GENERAL PARASITOLOGY

POINTS DETAILS
 Definition: e science that deals with organisms that take up their abodes, temporarily or permanently, on or within
OVERVIEW other living organisms for e purpose of procuring food, & with e relationship of these organisms to their hosts.
 Parasites refer to protozoa, helminthes, & arthropods.
 Adaptation b/w 2 organisms:
ADAPTATION 1. Symbiosis: a permanent association of 2 organisms that can’t exist independently.
2. Mutualism: an association of 2 organisms which benefits both & can live apart.
B/W 2 3. Commensalism: an association which benefits only e parasites while e host is not harmed.
ORGANISMS 4. Parasitism: an association which benefits only e parasites, who r weaker & obtain food & shelter from e host, who
is harmed.
1. Definitive host: an animal that harbors e adult or sexual stage of e parasites.
2. Intermediate host: an animal that part or all of e larval or asexual stage take place.
3. Paratenic host: an animal that harbors e parasites in an arrested state of development.
TYPES OF HOST 4. Incidental host: an animal that is infected by parasites but is not necessary for e parasites’ survival or development.
5. Dead-end host: an animal in which e cycle for transmission of e parasite is such that it can’ be transmitted further.
6. Reservoir host: an animal that harbors parasites to ensure e continuity of e parasites life cycle. It also acts as additional
sources of human infection.
1. Based on choice of e host:
1. Obligate: e parasites r completely dependent upon e host & take up a permanent residence in e host.
2. Facultative: e parasites that r capable of leading both a free & a parasitic life.
2. Based on habitat in e host:
a. Endoparasites: e parasites that live within e body of e host (infection).
b. Ectoparasites: e parasites that live on e outside of e host (infestation).
3. Based on e no. of types of species of e host::
a. Monoxenic: e parasites that act on one species of host only.
TYPES OF
b. Polyxenic: e parasites that act on multiple specie of e host.
PARASITES 4. Based on e period occupying e host:
a. Temporary: e parasite that r free-living during part of its existence & seeks host intermittently to obtain
nourishment.
b. Permanent: e parasites that remain on or in e host from early life until maturity or until death.
5. Others:
a. Incidental: e parasites that establishes itself in a host in which it does not ordinarily live.
b. Pathogenic: e parasites that cause injury to e host by its mechanical, traumatic, or toxic activities.
c. Pseudoparasites: an artifact mistaken for a parasite.
 E endemic parasites depend upon:
a. E presence & habits of a suitable host.
GEOGRAPHIC b. E easy escape from e host.
DISTRIBUTION c. E environmental conditions.
d. E economic & social conditions of e parasites of man.
 E parasites with simple life cycles r > likely to have a cosmopolitan distribution.
1. Inadequate individual & community sanitation.
PARASITIC 2. Low standards of living & ignorance.
SPREADING 3. Contamination of water.
FACTORS 4. Migrations of populations throughout e world.
5. Presence of optimal condition of temperature & humidity as well as moisturity.
 E transmission of parasites involves:
1. A source of infection.
FACRTORS
2. A mode of transmission.
PARASITIC 3. E presence of suitable host.
TRANSMISSION  E modes of transmission r either direct or indirect involving food, water, vectors & transplacentaly.
 E chance of transmission & infection depend on:
MODES
1. E parasites: its ability to be transmitted.
2. E host: depend on e host’s habit, communal associations & e resistance of e wall.
1. Prepatent: no symptoms & e parasites r not detected.
HUMAN 2. Patent: symptoms present & e parasites r seen.
CARRIER STATE 3. Acute: increased symptoms present & e parasites r seen in a very short time.
4. Chronic: mild & reduced symptoms present & e parasites r seen in a long time.
1. Pathogenecity depends on: 2. Parasites cause pathology by:
 E no. of parasites & their tissue tropism. 1. Invasion & destruction of host cells by e parasite
 E various specific mechanisms of tissue damage. itself.
PATHOLOGY 2. Exerting e mechanical effects.
 E worm burden or intensity of e infection.
 Tissue specificity. 3. Inflammatory response to e parasite & its products.
4. Competition for host nutrients.
3. E ability of e host to withstand infection by a parasites is due to:
1. Physiochemical barriers.
2. Factors that confer innate or natural resistance.
IMMUNITY 3. E specific immunity acquired from previous infection with e parasites.
4. E host specificity.
5. E genetic influence over susceptibility or resistance.
6. E age & e nutritional status.
PREVENTION 1. Reduction of e sources of infection in human by therapeutic measures.
2. Education in personal prophylaxis to prevent dissemination of infection.
3. Sanitary control of water, food, living, & working conditions & waste disposal.
4. Destruction or control of reservoir hosts & vectors.
 5. Erection of biologic barriers to e transmission of e parasites.

