothes  hatch  larvae
penetrate intact skin  nodular cutaneous myiasis.
➢ Hypoderma (cattle botfly) and Gasterophilus (horse botfly): Eggs are
accidentally deposited on the human intact skin  hatch  larvae 

penetrate and creep under intact skin  creeping eruption.

➢ Oestrus (sheep botfly): Female deposits eggs accidentally in the eye
(conjunctiva) or nose of man  hatch  larvae  ocular and
nasopharyngeal myiasis.
 54

➢ Chrysomyia and Wohlfahrtia: Female deposits eggs on broken skin 

hatch  larvae  penetrate wounded or diseased tissues only (not intact
skin).
2) Semispecific myiasis (obligatory necrobiots): Caused by larvae
of certain flies which mainly bread on decaying matters and animals, but
occasionally bread on living tissues of man or animals if open wounds or
ulcers are present (facultative sarcobiots) e.g. Calliphora, Lucilia and
Sarcophaga.
3) Accidental myiasis: Caused by larvae of some flies that may get in
human tissues accidentally through ingestion of contaminated food or
drink, contamination of wounds or deposition on urethral opening or anal
orifice e.g. Musca, Stomoxys and Fannia.

 N.B: Pseudomyiasis: It is the accidental ingestion of dead or living fly larvae with
no associated pathogenic changes or symptoms.
II. According to affected tissues:
1) Gastric myiasis: Due to ingestion of larvae of some flies which resist
gastric juice, with food or drink e.g. Eristalis larva (rat-tailed larva) in
man and Gastrophilus larva in horse.
2) Intestinal myiasis: Due to either ingestion of eggs or larvae of some
flies with food or drink (e.g. Musca, Calliphora, Lucilia and Sarcophaga)
or deposition of eggs or larvae of other flies (e.g. Fannia) near the anal
orifice during sleep or defecation in open latrines where larvae reach the
intestine through the anus. It presented by nausea, vomiting, abdominal
pain, diarrhoea and may be bloody stool in severe cases.
 55

CNS 2

3) Urogenital myiasis: Due to deposition of eggs of Fannia (latrine

fly):-
• On the urethral opening during sleep or defecation  eggs hatch 

larvae migrate along the urethra  urinary bladder  cystitis, pain,

haematuria or may be urethral obstruction.
• On vaginal opening in female  Larvae enter the vagina  vaginitis.
4) Ocular and nasopharyngeal myiasis: Due to invasion of larvae
of some flies to the conjunctiva and the nose  severe irritation, oedema,
sinusitis and may reach the brain e.g. Oestrus, Wohlfahrtia and
Sarcophaga.
5) Aural myiasis: Due to the attraction of some flies to purulent discharge
from inflammed ears where eggs are deposited  hatch  larvae enter
the external ears  middle and internal ears and may reach the brain 
severe lesion e.g. Wohlfahrtia and Sarcophaga.
6) Cutaneous myiasis:-
A. Intact skin:-
➢ Nodular myiasis: Where larvae remain in one spot causing a fruncle
like lesion (boil) that last for long time e.g. Dermatobia and
Cordylobia.
➢ Creeping eruption: Where larvae of some flies burrow through or
under the skin  forming tunnels e.g. Hypoderma and Gastrophilus.
B. Broken skin (wounds or ulcers): Where larvae of some flies
invade the skin lesions  traumatic cutaneous myiasis e.g. Calliphora,
Lucilia and Sarcophaga.
 56

 N.B. Nosocomial myiasis: Occurs in hospitals. It is frequent as the patients with

open wounds can be infested with larvae if flies are present.

❖ Diagnosis:-
1- Clinical: Appearance of the lesions and symptoms.
2- Laboratory:-
- Identification of larvae by its posterior spiracles.
- Breading of the larvae to adult stage for identification.
- Dermoscopy and ultrasonography may be helpful.
- Serological tests have been used to diagnose ocular myiasis.
❖ Treatment:-
1) Occlusion / suffocation substances in case of nodular or traumatic cutaneous
myiasis by using paraffin, beeswax, mineral oil or tobacco for at least 24 hours
to suffocate larvae in the skin lesion.
2) Manual removal of larvae by forceps under local anaesthesia from skin
wounds, eye, ear and nose.
3) Extraction of larvae after surgical incision in case of creeping eruption.
4) Purges for intestinal and gastric myiasis.
5) Larvicides: Ivermectin is a broad spectrum anti-parasitic agent that may kill
larvae (orally or topically).
❖ Prevention and control:-
1) Window screens and mosquito netting.
2) Insect repellents and insecticides.
3) Adequate protective clothing.
4) Good skin and wound hygiene to keep flies and mosquitoes from reaching the
skin.
5) Covering open wounds and change dressings daily.
6) Covering food.
7) Proper sanitary measures (e.g. remove rubbish from around living areas).
 57