PARASITIC PROTOZOA
POINTS DETAILS
4. Protozoa: Unicellular animals that occur singly or in colony formation.
OVERVIEW 5. Most r free-living, but some r parasitic.
1. Functions:
 Movement: By e action of prolongations of ectoplasm known as pseudopodia, cilia, flagella,
or undulating membrane.
ECTOPLASM
 Ingestion of food: Food may be taken from any part of ectoplasm or at any particular point
Thin outer layer
such as peristome. Peristome → Cystotome → Cytopharynx → Endoplasm.
 Excretion
 Respiration
 Protection
2. Functions:
1. Nutrition: digestion & absorption.
2. Reproduction: due to e presence of nucleus.
3. Contains:
1. Food vacuoles & reserves.
ENDOPLASM
2. Foreign bodies.
MORPHOLOGY Voluminous inner
3. Contractile vacuoles: function in e regulation of osmotic pressure & e elimination of waste
thick layer.
Protoplasm: coarsely or material.
finely granular 4. Chromatoidal bodies.
substances. 5. Kinetoplast (in flagellates):
1. Parabasal body.
2. Blepharoplast: where e flagella arise.
4. Consists of:
a. Nucleus:
1. Essential for maintaining & reproducing life.
2. Near e centre of e nucleus is a deeply staining karyosome (functions in promitosis).
3. Centrosome may also present.
b. Nuclear membrane:
CLEOPLASM
 Envelops fine reticulum filled with nuclear sap & chromatin.
 In vesicular nucleus, e chromatin is concentrated in a single mass.
5. 2 types (in infusoria):
1. Macronucleus: concerns with vegetative activities & metabolic activities.
2. Micronucleus: concerns with reproduction.
6. E arrangement of chromatin & karyosome is pathognomonic, differentiation of species.
7. Functions: to obtain food & to react to physical & chemical stimuli.
8. Types of locomotion:
 Pseudopodia: produce ameboid movement such as in Sarcodina.
MOVEMENT
 Cilia: rhythmically propel e organisms such as Infusoria.
 Flagella & undulating membrane: permit e organisms to move in all direction, such as
Mastigophora.
1. Aerobics respire directly or by taking in oxygen & expelling carbon dioxide e.g. malaria &
leishmania.
RESPIRATION
2. Anaerobics respire indirectly by using oxygen liberated from complex substances by e action of
ezymes e.g. most parasites.
3. Feed on already formed food. 2 types:
PHYSIOLOGY  Ingestion of solid food particles through cystostome & engulfment by pseudopodia.
NUTRITION  Absorption of liquid food from tissues or fluids by osmosis. E.g. blood & tissue flagellates.
4. Requirements r: inorganic salts, carbohydrates, fats, proteins, & vitamins.
5. Undigested particles R extruded through ectoplasm or special anal opening called cytopyge.
1. Excretion is effected through:
 Osmosis or effusion through ectoplasm.
EXCRETION
 Precipitation or deposition in endoplasm as in malarial pigments.
 Excretory or contractile vacuoles burst on surface of ectoplasm.
2. Protozoa secretes digestive ferments, pigments, & material for resistant cyst wall.
SECRETION 3. Protozoa cause pathology by secreting proteolytic enzymes, haemolysins, cytolysins, toxic, &
antigenic substances.
1. In cystic stage, protozoa secrete a resistant membranous wall & undergo nuclear division.
2. Purposes of encystation:
ENCYSTATION  For survival outside e host.
 For protection against digestive juice.
 To constitute e infective stage.
REPRODUCTION 1. Asexual reproduction:
 Simple binary fission as in amoebae, ciliates (transverse), & flagella (longitudinal).
 Endodiagony as in toxoplasma: cell undergoes single internal budding results in e formation of 2 daughter cells.
 Schizogony as in sporozoa.
 Endopologny as in toxoplasma.
2. Sexual reproduction: (syngamy) – sexual union of 2 cells:
1. Conjugation: temporary union b/w 2 ciliates for exchange of nuclear membrane. No increase in no.
2. Copulation: in spores. Male & females gametes → Zygotes → Oocysts containing sporozoites. Also known as
 sporogony.
3. Nuclear division may be amitotic, mitotic, or modified.
a. In simple life cycle & transmission in intestinal & luminal protozoa, parasites pass directly from host to host through
food or water. E infective stage r cysts & oocysts containing sporozoites.
TRANSMISSION b. In indirect life cycle protozoa, alternate existence in 2 hosts, human & arthropods r required:
a. Cyclic development occurs in blood sucking insects before it attains e infective stage.
b. Temperature & humidity affects abundance of insects vectors & developmental cycle of parasites in insect.
 Modes of infection:
 Ingestion: all protozoal cysts as in E. coli.
 Inhalation as in P. carinii & Cryptosporidium.
 Vectors bite as in malaria & leishmania parasites.
INFECTION  Sexual intercourse as in T. vaginalis.
 Transplacental as in T. gondii.
 Blood transfusion as in malarial parasites.
 Organ transplantation as in T. gondii.
 Protozoa multiply in their hosts & infection by only few parasites can initiate disease.
PATHOLOGY  Invasion & destruction of cells & tissues by parasites or its products
 Tissue damage secondary to immune response or immunopathology.
 Clinically depends on suggestive signs & symptoms.
 Laboratory diagnosis confirms clinical diagnosis. It identifies parasites in intestinal contents o in blood tissues by:
1. Direct smear.
DIAGNOSIS 2. Concentration methods.
3. Culture.
4. Animal inoculation.
5. Serological tests.
 E prevention:
1. Block channel of transmission.
2. Protect susceptible persons.
PREVENTION 3. Precaution specific for each disease:
 Intestinal protozoa & helminths r problems of satiation & hygiene.
 Blood & tissue protozoa can be controlled by control of vectors.
 Entamoeba histylotica
POINTS DETAILS
 Ent: intestinal lumen & hystolytica: lysis of tissue.
 Disease: Amebiasis, amebic dysentery, & amebic hepatitis
 Geographical distrubution: in cosmopolitan area – pathogenic & non-pathogenic.
 Strains:
a. E. hartmanni:
OVERVIEW
 Small strain, cyst 5-8 µm, & trophozoites 6-10µm morphologically identical.
 Non-pathogenic, a commensal in lumen of intestine.
b. E. hystilotica:
1. Has a commensal phase.
2. Pathogenic due to lowered bacterial resistance, bacterial & viral infection, change of diet, & etc.
1. Incidence 0.2% to 50% & directly correlated with sanitary conditions which is poor in tropical & subtropical areas.
2. Prevalent in people living under crowded conditions.
3. Inadequate toilet & sanitary facilities such as in mentals hospitals & migrant labor camps.
EPIDEMIOLOGY 4. Generally poor socioeconomic circumstances.
5. Also high in male homosexuals (as high as 25% to 35%) due to oral & anal intercourse.
6. Amoebic liver abscess, high in Mexico, India, Indonesia, & some African counteries.
 Size: 10 - 60µm, majority 15 to 30µm.
 Ectoplasm: wide, clear, refractile, hyaline body, constitutes about 1/3 of e entire organism.
 Ectoplasmic pseudopodia: thin & fingerlike-shape for movement.
 Endoplasm: fine & granular w/o bacteria & foreign particles but sometimes contain RBC in
invasive stage.
TROPHOZOIT  Nucleus: single, eccentric, & may be faintly discerned as a finely granular ring.
E  Nuclear membrane: clearly defined by hematoxylin staining which is lined with uniform &
closely packed fine granules of chromatin.
 Karyosome: small, deeply stained, & centrally located which consists of several granules in a
halo-like capsule, from which a lining network of fine fibrils radiates toward e periphery of e
nucleus.
 Easily destroyed than cyst. Survive up to 5 hours at 37oC & 96 hours at 5oC.
 Colorless round or oval cells that r smaller than trophozoites but larger than e cyst.
MORPHOLOGY  Intermediate stage with no food inclusions.
PRECYST
 Pseudopodial action is sluggish, & there is no progressive movement.
 Becomes cyst quickly.
 Shape: round or oval, & slightly asymmetrical hyaline bodies.
 Size: ranging from 10 to 20 µm in diameter.
 Cell wall: smooth, refractile, & nonstaining about 0.5µm thick.
 Cytoplasm of young cyst: contains vacuoles with glycogen & dark-staining, refractive, sausage-
shaped bars with rounded end chromatoid bodies (contain RNA, DNA, phosphate, & stored
CYST
food) – disappear when e cyst matures.
 Nucleus:
1. Immature cyst: has a single nucleus, about 1/3 of its diameter.
2. Mature cyst: has 4 smaller nuclei.
 Cyst with 1 to 4 nuclei may be passed in e feces.
1. Reproduction:
a. Excystation:
 In cyst form via simple binary fission.
 Each metacystic amoeba produces 8 amebulae.
b. Encystation:
 Occurs in e lumen of gut.
 Essential for transmission because only mature cyst is infective.
2. Respiration:
 Anaerobes because grow best under reduced oxygen tension. However, readily consume oxygen when provided.
PHYSIOLOGY  Have iron-sulfur proteins which r important electron carriers in e respiratory chain.
 Substrates for respiration: D-glucose, D-galactose, alcohols, & L-serine.
3. Nutrition:
 Absorb nourishment from e tissue dissolved by its cytolitic enzymes.
 Ingest RBC & fragments of tissues through pseudopodial encirclement.
 Consume bacterial & other particulate elements from e intestinal contents.
4. Waste disposal:
 Soluble or granular waste products r eliminated in excretory vacuoles at e surface.
 Undigested particles r egested through cytoplasmic protuberances.
 E main source of infection is cyst passing chronic patients or asymptomatic carriers.
 Mode of transmission:
TRANSMISSION & 1. Water & vegetable contaminated with infective feces or night soil.
2. Food contaminated by flies & hands of infected food handlers.
INFECTION 3. Wells & springs which is contaminated with local sewage.
4. Direct transmission through homosexuality.
5. Poor sanitary & sewage control.
PATHOLOGY SITES 1. Primary lesions:
 Wall of lumen of colon especially in cecal & sigmoidorectal regions where colonic flow
is low.
 Less frequently involves ilio-cecal valve, ascending colon, rectum, sigmoid, & hepatic
 flexture of transverse colon or appendix.
2. Secondary lesions: liver is most frequently involved, but nearly all organ may be infected.
 Depends on: 2. E virulence & invasiveness of e amebic
1. E resistance of e host, depens on: strain:
a. Innate immunity. 3. E condition in e intestinal tract, whish is
PATHOGENECITY b. E state of infection. facilitated by:
c. Freedom from infectious & a. Carbohydrate diet.
debilitating diseases. b. Physical & chemical injury of e mucosa.
c. Stasis & bacterial flora.
 Early lesion: tiny area of necrosis n e superficial mucosa or a small nodular elevation with a
minute opening that leads to a flask-shaped cavity containing cytolyzed cells, mucus, &
amebas.
 In acute or chronic dysentry: rapid lateral & downward extension of e ulcerative process to
both superficial & deep layers of e intestine.
GROSS LESION
 E lesion: vary from small, punctate, crariform ulcers distributed over e mucosa to large,
irregular ulcers with undermined edges & necrotic gelatinous bases, often covered with a
yellow, purulent, leathery membrane.
 Communicating sinuses produce honeycombed areas beneath intact mucosa that may slough
off & exposing large necrotic areas.
 E histologic changes (regenerative rather than inflammatory):
1. Histolysis. 3. Petechial hemorrhages.
2. Thrombosis of e capillaries. 4. Rounded-cell infiltration & necrosis.
 E ameba:
HISTOPATHO
 Destroy PMNs results in e scarcity of e cells.
 May be found in e floor of e ulcer, particularly at e base of e intestinal glands or
scattered through e tissues.
 E ulceration: extensive & often accompanied by 2o bacterial infection.
 E complications r:
1. Appendicitis: nongangrenous, slightly thickened, has irregular superficial ulcers in e
mucosa.
2. Intestinal perforation: occurs frequently in cecum.
INTESTINAL
3. Hemorrhage: a massive one can be produced by e erosion of a large blood vessel.
(Local intestinal
4. Granulomas:
amoebiasis)
 Firmly, painful, movable, nodular, inflammatory thickened, & occurs mostly in
cecum or sigmoid.
 Histologically they showncollagen, fibroblasts, & chronic inflammatory elements.
5. Pseudopolyposis & stricture.
1. Hepatic amebiasis:
 Tissue forms reach e liver as emboli in portal circulation & direct extension from
COMPLICATIONS amoebic ulcer in hepatic flexture of transverse colon.
 E abscess:
 Small, oval, or rounded mass with grayish brown matrix of necrosed hepatic cells.
 E centre liquefies, e wall thickens, & e contents become viscid chocolate, reddish,
or cream-colored mass of auto-lysed hepatic cells, RBCs, bile, fat, & etc.
EXTRA –  May be single or multiple.
INTESTINAL
 Commonest site is Rt. dome (85%).
2. Pulmonary amebiasis:
 Usually results from direct extension of a hepatic abscess & < frequently from emboli.
 Often 2o infected with bacteria & results in peumonic consolidation in lower Rt. lung.
3. Others:
 Other abscess can be observed in brain, spleen, & anarectal region.
 Ulcerative, vaginitis, cervitis, & involvement of penis may occur in homosexual.
 At onset: vague abdominal discomfort, weakness, & neurasthenia.
 Next stage: malaise, constipation alternate with diarrhea, & irregular colicky abdominalpain with or w/o abdominal
tenderness.
 Acute intestinal amebiasis (incubation period of 1 to 14 weeks):
1. Severe dysentry with numerous small stools containingblood, mucus, & necrotic mucosa.
CLINICAL 2. Acute abdominal pain & tenderness as well as fever.
3. Dehydration, toxemia, & prostration.
MANIFESTATION  Chronic amebiasis:
1. Recurrent attacks of dysentry with intervening periods of gastrointestinal disturbances & constipation.
2. Localized abdominal tenderness, hepatomegally, weight loss, & weakness.
 Amebic hepatitis:
1. Enlarged & tender liver with pain in e upper Rt. hypochondrium & radiate to e Rt. shoulder.
2. Leukocytosis is present as well as increased in PMNs, ESR, & alkaline phosphatase.
1. Identification of e parasites in e feces or tissues for 3 successive days.
2. Identification of traveling history & general signs & symptoms on physical examination, sigmoidoscopy, &
DIAGNOSIS roentgenology.
3. Microscopic examination of aspired or biopsied specimens.
4. Serological test via IHA or ELISA.
1. Remain in bed & receive a bland high protein & high vitamin dietwith adequate fluid.
TREATMENT 2. Drugs such as metronidazole, iodoquinol, dehydrometine or emietine, & tetracycline.
PREVENTION 1. Clean & proper personal hygiene.
2. Effective environmental sanitation to prevent water & food contamination.
3. Sanitary methods of sewage disposal.
 4. A properly safeguarded, filtered water supply as well as boiling water.
5. Control of insects with insecticides.

LIFE CYCLE OF Entamoeba histylotica

Infection by Entamoeba histolytica occurs by ingestion of mature cysts (1) in fecally

contaminated food, water, or hands. Excystation (2) occurs in the small intestine and
trophozoites (3) are released, which migrate to the large intestine. The trophozoites multiply by
binary fission and produce cysts (4) , which are passed in the feces. Because of the protection
conferred by their walls, the cysts can survive days to weeks in the external environment and are
responsible for transmission. (Trophozoites can also be passed in diarrheal stools, but are
rapidly destroyed once outside the body, and if ingested would not survive exposure to the
gastric environment.) In many cases, the trophozoites remain confined to the intestinal lumen
(A: non-invasive infection) of individuals who are thus asymptomatic carriers and cysts passers.
In some patients the trophozoites invade the intestinal mucosa (B: intestinal disease), or,
through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (C: extra-
intestinal disease), with resultant pathologic manifestations. It has been established that the
invasive and noninvasive forms represent separate species, respectively E. histolytica and E.
dispar, which are morphologically indistinguishable. Transmission can also occur through fecal
exposure during sexual contact (in which case not only cysts, but also trophozoites could prove
infective).
 Balantidium coli
POINTS DETAILS
OVERVIEW  Balantidium: little bag.
 Disease: Balantidiasis balantidosis, balitidial dysentry.
 Geographical distribution: Worldwide.
 Largest intestinal protozoa & e only pathogenic ciliate.
EPIDEMIOLOGY  E incidence is low in human but higher in pigs (65% – 91%).
 Pigs r important source of human infection:
1. Persons engaged in occupation & living in areas closely associated with pigs r at high risks.
2. Faecal-rout is e commonest mode of transmission.
3. Zoonosis.
MORPHOLOGY TROPHOZOITE  Color: grayish green & unstained trophozoite.
 Size: 60 x 45 µm (50-80 by 40-60 µm).
 Shape: like a sac enclosed in a delicate protective pellicle covered with spiral longitudinal
rows of cilia.
 At ant. end, peristome & cytostom continue in e cytopharynx r lined wth long cilia adapted for
procuring food.
 At post. end, an excretory opening e cytopyg is found for discharged of watse material.
 Cytoplasm:
 2 contractile vocuoles.
 Large, elongated, kidney-shaped macronucleus.
 Small, subspherical micronucleus.
 Numerous food vocuoles.
CYST  E trophozoite forms resistant cyst, double walled.
 Size: 52-55 µm (45-65 µm).
 Color & shape: unstained, greenish yellow subspherical or oval cyst.
 Shows only macronucleus, contractile vocuoles, & cilia.
PHYSIOLOGY 1. Movement: moves actively by e rhythmic motion of its cilia.
2. Reproduction: divides by transverse binry fission to form 2 new individual.
3. Resistance: trophozoites do not survive long extracorporeally, but cyst may remain viable for several weeks.
PATHOLOGY SITES  Lumen, mucosa, & submucosa of large intestine, especially in e cecal region & terminal
portion of ileum.
PATHOGENECITY  Produce hyaluronidase which facilitates tissues invasion in mucosa & submucosa of e
large intestine.
 E multiplying parasites forms nests & small abscesses that breakdown into oval, irregular
ulcers with red, undermined edges.
 Severity varies from simple catarrhal hyperaemia to marked ulceration.
HISTOPATHO  Presence of hemorrhagic areas, round-cell inflitration, abscesses, necrotic ulcers, &
invading parasites.
 Predominating reaction being mononuclaer unless 2o bacterial infection is present.
PROGNOSIS  Prognosis depends on:
1. E severity of e infection.
2. E response to e treatment.
 Prognosis is good in asymptomatic & chronic infections.
CLINICAL  Many patients r asymptomatic carriers of infection.
MANIFESTATION  In acute infection:
1. 6 – 15 liquid stools per day.
2. Present with mucus, blood, & pus.
 In chronic disease:
1. Intermittent diarrhea alternating with constipation.
2. Present of tender colon, anaemia, & cachexia.
DIAGNOSIS 1. Identification of trophozoites in diarrheic stools, < frequently cysts is found in formed stools.
2. Sigmoidoscope: used in patient with sigmoidorectal infection.
TREATMENT  Treatment by oxytetracycline, iodoquinol or metronidazol.
PREVENTION  Same as in prevention of amoebic dysentry.

The Book of Gifts (Kitab Al-Hibat)

Muslim: Book 12: Hadith 3949

Umar b. Khattab (Allah be pleased with him) reported: I donated a pedigree horse in the path of Allah. Its possesser made it languish. I thought
that he would sell it at a cheap price. I asked Allah's Menengsr (May peace be upon him) about it, whereupon he said: Don't buy it and do not
get back your charity, for one who gets back the charity is like a dog who swallows its vomit. This hadith has been narrated on the authority of
Malik b. Anas with the same chain of transmitters but with this addition:" Don't buy that even if he gives you for one dirham."
 LIFE CYCLE OF Balantidum coli

Cysts are the parasite stage responsible for transmission of balantidiasis .  The host most often
acquires the cyst through ingestion of contaminated food or water .  Following ingestion,
excystation occurs in the small intestine, and the trophozoites colonize the large intestine .  The
trophozoites reside in the lumen of the large intestine of humans and animals, where they replicate by
binary fission, during which conjugation may occur .  Trophozoites undergo encystation to produce
infective cysts .  Some trophozoites invade the wall of the colon and multiply.  Some return to
lumen and disintegrate.  Mature cysts are passed with feces

Giardia lambia
POINTS DETAILS
 OVERVIEW  Disease: Giardiasis, lambiasis.  Hosts:
 Geographical distribution: 1. Man, especially children, less in adult.
1. Worldwide: > prevalent in developing world. 2. Mice & rat can be infected.
2. > common in warm than in cool climate.
MORPHOLOGY TROPHOZOITE  Size: 7 – 22 µm, average: 14 – 15 µm.
 Shape: bilaterally symmetrical, pear-shaped flagellate, broad & rounded anterior, tapering
posterior end, & convex doral surface.
 Sucking disk: ovoid, concave, occupies about ¾ of e flat ventral suface, bordered by e curved
intracytoplasmic portion of ant. flagella axoneme, & modified for attachment (mechanical
irritation). Also used to resist ordinary peristalsis.
 Axonemes: straight, closely approximated, run parallel to each other dividing e body into 2
halves through e whole length.
 Others: 2 nuclei with 2 large central karyosomes, 2 blepharoplasts, 2 deeply coma-shaped
staining bars considered to be parabasal bodies, & 4 pairs of flagella.
 Could be seen in diarrheic stool.
CYST  Size: 10 – 14 µm.
 Shape: elipsoidal with a smooth, well-defined wall.
 Contains 2 or 4 nuclei, axostyle which r visible as 2 rods dividing cyst, parabasal bodies across
axostyle, & remnant of flagellae which r coiled.
 Under moist condition, cysts remain viable for months outside e host.
 More commonly seen in stool.
PHYSIOLOGY 1. Motion: e lashing flagella propel e trophozoite with a rapid, jerky, & twisting motion.
2. Nutrition: food is absorbed through intestinal content from epithelial cells through sucking disk.
3. Reproduction:
 Multiplication occurs by mitotic division (longitudinal binary fission) during encystment, followed by
separation into daughter trophozoites after excystation.
 An alkaline environment, increased by achlohydria, & rich carbohydrate diet favor multiplication.
TRANSMISSION &  Through food & water contaminated with sewage, flies, or food handlers, & hand to mouth.
INFECTION  Many outbreaks have been observed all over e world including in day care centre & nurseries, most probably due to
contaminated water.
 It is > common in population practicing anal-oral intercourse.
PATHOLOGY SITES 1. Small intestine especially duodenum, jejunum, & upper ileum.
2. Swim freely & rapidly in spiral motion & attached to intestinal epithelium.
3. Bile duct & gall bladder occasionally invaded.
PATHOGENESIS  Only small no. of cyst r needed to initiate infection, as few as 10 cysts r able to produce
infection.
 Excystation occurs in e upper regions of e small intestine, where e parasites multiply by
simple binary fission.
 Prepatent period ranged from 6 – 15 days & usually lasted up to 41 days.
 Light infection r usually asymptomatic.
HISTOPATHO  Mechanism of mucosal injury:
1. Attachment of trophozoite to e epithelium can disrupt & distort microvilli.
2. Trophozoites produce cytopathic substances responsible for this disruption of epithelial
structure & function (proteinases & surface lectin).
3. Mucosal damage occurs by both mechanical & biochemical factors.
 Histologically:
1. Mast cell mediated reactions contributes to e inflammation & edema seen in e mucosa
& lamina propia.
2. There is shortening of e villi & a cellular infiltration of e lamina propia of e mucous
membrane.
COMPLICATIONS 1. Attachment to mucous membrane → inflammation & hyperaemia → diarrhea.
2. Associated with inability to absorb fats & vitamin A → malabsorption → fatty stool or steatorrhea.
3. Duodenitis → duodenal ulcer → hunger pains → picture of peptic ulcer.
4. Extra intestinal invasion → cholecytitis.
5. Motility disturbance causes by parasites → abdominal cramps.
CLINICAL 1. Diarrheic syndrome in children & adults: 2. Dyspeptic syndrome in adults stimulates gall bladder dyspepsia:
MANIFESTATION  Recurring or persistent diarrhea  Anorexia, nausea, & vomiting.
 Irregular bowel movements.  Epigastric pain.
 Epigastric discomfort & pain.  Alternating diarrhea & constipation.
 Flatulence & loss of weight.  Flatulence.
DIAGNOSIS 1. Clinical picture. 3. Duodenal aspiration: if no cysts r
2. Stool examination: passed (contents may be
a. Macroscopically: Steatorrhea – pale yellow & loose stool, lentil soup cultured). Duodenal content may
appearance, & contains excessive mucous & fat. be sampled by e “Enterotest
b. Microscopically: multiple cysts, no RBCs or Charcoat Leyden crystals, capsule” which is gelatin capsule
& presence of fat globules. In diarrheic stools, it is usual to find only containing a coiled thread.
trophozoites.
TREATMENT 1. Metronidazol (flagyl). 2. Tinidazol.

PREVENTION 1. Treatment of cases. 5. Proper water supplies.