❖ Table 6: Morphological differences between members of

family Muscidae:-
Musca Stomoxys Glossina Glossina
Items domestica calcitrans palpalis moristans
(House fly) (Stable fly) (Tsetse fly) fig.(6 – 1, 2)
Colour Grey Grey fig.(5 - 1) Black Brown
Size 5 - 10 mm 5 - 10 mm 10 - 15 mm
Proboscis - Sucking only - Piercing and - Piercing and sucking
sucking
- Retractile fig.(4 - 3) - Rigid fig.(5 - 3) - Rigid fig.(6 - 4)
Adult

4 segments, median 4 segments, dark 8 segments, 8

dark strip spots median segments,
Abdomen
pale strip transverse
bands
Egg White, banana shaped, laid in batches Larviparous
Triangular, central Cylindrical larva with 2
D-shaped, median button & 3 S- posterior knobs
button & 3M shaped slits
shaped sinuous slits
Larval
posterior
spiracle

Pupa Barrel- shaped Barrel with 2 post.

Knobs
 58

Plate 7: Muscidae members and life cycle

 59

❖ Table 7: Habits, medical importance and control of Muscidae members:-

Items M. domestica S. calcitrans G. palpalis G. morsitans
-Lives in contact with -Attacks domestic -Attracted by moving objects,
man. animals as horses. body heat and smell.
-Feeds on liquid, semi- -Blood suckers. -Blood suckers.
liquid & solid
substances after
Habits

softening with saliva.

-Daytime feeders (diurnal).
-Active in daytime & -Daytime feeders
rest at night. (diurnal). - G. palpalis breeds on soil
-They breed on -They breed on under trees along river banks.
garbage, manure & horse dung. - G. morsitans breeds on soil
human faeces. in open land (jungles).

-Indirect mechanical -Direct mechanical - They are vectors of African

transmission of transmission of sleeping sickness in man:-
Medical importance

parasitic, bacterial and blood parasites as - G.palpalis transmits T.

viral diseases Trypanosoma (T), gambiense West African
leishmania, malaria sleeping sickness
-Accidental myiasis -Accidental myiasis - G. morsitans transmits T.
rhodesiense  East African
-Irritation & annoyance - Painful bite sleeping sickness
-They transmit a fatal disease
in animals  Nagana
-Wire screening of -Wire screening of - Wire screening and wearing
windows & doors animal's stables protective clothes
Prevention & control

- Sanitary disposal of - Sanitary disposal - Clearing of river banks from

garbage, refuse & of horse manure trees and vegetations
manure - Manual collection of pupae
-Proper sewage disposal
- Application of - Application of - Application of insecticides
insecticides insecticides & repellents.

- Health education & - Elimination of wild game

personal hygienic animals (R.H)
measures
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❖ Table 8: Comparison between members of Calliphoridae:-

Calliphorinae Sarcophaginae
Items
Calliphora Lucilia Sarcophaga Wohlfahrtia

Metallic Metallic
Colour Grey with red eyes Grey
blue Green fig.(8 – 1, 2) fig.(9 – 1, 2)
fig.(7 - 1)
Slightly bigger than
Size Bigger than Musca
Musca
Probosci
Non blood sucking
s
Adult

Abdome As Musca Chess-board Dark spots

n pattern

Egg As Musca Larviparous

Triangular complete Rounded incomplete peritreme with 3
peritreme with 3 straight slits
Larval straight slits
posterior
spiracles

-They mainly bread on decaying animals or -Breads on

Habits
plants (obligatory necrobiots) wounded or
diseased tissues
- May bread on wounds (facultative (obligatory
sarcobiots) sacrobiots)

Medical Semispecific myiasis

Specific myiasis
importance
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CNS 2

Cercarial dermatitis
(Swimmer`s itch, Bather`s itch)