2. Personal hygiene. 6. Chlorinating water does not kill e cyst, water should be
3. Fly control. boiled or filtered to remove e parasite.
4. Proper sewage disposal.
 LIFE CYCLE OF Giardia lambia

Cysts are resistant forms and are responsible for transmission of giardiasis.  Both cysts and trophozoites
can be found in the feces (diagnostic stages) .  The cysts are hardy, can survive several months in cold
water.  Infection occurs by the ingestion of cysts in contaminated water, food, or by the fecal-oral route
(hands or fomites) .  In the small intestine, excystation releases trophozoites (each cyst produces two
trophozoites) .  Trophozoites multiply by longitudinal binary fission remaining in the lumen of the
proximal small bowel where they can be free or attached to the mucosa by a ventral sucking disk . 
Encystation occurs as the parasites transit toward the colon.  The cyst is the stage found most commonly
in non-diarrheal feces .  Because the cysts are infectious when passed in the stool or shortly afterward,
person-to-person transmission is possible.  While animals are infected with Giardia, their importance as a
reservoir is unclear.
 OPPORTUNISTIC INFECTIONS
Genus Cryptosporidium
POINTS DETAILS
 Disease: cryptosporidiosis.
 In human involved Cryptosporidium parvum.
 Parasites of rodents, birds, reptiles, fish, & cattle.
 Geographical distribution: worldwide in travelers & day care centres.
OVERVIEW
 Can occur as water born outbreak.
 Host: Definitive host varies according to species but w/o intermediate host.
1. Young children.
2. AIDS patients.
 Sporulated oocyst with 2 x 4 – 5 µm.
 Rounded or oval.
 Contains 4 slender fusiform sporozoites.
MORPHOLOGY  Difficult to distinguish fromyeasts in wet mount preparations.
OOCYST
 2 types:
1. Thin-walled: releases sporozoites in situ to initiate autoinfection.
2. Thick-walled: excreted.
 Iniated by ingestion of sporulated oocyst.
TRANSMISSION &
 Excystation in upper GIT.
INFECTION  Sporozoites invade e epithelial cells of ileum.
 GIT & respiratory tract:
1. On brush border.
2. Just under e surface membrane.
SITES
3. Not in cell proper.
4. Free in crypt.
PATHOLOGY  May be in bile & pancretic ducts & gallbladder.
 Cryposporidial meronts & oocyst r difficult to detect on e surface mucosal cells because
they r small.
PATHOGENECITY
 E prepatent period ranges from 5 to 21 days, & e duration of sheddig can be > than a month
in e normal hosts & much longer in immunocompromised hosts.
1. Immunocompetent individuals:
 Gartroenteritis: leads to self-limiting diarrhea for 3 – 10 days.
CLINICAL 2. Immunocompromised individuals:
MANIFESTATION  Persistent, cholera-like diarrhea with vomiting: can lead to fatal outcome in children.
 Protracted watery diarrhea.
 Cramping abdominal pain, fever, & dehydration.
1. Stool examination:
 To identify oocysts.
 If large no. of oocysts r not being excreted, a sucrose flotation or formalin-ether or formalyn ethyl-acetate
DIAGNOSIS concentration procedures with subsequent staining is recommended.
 Acid-fast stain leads to bright red or pink oval or rounded bodies against green background.
2. IgG & IgM demonstration by ELISA or IFA after acute infection.
3. Indirect or direct fluorescent Ab techniques (FAT) for staining oocyst in stools.
 Mainly supportive to sustain & improve general condition.
TREATMENT  Spiramycin 1 gm t.d.s. for 2 weeks.
1. Good personal hygiene.
2. Avoid contact with infected hosts.
3. Proper disposal of feces.
PREVENTION 4. Clean drinking water supply.
5. For veterinary, medical, & laboratory personnel:
a. Avoid contact with infected materials by using gloves, gowns, & hand-washing.
b. Potentially contaminated instruments & equipment should be autoclaved or heated.

Times of the Prayers

Bukhari :: Book 1 :: Volume 10 :: Hadith 505
Narrated 'Abdullah:

I asked the Prophet "Which deed is the dearest to Allah?" He replied, "To offer the prayers at their early stated
fixed times." I asked, "What is the next (in goodness)?" He replied, "To be good and dutiful to your parents I
again asked, "What is the next (in goodness)?" He replied, 'To participate in Jihad (religious fighting) in Allah's
cause." 'Abdullah added, "I asked only that much and if I had asked more, the Prophet would have told me
more."
 LIFE CYCLE OF Cryptosporidium

Sporulated oocysts, containing 4 sporozoites, are excreted by the infected host through feces and possibly
other routes such as respiratory secretions .  Transmission of Cryptosporidium parvum occurs mainly
through contact with contaminated water (e.g., drinking or recreational water).  Occasionally food
sources, such as chicken salad, may serve as vehicles for transmission.  Many outbreaks in the United
States have occurred in waterparks, community swimming pools, and day care centers.  Zoonotic
transmission of C. parvum occurs through exposure to infected animals or exposure to water
contaminated by feces of infected animals .  Following ingestion (and possibly inhalation) by a
suitable host , excystation occurs.  The sporozoites are released and parasitize epithelial cells ( ,
) of the gastrointestinal tract or other tissues such as the respiratory tract.  In these cells, the parasites
undergo asexual multiplication (schizogony or merogony) ( , , ) and then sexual multiplication
(gametogony) producing microgamonts (male) and macrogamonts (female) .  Upon fertilization of
the macrogamonts by the microgametes ( ), oocysts ( , ) develop that sporulate in the infected
host.  Two different types of oocysts are produced, the thick-walled, which is commonly excreted from
the host , and the thin-walled oocyst , which is primarily involved in autoinfection.  Oocysts are
infective upon excretion, thus permitting direct and immediate fecal-oral transmission.  
Note that oocysts of Cyclospora cayetanensis, another important coccidian parasite, are unsporulated at
the time of excretion and do not become infective until sporulation is completed.
 Isospora beli
POINTS DETAILS
 Disease: human coccidiasis & isoporiasis.
 Geographical distribution:
1. Worldwide, Central & South America, Africa, & South East Asia.
2. Egypt: 3 cases reported, 1 from Ain Shams University Hospital.
OVERVIEW  Definitive hosts:
1. E only known coccidian for which man is DH.
2. Opportunistic infection in patients with AIDS.
3. No intermediate host.
 Normally found in e stools.
OOCYST  Shape: elongated or ovoid with a typical ellipsoidal shape
 Size: 25 – 33 µm by 12 – 16 µm.
MORPHOLOGY  When excreted, e oocyts r immature & contain 1 sporoblast (granular cytoplasm within a
IN FRESH smooth, colorless, 2 layered-wall & unsporulated).
FECES  Division of oocyst into 2 sporoblasts secretes a cyst wall & becoming sporocyst.
 Further division produces 4 elongated nucleated sporozoites.
 Intestinal epithelium (e cycle):
1. Asexual schizogony.
SITES 2. Gametogony.
3. Oocyst formation, discharged in any stage of maturation.
4. Sporulation needs few days.
PATHOLOGY
 Accidental hand-to-mouth ingestion of sporulated oocyst.
MODE OF INFECTION
 Through food or water contamination.
 Malabsorption: mucosal lesions of shortened villi, hypertrophied crypts, & infiltration
LESION
of lamia propia with eosinophils, polys, & round cells.
 Prepatent period: 7 days, oocysts r discharged for 9 – 16 days & up to 120 days in one case.
 Majority symptomless: self-limiting infection.
CLINICAL  Mild gastrointestinal distress: nausea, pain, & chronic diarrhea.
MANIFESTATION  Severe dysentry or diarrhea especially in AIDS patients.
 Fever, malaise, diarrhea, & abdominal pain.
 Loss fecal fat suggestive of malabsorption which results in weight loss & even fatal outcome.
1. Intestinal biopsy: by demonstrating oocysts in e feces, oocysts or sporocysts in duodenal contents, & intracellular
stages of e parasites.
2. Stool examination:
DIAGNOSIS  Positive only in heavy infection.
 Concentration methods r required.
 Unless iodine stained oocysts, very difficult to recognize.
1. Rest & balanced diet.
2. it is self-limiting.
TREATMENT 3. Specific treatment is unknown but immunosuppressed indviduals can be treated by trimethprim &
sulphamethoxazole mixture.
PREVENTION  Similar to E. hystilotica.