❖ Definition and cause: Penetration of human skin by cercariae of non -

human schistosomes (avian and animals). Cercaria penetrates the skin but can`t
go beyond the germinal layer. It is rapidly destroyed by host defense mechanism.
❖ Clinical picture: Dermatitis, irritation, itching, urticarial rash, papules and
2ry bacterial infection.
❖ Diagnosis: History of skin rash after contact with infected water canal.
❖ Treatment :-
• Antipruritics.
• Local antihistaminic.
• Antibiotics for 2ry bacterial infection.
❖ Control :-
• Snail control.
• Avoid swimming in polluted water canals.
• Rapid drying of the skin before evaporation to prevent cercarial
penetration.
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Plate 8: life cycle of unhuman schistosomiasis

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Larva migrans
❖ Definition: It is a condition caused by migrating larvae of non-human
nematodes in unsuitable host. Rarely caused by larvae of human nematodes.
- Larva migrans in man includes: Cutaneous larva migrans and visceral
larva migrans.
Cutaneous larva migrans
(Creeping eruption)
❖ Definition: Invasion of human skin by filariform larvae of dog and cat
hookworms, Ancylostoma caninum & Ancylostoma braziliense. It is a blind
cycle.
❖ Geographical distribution: Cosmopolitan.
❖ Mode of infection:-
• Human infection is caused by penetration of the skin by animal hookworm’s
filariform larvae.
• Infection occurs due to contact with contaminated soil (moist or sandy) with
dog & cat excreta.
• The larvae migrate in the superficial layers of the skin and not go beyond the
basal layer of the skin and keep migrating in the epidermis without
development and rarely reaching the circulation.
❖Other causes of cutaneous larva migrans:-
Hookworms filariform larvae.
Strongyloides stercoralis filariform larvae.
 Cutaneous myasis by larvae of some flies as Gastrophilus and Hypoderma.
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CNS 2

❖ Pathogenesis and symptomatology:-

1) At the site of entry  red itchy papule  tunnel (1-2 mm)  vesicles  2ry
bacterial infection  sever irritation and pruritis.
❖ Diagnosis:-
1) Clinical.
2) Laboratory: Skin biopsy for larval identification.
❖ Treatment:-
1) Antihistaminics.
2) Antibiotics for 2rybacterial infection.
3) Spray of skin by ethyl chloride (local freezing) or carbon dioxide snow which
produce freezing of larvae till death  larvae are lost with epidermal sloughs.
4) Thiabendasole and Ivermectin
❖ Prevention and control:-
 Dog and cats:-
1) Regular examination and treatment of pet animals.
2) Elimination of stray animals.
❖ Protection by:
1) Wearing shoes and avoid walking bare feeted.
2) Keeping dogs and cats off beaches.
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Plate 8: life cycle of cutaneous larva migrans

 66

Family: Demodicidae
Demodex folliculorum
(Hair follicle mite)
❖ Geographical distribution: Cosmopolitan.
❖ General characters fi
• Small (100 - 300µm) elongated, worm like parasite lives in hair follicles.
• Cephalothorax carries capitulum & 4 pairs of short 5 segmented legs.
• Long striated abdomen.
❖ Life cycle (18 - 24 days):-
➢ Adults live in the sebaceous glands and hair follicles
especially the face around the nose, lips, cheeks, eyebrows,
eye lashes, forehead and external ear.
➢ The female lays eggs (20 - 24 eggs)  hatch  larvae (3
pairs of legs) moult  nymph (4 pairs of legs)  adults.
❖ Mode of infection:-
1) Direct contact with patients.
2) Contact with infected towels.

❖ Pathogenesis and symptomatology:-

• Acne like lesions, blepharitis with itching of the eye lids, eye
brows itching, red skin and discomfort.
❖ Diagnosis:-
• Pressing and squeezing the lesion and examining the extruded materials
under microscope for parasitic stages.
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❖ Treatment:-
1) Cleanliness and washing of face with sulfer soap.
2) Local treatment with benzyle benzoate or sulfer ointments.
3) Oral ivermectin and topical permethrin cream.
4) Mercury oxide ointment (1%) for infested eye lashes.

Chigger’s (Jigger’s) disease (TBL)

Definition: Invasion of human skin by female Tunga penetrans or larva of
Trombicula akamushi.

• Geographical distribution: Tropical regions of America, Africa & Far East.