At time of excretion, the immature oocyst contains usually one

sporoblast (more rarely two) .  In further maturation after
excretion, the sporoblast divides in two (the oocyst now contains
two sporoblasts); the sporoblasts secrete a cyst wall, thus
becoming sporocysts; and the sporocysts divide twice to
produce four sporozoites each .  Infection occurs by ingestion
of sporocysts-containing oocysts: the sporocysts excyst in the
small intestine and release their sporozoites, which invade the
epithelial cells and initiate schizogony .  Upon rupture of the
schizonts, the merozoites are released, invade new epithelial
cells, and continue the cycle of asexual multiplication . 
Trophozoites develop into schizonts which contain multiple
merozoites.  After a minimum of one week, the sexual stage
begins with the development of male and female gametocytes
.  Fertilization results in the development of oocysts that are
excreted in the stool .  Isospora belli infects both humans and
animals.
 Microsporidia
POINTS DETAILS
OVERVIEW  Genus (in man):  Geographical distribution:
1. Encephalitozoon hellem. 1. Australia, USA, Netherlands, Engand, 15% – 30% of
2. Enterocytozoon bieneusi. AIDS patients infected most commonly by E.
3. Pleistophora spp. bieneusi, E. hellem, & S. intestinalis.
4. Septata intestinalis. 2. E. bieneusi is largely restricted to RBC of small
 A new group of human opportunistic pathogens. intestine where it causes villous atrophy &
 Unicellular obligate intracellular parasites. malabsorption. Bile duct & gall bladder involvement r
associated with sclerosing cholangitis & infection in
nasal sinuses & bronchial epithelium.
3. In Africa, prevalence is lower.
HOST 1. Most invertebrate phyla & all 5 classes of vertebrates.
2. Pets, particularly dogs may be infected.
3. In man:
 Opportunistic in immunocompromised
 Recorded in immunocompetents as in apparent or clinically transient infections.
 Presence of coiled polar filament that is extruded from a spore to inject infectious material, e sporoplasm, into a host
MORPHOLOGY cell to initiate infection.
 Size: 1 – 4 µm.
TRANSMISSION &  Routes of infection:  Mode of transmission:
INFECTION 1. Ingestion: fecal-oral, enteric infection. 1. Transmitted by highly resistant spores.
2. Inhalation: respiratory infection. 2. Spores contain infection sporoplasm & coiled tube.
3. Inoculation or spores in an abrasion (ocular).
PATHOLOGY SITES  Intestine, eye, CNS, trachea-bronchial tree, nasal sinuses, & kidney.
PATHOGENECITY  On entering a new suitable host, e polar tube is everted, e sporoplasm migrates through it
& is injected into a host cell, primarily e GIT & RT.
 Inside host cell replication (merogony) precedes spore formation (sporogony).
 Mechanism of dissemination to ther organs is not understood yet.
 Infection in immunocompetent people is recorded as ocular, neurological, muscular, &
disseminated infection.
 E. bieneusi is associated with severe diarrhea.
CLINICAL 1. In AIDS patients: severe enteritis.
2. Keratoconjunctivitis caused by Nosema in both AIDS & HIV-negative patient.
MANIFESTATION 3. Myositis & hepatitis r unusual types.
DIAGNOSIS  Specific Trichrome stain.
 Giemsa stain.
 Fluorescent Dye: Uviltex-2 B.
TREATMENT  Enteric infection responds to Albendazol.  Resistant to:
 Corneal infection responds to Itraconazzole & Borline 1. Penicillin, streptomycin, & gentamycin.
(propamidine isethionate). 2. Sonication, freezing, & thawing.
3. Distilled water.
 Toxoplasma gondii
POINTS DETAILS
 An obligate intracellular parasite.
 Geographical distribution: worldwide.
OVERVIEW  Hosts:
1. Definitive host: cat.
2. Accidental or non-specific: mammals (man), avian, cold-blooded vertebrates.
1. In areas where cats r numerous, e sanitation is poor & e climate is humid & mild, favoring long-term oocyst
EPIDEMIOLOGY viability, e presence of Abs to Toxoplasma is highly in children.
2. Outbreaks of toxoplasmosis have been recorded, one involving 5 medical students in New York City.
1. Tachyzoites:
 Actively multiplying asexual form in e human form.
 Pyriform in shape & approximately 3 by 6 µm.
 Contains a cell membrane, nucleus, & various organelles. Tachyzoites r
antigenically
 Prominent in acute infection.
distinguish-
 Can develop a parasite membrane around them & become a cyst.
TROPHOZOITE able from
2. Bradyzoites:
bradyzoites.
 Crescent-shaped & slender form with a nucleus situated towards
e posterior end.
 Metabolically quiescent but remains viable.
 Prominent in chronic infection.
MORPHOLOGY  In e encysted stage.
PRECYST  Found in e macrophages.
 Contains 50 to several thousand bradyzoites & measure from 10 to 100 µm in diameter.
CYST
 Can be found in brain tissue & muscle.
 Formed within e epithelial cells of e small intestine of e cat.
 E fertilized macrogametes develop into nearly spherical oocysts that rupture out of intestinal
epithelial cells.
OOCYST  When passed in cat’s feces, e oocysts measure 10 – 13 µm in diameter.
 Oocyst wall contains 2 colorless layers & undifferentiated materials which develop into 2
sporocysts.
 Each sporocyst contains 4 sporozoites.
REPRODUCTION  Depend on virulence & state of immunity.
&  Types:
1. Acute infection:
MULTIPLICATION  Tachyzoites divide repeatedly by endodyogony.
 Host cells may swell up.
 Develop a membrane & become a cyst (pseudocyst).
2. Chronic infection:
a. Bradyzoites: multiply slowly by endodyogony within true cysts with tough wall.
b. Cyts formed in brain, liver, heart, & muscles & persist for month or years.
c. Release of bradyzoites stimulates persistence of immunity.
d. When immunity is lowered: parasites multiply as tachyzoites resulting in localized or generalized relapse.
e. When immunity returned to normal: cysts r formed.
1. Cat infected by ingestion of:
 Raw meat.
Cysts Long-term oocyst viability is
 Rodents.
favored by poor sanitation &
 Pseudocyst.
humid climate.
 Oocyst.
TRANSMISSION & 2. Non-specific hosts infected by ingestion of:
 Oocyst (only source for herbivores or man). Can be ingested directly or by aerosol dispersion or by ingestion of
INFECTION material contaminated with infected cat feces.
 Cysts in raw or improperly cooked beef, pork, or mutton meat (carnivores & omnivores).
3. Transplacental from mother who develop toxoplasmosis during pregnancy to foetus.
 Immunity to mothers who have already been infected before pregnancy.
4. Blood transfusion (within white cells, platelets, but packed RBC transfusion is safe).
5. Organ transplantation.
SITES OR 1. Definitive host: clumnar epithelial cells of small intestine.
2. Accidental host:
HABITTAT
 Develop in vocuoles in any nucleated cell.
 Specific predilection for brain & retinal cell.
 Liver & lymph nodes.
COMPLICAION & 1. Congenital toxoplasmosis:
CLINICAL  Occurs in about 1 to 5 per 1000 pregnancies.
 Often severe & fatal depends on e age of e fetus during infection & Ab protection from e mother.
MANIFESTATION  Infection of e mother is usually asymptomatic.
 Primary infection during:
a. E 1st trimester results in abortion.
b. E 2nd trimester results in still birth.
c. E 3rd trimester results in congenital infection.
 Typical syndromes:
a. Intracerebral calcification. Occasionally, e infection is
b. Chorioretinitis. milder & there may be a
complete recovery.
 c. Hydrocephaly.
d. Microcephaly.
e. Psychomotor disturbance.
f. Convulsion as well as visceral & muscular lesions.
 Complication in severe overt cases: xanthochromia, increased cells & proteins.
 There may be also chorioretinal lesions in infant which is severe, extensive, & bilateral:
a. Intense edema of e retina.
b. Various degrees of degeneration & necrotic inflammation with perivascular & general cellular inflitration.
c. Optic neuritis or may be retinochoroiditis.
2. Acquired or reactivated toxoplasmosis:
 Acute form in children & adults that resembles thypus & usually fatal.
 Parasitemia persists for several weeks & with e production of Ab, cysts form in various tissues.
 2 main clinical types:
a. > common & mild lymphatic form resembling infectious mononucleus.
 Ch aracterized by:
 Cervical & axillary lymphadenopathy.  Slight anemia, leukopenia, & lymphocytosis.
 Malaise & muscle pain.  Low blood pressure.
 Irregular low fever.  Slightly altered liver function.
b. Acute, fulminating, disseminated infection.
 Characterized by:
 Skin rash, high fever, chills, & prostration.
 Meningoencephalitis, hepatitis, pneumonitis, & myocarditis.
 Opportunistic infection:
 Usually associated with immunosuppression due organ transplantation & treatment of neoplastic disease.
 Also occurs in AIDS patients.
 Early symptoms:
 Headache & fever.
 Lethargy & altered menta status.
 Progression to focal neurological deficits & convulsion.
1. Direct methods:
 Tissues or fluids suspected of containing parasites (if available): biopsied lymph nodes or muscle.
 Blood.
 R used for detection of parasites by:
a. Staining by Giemsa or immunofluorenscence.
b. PCR for detection of parasite DNA in AIDS patients whose Ab testing is useless.
c. Tissue culture.
2. Indirect methods:
DIAGNOSIS  Most important method.
 Depends on e demonstration of immunity.
 Serologic diagnosis requires demonstration of Ab titers.
 A very high Ab level is not sufficient evidence:
a. Acute infection: rising titre of IgM.
b. Reactivated form: rising titre of IgG.
 IFAT & ELIZA rising titre is important, repeat e test after 2 or 4 weeks.
 In Asia, even vegetarians have a high Ab titer.
 Congenital infection: Demonstration of IgM, not IgG.
1. Pyrimethamin (daraprim).
TREATMENT 2. Spiramycin (rovamycin) for pregnant females.
1. General prevention:
 Mainly through cooking of all meats: barbeque must be cooked completely.
 Careful attention to cat feces (oocysts remain infective for 18 months).
2. For pregnant women:
 Avoiding tasting raw meat.
 Wash hands with soap & water after handling meat.
PREVENTION  Cook all meat thorough, including harmburgers & frozen meats.
 Get rid of cats or keep them in house where r no rodents, however:
a. Feed cats dry or cooked-canned cat food.
b. Empty liter box daily.
c. Disinfect litter box with boiling water & wash hands after these activities.
 Better delegate this job to other member of e family.

Good manner and Form (Al-Adab)

Bukhari: Book 8: Volume 73: Hadith 160
Narrated Abu Huraira:

The Prophet said, "Whoever believes in Allah and the Last Day, should serve his guest generously; and
whoever believes in Allah and the Last Day, should unite the bond of kinship (i.e. keep good relation with
his Kith and kin); and whoever believes in Allah and the Last Day, should talk what is good or keep quit.”
 LIFE CYCLE OF Toxoplasma gondii

Members of the cat family (Felidae) are the only known definitive hosts for the sexual stages of T.
gondii and thus are the main reservoirs of infection.  Cats become infected with T. gondii by carnivorism
(1).  After tissue cysts or oocysts are ingested by the cat, viable organisms are released and invade
epithelial cells of the small intestine where they undergo an asexual followed by a sexual cycle and then
form oocysts, which are then excreted.  The unsporulated oocyst takes 1 to 5 days after excretion to
sporulate (become infective).  Although cats shed oocysts for only 1 to 2 weeks, large numbers may be
shed.  Oocysts can survive in the environment for several months and are remarkably resistant to
disinfectants, freezing, and drying, but are killed by heating to 70°C for 10 minutes.
Human infection may be acquired in several ways: A) ingestion of undercooked infected meat
containing Toxoplasma cysts (2); B) ingestion of the oocyst from fecally contaminated hands or food
(3); C) organ transplantation or blood transfusion; D) transplacental transmission; E) accidental
inoculation of tachyzoites.  The parasites form tissue cysts, most commonly in skeletal muscle,
myocardium, and brain; these cysts may remain throughout the life of the host.
 Trichomonas vaginalis
POINTS DETAILS
 E most common pathogenic protozoan of humans in industrialized countries.
 Geographical distribution: worldwide.
OVERVIEW  Disease: trichomonad vaginitis, urethritis, & prostatovesiculitis.
 Comprises flagella, an undulating membrane, an axostyle (a prominent central rod), & usually a cytostome.
 Host: man.
 Women: 3. 1/7 of infected women complain of symptoms.
EPIDEMIOLOGY 1. Incidence is 10% -25%.  Male: usually asymptomatic.
2. Higher when hygiene is deficient.
 Colorless pyriform flagella, 15 – 18 µm in fresh preparations but smaller when fixed.
 Single nucleus.
 No cysts.
MORPHOLOGY  Anterior 4 flagella: run backward along e surface.
TROPHOZOITE
 Rounded or pyriform.
 Form undulating membrane, 1/3 – ½ body surface: supported by marginal filament (costa).
 Contains thicker parabasal body.
1. Motility: rapidly, rotating through debris by e lashing of e anterior flagella & by e action of undulating membrane.
2. Nourishment: ingest bacteria, starch, & RBCs. Dextrose, maltrose, maltose, & other carbohydrates stimulate growth.
PHYSIOLOGY 3. Reproduction: takes place by binary logitudinal fission with mitotic division of e nuclei.
4. Resistance: loses its vitality below pH 4.9, thus it can’t live in e normally acid vaginal secretion (pH 3.8 to 4.4) of
health adults.
1. Sexual intercourse.
TRANSMISSION & 2. Sharing douche equipment.
INFECTION 3. Contact with contaminated toilet seats & toilet articles.
4. During passage in birth canal in newborns.
1. Female: vagina, cervix, urethra, & bladder.
SITES
2. Male: prostate, urethra, bladder, & seminal vesicle.
 Is a causative agent of a persistent vaginitis.
 E flagellate is reponsible for a low-grade inflammation, furnished by its toxic action on
cells in tissue cultures & e production of vaginitis in women by bateria-free cultures.
 Requires a pH of 5.0 – 5.5 eventhough e normal acidity of vagina 4.0 – 4.5.
 Prediposing conditions leading to decrease of lactic acid:
1. Decrease in no. of Doderlin bacilli.
PATHOGENESIS 2. Superadded infection e.g. Gonorrhea:
PATHOLOGY  E organism is frequently coexistent with other infection.
 It has almost 3-folds high risk in AIDS patients.
3. In young girls & menopouse pH is neutral.
 Burrows in epithelium by its wedge but no penetration power, not pass to sub-epithelial
layer.
 Inflammation with hyperaemia & peticheal haemorrhages resulting in strawberry vagina.
 Factors that determine infection:
PATHOGENICIY 1. Bacterial flora.
2. Physiologic status of e vagina: pH.
 E incubation period is 5 to 28 days.
 Infection in women is frequently symptomatic.
 Complications:
 Hyperemia & petechial hemorrhages, in advance cases, granuloma areas.
COMPLICATIONS  E surface s covered with a frothy, seropurulent, creamy, or yellowish discharge, frequently forming a pool in e
post. fornix is e prominent symptom.
& CLINICAL  Valvular pruritis & vaginal discharge which can be accompanied by vulvar & cervical lesion (erosion),
MANIFESTATION abdominal pain, dysuria, & dyspareunia.
 Signs: vaginal & cervical inflammation, itching & burning, presence of profuse irritating leukorrheic discharge.
 Mucosal erosion & necrosis r also observed.
 In men, it is frequently asymptomatic, ocassionally, urethritis, epididymitis, prostatovesiculatis & prostatitis can
occur.
1. Suggestive symptoms: vaginal discharge, punctuate lesion, & hyperaemia.
2. Microscopic examination of wet mounts for demonstration of actively motile parasites in vaginal discharge collected
DIAGNOSIS from post. fornix by e introduction of bivalve speculum (can be stained by Giemsa).
3. In male, examination of prostatic secretions following prostatic massage & urine of e male.
4. Culture when microscopic examination is –ve (e ost sensitive method but results r not available for 3 to 7 days).
1. Treatment of husband.
2. Restoration of normal condition (pH) of vagina by local cleaning of vaginal mucosa.
TREATMENT 3. Metronidazole via vaginal insertment (female only) & orally taken (both male & female), however, it should not be
given to pregnant patients.
1. Proper concern & care on personal hygiene.
PREVENTION 2. E detection & treatment of infected males.
 Life cycle of Trichomonas vaginalis

Trichomonas vaginalis resides in the female lower genital tract and the male urethra and prostate ,
where it replicates by binary fission .  The parasite does not appear to have a cyst form, and does
not survive well in the external environment.  Trichomonas vaginalis is transmitted among humans,
its only known host, primarily by sexual intercourse
 Naegleria sp. & Acanthamoeba sp.
Naegleria sp. POINTS Acanthamoeba sp.
 Disease: Primary Amoebic Meningoencephalitis OVERVIEW  Disease: Granulomatous Amoebic Encephalitis
(PAM). (GAE), a sub-acute opportunistic infection, spread
 Found in soil & water. hematogenously from lungs to e CNS, & kerato-
conjuctivitis.
 Do not necessarily involve contact with soil or
stagnant water.
GEOGRAPHICAL DISTRIBUTION:
1. Many part of e world.
2. First cases in 1965 in USA (Florida) & in Australia.
 Trophozoites:  Trophozoites:
1. Broad pseudopodia. 1. Filamentous pseudopodia called acanthopodia.
2. Actively motile. 2. Irregular with e size of 15 – 45 μm.
3. Form flagellate stage. 3. Sluggishly motile.
 Cysts:
MORPHOLOGY 4. Do not form flagellate stage.
1. Single-walled.  Cysts:
2. Do not encyst in tissue. 1. Double-walled.
2. May encyst in tissue.
 Infection occurs during swimming & diving in TRANSMISSION &  Infection via inhalation of e cysts through e respiratory
contaminated water of still water lakes, ponds & tract or through skin penetration.
backwater. INFECTION
PATHOLOGY
 Invade e brain through e mucosa of nasal cavity,  Final spread to CNS is hematogenous after initial
presumably penetrate e cribriform plate of e ethmoid invasion.
PATHOGENESIS
bone through e olfactory neuroepithelium.  Infection of e brain occurs in debilitated patients due
 Multiply in e Grey matter along e base of e brain. to immunosuppression or other diseases.
PAM: 1. GAE:
 E symptoms:  Course is sub-acute with a variety of CNS
1. Severe frontal headache. manifestation:
2. Fever. a. Meningeal signs.
3. Blocked nose. b. Alteration of mental status.
4. CNS involvement: altered taste & smell, stiff c. Neurologic deficits mimicking brain abscess or
neck, & Kernig’s sign. tumor.
 E signs:  Some cases of disseminated cutaneous infection
1. Peripheral WBL: 24000, with a preponderance of COMPLICATIONS have been reported in AIDS patients.
neutrophils (92%).. & CLINICAL  Skin lesons, nodules, or ulcers focus for spread to
2. Spinal fluid contains many neutrophils without CNS.s maybe found in CNS.
MANIFESTATION
any bacterial growth.  cyst
3. Spinal fluid protein is moderately elevated. 2. Amoebic Keratitis:
4. Spinal fluid glucose is moderately reduced.  Unilateral severe ocular pain.
 Rapid course, death usually following within 4 – 5  Stromal infiltrate in e shape of a complete ring.
days aftr onset of e symptoms.  Recurrent breakdown & healing.
 On post-mortem: nests of trophozoites & extensive  E course is chronic over months.
haemorrhagic reaction in basilar portion of e 3. Acanthamoeba kerato-conjunctivitis & corneal ulcer:
cerebllum. minor trauma due to use of soft contact lenses.
 Suspected in individuals with meningoencephalitis, 3 DIAGNOSIS  Amoebic keratitis:
– 7 days after swimming in fresh water pools, ponds, Amoeba can be recovered 1. Trophozoites & cysts of Acanthamoeba
or hot water spring. by intracerebral identified in Giemsa or Periodic-acid-shiff-
 Identfication of trophozoites in wet-preparation of inoculation of CSF into stained smears from scraping or corneal biopsy
CSF. mice or on to non-nutrient specimens.
 CSF should not be centrifuged or refrigated as agar plates previously 2. Staining with IFA.
trophozoites r destroyed. seeded with E.coli. 3. Culture or scraping on to non-nutrient agr plates.
 E only effective drug is Amphotrericin B, by IVI at a  GAE: no cure of human cases.
maximum dose.  Keratitis: topical application of 1% Miconazole
TREATMENT nitrate, 0.1% Propamidine isothionate, & Neosporin
for 3 – 4 weeks.
 Corticosteroids r contra-indicated.
PREVENTION:
1. Avoid swimming in small lakes & ponds which have warm water & algal growth.
2. Swimming pools should be adequetly chlorinated.
3. Users of contact lenses should adhere closely to recommended procedures for use & care of lenses.

“Hidup ini – kata Ahmad Syauqi, sang raja penyair Arab – adalah keyakinan & perjuangan. Dan perjuangan
seorang muknin sejati itu – kata Imam Ahmad Bin Hambal – tidak akan berhenti kecuali setelah kedua telapak
kakinye telah menginjak ke pintu syurga.”

Oh Allah, please love me, always love me, never hate me, never ever hate me.
Oh Allah, please be with me, always with me, never leave me, never ever leave me.
 LIFE CYCLE OF Naegleria sp. & Acanthamoeba sp.

Free-living amebae belonging to the genera Acanthamoeba, Balamuthia, and Naegleria are important
causes of disease in humans and animals.  Naegleria fowleri produces an acute, and usually lethal, central
nervous system (CNS) disease called primary amebic meingoencephalitis (PAM).  N. fowleri has three
stages, cysts , trophozoites , and flagellated forms , in its life cycle.  The trophozoites replicate by
promitosis (nuclear membrane remains intact) .  Naegleria fowleri is found in fresh water, soil, thermal
discharges of power plants, heated swimming pools, hydrotherapy and medicinal pools, aquariums, and
sewage.  Trophozoites can turn into temporary flagellated forms which usually revert back to the
trophozoite stage.  Trophozoites infect humans or animals by entering the olfactory neuroepithelium and
reaching the brain.  N. fowleri trophozoites are found in cerebrospinal fluid (CSF) and tissue, while
flagellated forms are found in CSF.
Acanthamoeba spp. and Balamuthia mandrillaris are opportunistic free-living amebae capable of causing
granulomatous amebic encephalitis (GAE) in individuals with compromised immune systems. 
Acanthamoeba spp. have been found in soil; fresh, brackish, and sea water; sewage; swimming pools;
contact lens equipment; medicinal pools; dental treatment units; dialysis machines; heating, ventilating,
and air conditioning systems; mammalian cell cultures; vegetables; human nostrils and throats; and human
and animal brain, skin, and lung tissues.  B. mandrillaris however, has not been isolated from the
environment but has been isolated from autopsy specimens of infected humans and animals.  Unlike N.
fowleri, Acanthamoeba and Balamuthia have only two stages, cysts and trophozoites , in their life
cycle.  No flagellated stage exists as part of the life cycle.  The trophozoites replicate by mitosis (nuclear
membrane does not remain intact) .  The trophozoites are the infective forms and are believed to gain
entry into the body through the lower respiratory tract, ulcerated or broken skin and invade the central
nervous system by hematogenous dissemination .  Acanthamoeba spp. and Balamuthia mandrillaris
cysts and trophozoites are found in tissue
 Pneumocystis carinii
POINTS DETAILS
 Extracellular opportunistic organism: pathogenic tissue parasite in 85% of AIDS patients.
 Disease: pneumocytosis, parasitic pneumonia, & interstitial plasma cell pneumonia.
 Geographical distribution: worldwide.
OVERVIEW  Mode of transmission: unknown, maybe through droplets to close contact.
 Attachment to but not invasion of host cells by e parasites was prominent.
 E exact type of multiplication is unknown.
 Infection is cosmopolitan in human, rodents, dogs, & several other domestic animals.
 Low virulence & multiply actively in hosts of lowered resistance:
1. Chemotherapy.
2. AIDS.
3. Radiation therapy.
EPIDEMIOLOGY 4. Organ transplantation.
5. Prematurity, etc.
 Infection occurs in 2 clinico-pathological forms:
1. In infants aged 2 – 7 months that suffer from immune deficiency state.
2. Sporadic in immunocompromised children or adults: immune deficiency, cytotoxic therapy, & association with
cytomegalic inclusion bodies.
 Unicellular, pleomorphic form of 1 -2 µm in diameter (ranging up to 5 µm).
TROPHOZOIT
 Thin-walled, pear-shaped, & crescentic or amoeboid.
E
 Contains a nuclear mass, a mitochondria, endoplasmic reticulum, & round bodies or vacuole.
MORPHOLOGY
 Size: 3 – 6 µm.
CYST  Thick-walled, round, ovoid, & crescent or cup-shaped.
 4 – 8 small intracystic oval bodies.
 Mainly lung.
SITES  Disseminated in ear, liver, & BM.
 In AIDS patients, can results in malignant lymphoma.
1. Generally:
 In adults, e disease is predominantly alveolar.
 In malnourished infants there is a major intestitial component.
 In both, e organism usually intermingles with alveolar macrophages in e alveolar
PATHOLOGY exudate.
2. Macroscopically: e lung r firm & e cut surface r gray & airless.
PATHOGENECITY
3. Microscopically:
 Thickened alveolar septa, inflitrated with plasma cells: interstitial plasma cell
pneumonia.
 E alveolar epithelium is partly desquamated.
 Alveoli r filled with fat-laden cells, parasites, & foamy vacuolated materials.
 Presence of P. carinii within e alveoli.
 Incubation period: 14 -21 days.
 2 types:
1. In infantile disease associated with malnutrition:
 Onset is insidious over weeks with poor feeding.
 Failure to thrive.
COMPLICATIONS  A rapid respiratory rate of up to 100 respiratory rates per minute
 Cynosis.
& CLINICAL 2. In immunosuppressed children & adults:
MANIFESTATION  A rapid onset over a few days.
 Associated with fever, rapid respirations, nonproductive cough, & cynosis.
 In both types, rales r not heard in e chest & radiographs show a diffuse inflitrate that is usually bilateral & often has
ground-glass appearance.
 E arterial oxygen tension is low & e CO2 is normal or low.
 Death is due to asphyxia.
1. Clinical pictures in a risky patients.
2. X-ray observation of lung.
3. High level of IgM r also of diagnostic test.
4. Identification of characteristic organism in pulmonary specimens stained with Gomori Methenamine silver stain.
5. IF & MCAbs to detect P. carinii in sputum specimens.