• Causative organism: 1- Tunga penetrans (Sand flea or Chigger's flea).
2- Trombicula akamushi larva, scrub mite, red bug).
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CNS 2

• Mechanism of transmission & mode of infection:

1- Both male and female Tunga penetrans feed on blood. After
fertilization, the female penetrates the skin of man and animals usually the
sole of the foot and interdigital spaces leaving the posterior part of its
abdomen in contact with the outer surface for respiration. The flea
becomes engorged with blood reaching the size of pea and deposits eggs
that fall down on the soil to complete the life cycle.
• Clinical pictures:-
The lesion appears as nodular swelling with ulceration and secondary
bacterial infection and may be tetanus or gas gangrene occurs. Severe pain
occurs if the flea is crushed and eggs are set free into the skin.
• Treatment:
- Removal of the flea with a sterile needle.
- Antiseptic dressings.
- Antibiotics and antihistaminic.
• Prevention and control: Control of fleas and wearing shoes.
2- Both the nymph and the adult live in the soil and feeds on plant juices or
small insects (they are never parasitic).
• After mating, the fertilized female lays eggs  hatch  larvae.
• The larva is ectoparasite of man, rodents and birds. It does not burrow into
the skin or suck blood. It pierces the skin by its capitulum and injects a
salivary secretion containing powerful digestive enzymes that break down
skin cells leads to formation of a tube called histosiphon or stylostome
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CNS 2

• through which the larva feeds on tissue fluid. Once the larva has finished
feeding, it drops to the ground to complete its life cycle  nymph  adult.
❖ Medical importance:-
1) Chigger dermatitis (scrub itch):- Manifested by red spots and severe itching at
the site of larvae bite. Scratching of the skin  breaks the skin  secondary
bacterial infection.
2) Vector of scrub typhus (Tsutsugamushi fever):-
- Causative organism: Rickettsia orientalis (R. tsutsugamushi).
- Reservoir host: Rodents.
- Mode of infection: Bite of the larvae.
- Mechanism of transmission: Infection passes from one generation of the
mite to the next generation by transovarian route.
• Larva feeds on organic debris in the breeding places thus acts as
intermediate host for some tapeworms.
• Season: Spring and autumn.
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Plate 9: life cycle of fleas

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CNS 2

Medical importance of fleas:-

1) Intermediate host of: Hymenolepis diminuta, Dipylidium caninum and
occasionally H. nana.
2) Dermatitis and allergy due to bite of fleas.
3) Disease transmission:
a. Vector of Plague (Black death):-
It is an enzootic disease transmitted from rats to man by rat flea. An
epidemic of human plague occurs after the spread of infection among rats
and their death.
- Causative organism: Yarisinia pestis ( Pasteurella pestis).
- Source of infection: Rat Rat flea Rat Rat flea Man Human flea Man.
- Mechanism of transmission & mode of infection: The bacilli multiply
rapidly and block the gut (proventriculus). When such blocked flea
feeds by biting the skin, the blood regurgitates carrying the organism
to the site of bite (anterior station transmission).The flea is unable

- to feed to reach satisfaction, so it moves rapidly from one host to

another transmitting the disease till it dies from starvation.
Xenopsylla cheopis is the most efficient vector as it easily blocked
and feeds on rodents and human.
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CNS 2

b. Vector of endemic typhus fever (Murine typhus):-

It is an enzootic disease transmitted from rats to man by rat flea.
It does not become epidemic as the rat flea unable to transmit the disease
from man to man.
- Causative organism: Rickettsia mooseri (R. typhi).
- Source of infection: Rat Rat flea Rat Rat flea Man.
- Mechanism of transmission & mode of infection: Rickettsia multiplies in
the epithelial lining of the mid gut of rat flea (X. cheopis is the most
common).The epithelial cells ruptured and organisms are released
into the lumen  pass out with faeces of flea (Posterior station
transmission). Infection occurs by contamination of wounds by
faeces, inhalation of dust containing faeces of infected fleas or
crushing the fleas against bite wound.

Prevention and control of fleas:-

1) Human flea:-
- Cleanliness of dust from floor & carpets by vacuum.
- Application of insecticides & repellents (Naphthaline) for corners, floor
cracks and under carpets.
2) Dog and Cat fleas:-
➢ Dusting animals and their places with insecticides (DDT).
3) Rat fleas:-
➢ Control of rat fleas first before killing rats by dusting rodent burrows with
DDT to avoid their attacking to human as in case of plague.
4) Rat control:-
➢ Using traps.
➢ Rodenticides as warfarin (anticoagulant  internal haemorrhage  death).
➢ Strict quarantine measures against ships coming from endemic places of
plague by fumigation with Calcium cyanide to kill rats and fleas.
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Activity 1:
Label the following diagrams

(a)

(b)