DIAGNOSIS Diagnostic approach for P.carinii

TECHNIQUE YIELD
Induced sputum 30% – 85%
BAL Fair (but over 90% in AIDS)
Open lung biopsy Over 95% (all patients)
1. Pyrimethamine & sulphadiazine.
TREATMENT 2. Steroids r contraindicated.
3. Prophylaxis by inhalation of aerosolized pentamidin in AIDS patients.
 LIFE CYCLE OF Pneumocystis carinii.

This is a generalized life cycle proposed by John J. Ruffolo, Ph.D. (Cushion, MT, 1988) for the
various species of Pneumocystis.  These fungi are found in the lungs of mammals where they reside
without causing overt infection until the host's immune system becomes debilitated.  Then, an
oftentimes lethal pneumonia can result.  Asexual phase: trophic forms replicate by mitosis to . 
Sexual phase: haploid trophic forms conjugate and produce a zygote or sporocyte (early cyst) . 
The zygote undergoes meiosis and subsequent mitosis to produce eight haploid nuclei (late phase
cyst) .  Spores exhibit different shapes (such as, spherical and elongated forms).   It is postulated
that elongation of the spores precedes release from the spore case.  It is believed that the release
occurs through a rent in the cell wall.  After release, the empty spore case usually collapses, but
retains some residual cytoplasm .  A trophic stage, where the organisms probably multiply by
binary fission is also recognized to exist.  The organism causes disease in immunosuppressed
individuals.
 Sarcocystis lindemani
POINTS DETAILS
 Parasites of mammals, birds, & reptiles.
 Species: S. lindemani (muscle sarcocystosis in man).
OVERVIEW  Geographical distribution: worldwide.
 Hosts: man & other mammals, birds, as well as reptiles.
 Infection is very common in cattle, sheep, & pigs.
EPIDEMIOLOGY  Reported in few cases (16) in man which r only accidentally at autopsy.
 One of e zoonosis.
 Male & female gametocytes develop in e lamina propia of e small intestine.
 Producing oocysts that sporulated & r passed in feces.
 Asexual cystic stages in muscles.
 Source of infection: mature tetrasporozoic sporocyst.
MORPHOLOGY  Size: according to stage of development & species.
 Shape: cylindrical, fusiform, rounded, or oval.
 2 sporulated sporocysts contain 4 sporozoites.
 Sporocyst measure 15 – 19 by 8 – 10 µm, seen in wet mount preparation.
1. Man & other mammals, birds & reptiles may:
 Harbour asexual cystic stages (S.lindmani).
 In skeletal & smooth muscles of trunk, limbs, esophagus, & diaphragm.
SITES
2. Animals & man:
 Harbour intestinal asexual & sexual stages.
PATHOLOGY  Man is e DH of 2 species.
1. Local symptoms: muscle tenderness associated with cystic changes in striated muscles.
2. Generalized symptoms:
PATHOGENECITY
 Pain & swelling of an isolated muscle.
Symptoms
 Dyspnea & wheezing.
3. Self-limiting.
1. Cysts in muscles.
2. Oocyst with sporozoites in feces.
DIAGNOSIS 3. Seropositivity is high among Orang Asli, Malay, Chinese, & Indian.
4. Prognosis: good.
TREATMENT  No known treatment.
 Genus Plasmodium – Malaria Fever
POINTS DETAILS
 E malarial parasites r from genus Plasmodium which cause malarial fever.
 E only blood protozoa whose sexual reproduction (gametocytes) in mosquitoes & asexual production (sporozoits)
in humans.
 4 species r known i.e. P. falciparum, P. ovale, P. vivax, & P. malariae.
OVERVIEW  E vectors:
1. Anopheles masculatus: Peninsula Malaysia.
2. Anopheles balabecensis: Sabah. Through anterior inoculation.
3. Anopheles donaldi: Sarawak.
 E endemicity of malarial fever is graded by e spleen enlargement or spleen rate in 2 – 9 years children.
1. Trophozoite or sporozoit: a ring of bluish cytoplasm with a dotlike nucleus of red chromatin.
MORPHOLOGY 2. Schizont: dividing parasite showing multiple masses of nuclear chromatin.
3. Gametocyte: compact cytoplasm & absence of nuclear division.
 Modes of infection:
1. Through e vector: infected female Anopheles mosquitoes.
2. Through blood transfusion: involves e erythrocytic cycle & therefore is usually easily eradicated.
3. Through contaminated syringe: multiple use of a syringe among drug addicts.
4. Transplacental: congenital infection.
 Types of infection:
INFECTION 1. Single infection: one species in one RBC.
2. Multiple infections: three P. vivax in one RBC.
3. Mixed infection: more than one species in one RBC.
 Nature of infection:
1. P. ovale & P. vivax: prefer to invade young RBC.
2. P. malariae: has an affinity for mature & older RBC.
3. P. falciparum: infects cells of all ages.
 According to phase:
1. Liver phase:
 No recognizable symptoms.
 Mainly in e incubation period (9 – 30 days).
2. RBC phase:
 Fever is present d/t e rupture of RBC & e release of pyrogenic substances trigger immune response.
 Anemia develops if RBC destruction is more than 5%:
a. Haemolytic anaemia: lysis of RBCs.
b. Normochromatic & normocytic anaemia.
 Splenomegaly d/t e clearance of destructed RBCs.
 Hepatomegaly d/t hyperreactive parasites (schizonts) & hyperplasia of Kupffer cells.
PATHOLOGY  P. falciparum gives e most dangerous infection because:
1. It has a shorter liver cycle: 6 days.
2. It has more liver schizonts: 40000 schizonts.
3. It has an ability to infect red cells of all ages including reticulocytes & erythrocytes thus produce a high
parasitemia.
4. It gives multiple infections of RBC: more than one parasite in one RBC.
5. It has an unsynchronized schizont rupture: quotidian fever.
6. E infected RBCs tend to stick to e endothelium of e vessels & to each other results in:
a. Blood vessels blockage.
b. Sequester of schizonts in visceral capillaries not in e peripheral circulation.
c. Preventing e deformed & infected RBCs from circulating through spleen to be destroyed.
d. Finally, all above lead to congestion & reduced blood flow to other organs which causes anoxia.
 D/t e ruptures of RBC schizonts which release e pyrogenic substance such as IL-1 & TNF.
 Types of fever:
1. Tertian fever: every 3 days for P. falciparum & P. vivax.
2. Quartan fever: every 4 days for P. malariae.
3. Quotidian fever: irregular schizont ruptures for P. falciparum.
 Malarial paroxysm:
 One of e most dramatic & frightening events in clinical medicine.
 3 stages:
MALARIAL 1. Cold stage:
 Up to one hour with chilly sensations that progress to a teeth-chattering & frankly shaking chill.
FEVER &  Peripheral blood vessels r constricted & e lips & nails r cyanotic.
PAROXYSM 2. Hot stage:
 Usually lasts from 1 - 4 hours.
 E body temperature begins to mount rapidly as e blood vessels dilate, ranging from 103 F to 106 F.
 E skin is hot & e face flushed with nausea, vomiting, headache, & rapid pulse.
 E patient may become euphoric & convulsion may occur in children.
3. Sweat stage:
 Usually lasts from 1 – 2 hours.
 E patient perspires profusely, e temperature falls, & e headache disappears.
 In a few hours, e patient is exhausted but symptomless.
CLINICAL  E symptoms:
MANIFESTATION  Depend on e level of parasitemia.
 Among e symptoms r headache, lassitude, vague pains in e bones & joints, chilly sensation, & fever.
& COMPLICATION  E complications (only P. falciparum which could give a fatal outcome):
1. E cerebral type:
  Results in cerebral malaria or pernicious malaria d/t:
a. Capillary sludging of internal organs.
b. Brain → vessels blockage → hypoxia → coma → death.
 Children with low immunity r most commonly infected.
2. E gastrointestinal symptoms: vomiting, abdominal pain, diarrhea, & intestinal hemorrhage.
3. Others: weakness, hypotension, circulatory collapse, pulmonary edema, cyanosis, & impaired oxygenation of
e blood.
 Diagnosis by BFMP: blood film for malarial parasites.
DIAGNOSIS  Thick (to ensure e infection is not missed) & thin (to identify e species) smears using Giemsa.
1. Chloroquine: parasite resistance.
2. Quinine & fansidar.
TREATMENT 3. Quinghaosu (artemesinin): plant used in China.
4. Omaria (Indian herbal medicine): under trial.
5. Malarone: paediatric tablets for travel (1 day priorly).

DIFFERENCES BETWEEN MALARIAL SPECIES

P. falciparum P. vivax PROPERTIES P. malariae P. ovale
 Many RBCs infected.  Large ring forms inside  Small ring inside RBC.  Large ring formed inside
 Multiple infections. RBC.  Band formed across RBC.
 Little stippling  Many RBCs infected. RBC.  Many RBCs infected.
(Schuffner’s dots).  Multiple infections.  Moderate no. of RBC  Multiple infections.
 Fine cytoplasm.  Much stippling. infected.  Much stippling.
 Cytoplasm is very active.  Little stippling.  Cytoplasm is very active.
 RBC is enlarged.  Cytoplasm is moderately  RBC shape becomes oval
active. & enlarged in smear.
TROPHOZOITE
S

 Few RBCs infected.  Many RBCs infected.  Few RBCs infected.  Many RBC infected.
 Absence in peripheral  Found in peripheral  Found in peripheral  Found in peripheral
circulation. circulation. circulation. circulation.
 18 – 24 merozoits in  12 – 24 merozoits in RBC.  6 – 12 merozoits in RBC.  6 – 12 merozoits in RBC.
RBC.  Much pigments.  Moderate pigments.  Much pigments.
 Moderate pigments.  Heavy stippling.  Moderate stippling.  Heavy stippling.
 Less stippling or  Daisy – shaped flower.  RBC is oval in shaped.
Maurer’s cleft.

SCHIZONTS

 RBC is distorted.  Many RBCs infected. GAMETOCYTE  Moderate RBC no. is  Many RBCs infected.
 Banana – shaped.  Male is less dense. S infected.  RBC is oval in shape.
 Male is slender.  Female has > cytoplasm.  Male is less dense.  Other features r similar to
 Female is dense.  Heavy pigmentation.  Female cytoplasm is P. vivax.
 Pigments & stippling as  Much stippling. dense.
in schizonts.  Moderate pigmentation
 Presence in peripheral & stippling.
blood.
1. Reticulocytes. CHOICE OF
1. Reticulocytes. 1. Erythrocytes. 1.Reticulocytes.
2. Erythrocytes. RBC
LIFE CYCLE OF Genus Plasmodium – MALARIAL FEVER

Liver Phase.
P. falciparum: 6 days.
P. vivax: 8 days.
P. malariae: 13 days.
P. ovale: 9 days.

RBC Phase.
P. falciparum: 3D,
20M.
P. vivax: 3D, 15M.
P. malariae: 4D, 8M.

The malaria parasite life cycle involves two hosts.  During a blood meal, a malaria-infected female Anopheles
mosquito inoculates sporozoites into the human host .  Sporozoites infect liver cells and mature into
schizonts , which rupture and release merozoites .  (Of note, in P. vivax and P. ovale a dormant stage
[hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks, or even years later.) 
After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual
multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect red blood cells .  The ring
stage trophozoites mature into schizonts, which rupture releasing merozoites .  Some parasites differentiate
into sexual erythrocytic stages (gametocytes) .  Blood stage parasites are responsible for the clinical
manifestations of the disease. 

The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles
mosquito during a blood meal .  The parasites’ multiplication in the mosquito is known as the sporogonic cycle
.  While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes .  The
zygotes in turn become motile and elongated (ookinetes) which invade the midgut wall of the mosquito where
they develop into oocysts .  The oocysts grow, rupture, and release sporozoites , which make their way to
the mosquito's salivary glands.  Inoculation of the sporozoites into a new human host perpetuates the malaria life
cycle

AFRICAN TRYPANOSOMIASIS
 E flagellates:
1. Trypanosoma brucei gambiense.
2. Trypanosome brucei rhodesiense.
 E vector: young Glossina palpalis (both male &
female), also known as tsetse fly.
 Transmission through anterior inoculation.
 Disease: African sleeping sickness.
1. T. brucei gambiense: zoonosis, prominent in central
Africa such as Savanna.
2. T. brucei rhodesiense: zoonosis, prominent in West
Africa such as Riverine.
 T. b. gambiense & T. b. rhodesiense r similar in
appearance.
 E organism measures 10 - 30 µm x 1-3 µm.
 It has a single central nucleus & a single flagellum
originating at the kinetoplast & joined to e body by
an undulating membrane.
 E outer surface of e organism is densely coated with
a layer of surface glycoprotein.
 Both species have e same reaction, however:
1. T. b. gambiense has a chronic reaction with a
slower progress, fatal in 1 – 2 years.
2. T. b. rhodesiense has an acute reaction with a
rapid progress, fatal in months.
 3 stages of disease:
1. Bite reaction: a non-pustular, painful, itchy
chancre forms 1-3 weeks after e bite & lasts 1-2
weeks w/out scar.
2. Parasitemia:
 E no. of parasites in blood is high.
 Parasites r present in all tissues.
 Lymph node enlargement.
 Winterbottom’s sign (post cervical LN): in
45% cases with hard LN & fever.
 Anemia & extreme weakness.
3. CNS involvement:
 Need an urgent treatment.
 Severe headache → muscular paralysis →
loss of coordination (d/t neuron damage) →
deep sleep coma (best time for Rx) → death.
 Early diagnosis is essential.
 Among e tests:
1. Winterbottom’s sign.
2. Trypanosomes in:
a. Blood.
b. CSF.
c. Bone marrow.
3. Immunological IgM increases 5 to 10 times.
4. Antigenic variations.
1. Suramin: a toxic drug.
2. Tbrh: more difficult to treat.
TRYPANOSOMIASIS
PROPERTIES AMERICAN TRYPANOSOMIASIS
 E flagellate: Trypanosoma cruzi.
 E vector: Triatoma infestan or kissing bug.
AETIOLOGY  Transmission through posterior contamination.
 Disease: Chaga’s disease.
 Scattered irregularly in Central & South America.
 Has many reservoir hosts.
EPIDEMIOLOGY  Zoonosis.
 50% – 80% vectors r infected.
 Occurs in 3 different forms:
1. E trypomastigote form is found in mammalian
blood, is 15 to 20 microns long & morphologically
similar to African trypanosomes.
MORPHOLOGY 2. E epimastigote form is found in e insect intestine.
3. E amastigote form is found intracellularly or in
pseudocysts in mammalian viscera is round or
oval shaped & measures 2-4 microns & lacks a
prominent flagellum.
1. Bite site:
 Parasites enter through wound (via stercorarian).
 Usually at mucous lining of e eyes & nose.
 Parasites phagocytosed → divide as amastigotes
→ inflammation → chagoma (1o lesion).
 Parasites in tissue or reticuloendothelial system:
a. Myocardium.
Organ dysfunction.
b. Neurons.
2. Acute stage:
 Usually lasts in 20 – 30 days.
 Mainly in children.
 Hepatosplenomegaly may be observed.
PATHOLOGY  Romana’s sign is present:
a. E unilateral conjunctivitis.
b. Orbital edema.
3. Chronic stage:
 Neurons r damage in esophagus, colon, & ureter
→ peristalsis is affected (d/t loss of autonomic
function) → megasyndrome → death.
 Megasyndromes:
a. Megaesophagus: substernal discomfort,
painful swallowing, & hypertrophy of
esophagus with eventual regurtation of food.
b. Megacolon: results in severe constipation.
c. Cardiomegaly: ventricular arrhythmias can
also present.
 E disease may be suspected when general, cardiac, or
DIAGNOSIS gastrointestinal symptoms r present.
 Xenodiagnosis.
1. No good drug.
TREATMENT 2. Nifurtimox: a toxic drug.
3. Early treatment is effective.
Forms of Trypansoma brucei obsreved in e tsetse fly & in e
human blood stream
T. brucei is transmitted by tsetse flies of e genus Glossina.
Parasites r ingested by e fly when it takes a blood meal on an
infected mammal. E parasites multiply in e fly, going through
several developmental stages in e insect gut & salivary glands
(procyclic trypanosomes, epimastigotes, metacyclic
trypanosomes). E cycle in e fly takes approximately 3 weeks. 
When e fly bites another mammal, metacyclic trypanosomes r
inoculated & multiply in e host's blood & extracellular fluids
such as spinal fluid. Humans are e main reservoir for T. b.
gambiense, but this species can also be found in animals. Wild
game animals are e main reservoir of T. b. rhodesiense.
 LIFE CYCLE OF AFRICAN TRYPANOSOMIASIS
During a blood meal on the mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic
trypomastigotes into skin tissue.  The parasites enter the lymphatic system and pass into the bloodstream
.  Inside the host, they transform into bloodstream trypomastigotes , are carried to other sites
throughout the body, reach other blood fluids (e.g., lymph, spinal fluid), and continue the replication by
binary fission .  The entire life cycle of African Trypanosomes is represented by extracellular stages. 
The tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an
infected mammalian host ( , ).  In the fly’s midgut, the parasites transform into procyclic
trypomastigotes, multiply by binary fission , leave the midgut, and transform into epimastigotes .  resumes only when the parasites enter another cell or are ingested by another vector.  The “kissing” bug
The epimastigotes reach the fly’s salivary glands and continue multiplication by binary fission .  The
cycle in the fly takes approximately 3 weeks.  Humans are the main reservoir for Trypanosoma brucei
gambiense, but this species can also be found in animals.  Wild game animals are the main reservoir of T.
b. rhodesiense.
LIFE CYCLE OF AFRICAN TRYPANOSOMIASIS
An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its
feces near the site of the bite wound.  Trypomastigotes enter the host through the wound or through intact
mucosal membranes, such as the conjunctiva .  Common triatomine vector species for trypanosomiasis
belong to the genera Triatoma, Rhodinius, and Panstrongylus.  Inside the host, the trypomastigotes invade
cells, 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 .  Trypomastigotes infect cells from a variety of tissues and transform into intracellular
amastigotes in new infection sites.  Clinical manifestations can result from this infective cycle.  The
bloodstream trypomastigotes do not replicate (different from the African trypanosomes).  Replication
becomes infected by feeding on human or animal blood that contains circulating parasites .  The ingested
trypomastigotes transform into epimastigotes in the vector’s midgut .  The parasites multiply and
differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut .
Trypanosoma cruzi can also be transmitted through blood transfusions, organ transplantation,
transplacentally, and in laboratory accidents.
 LEISHMANIASIS
VISCERAL LEISHMANIASIS PROPERTIES CUTANEOUS LEISHMANIASIS
 E flagellates:
 E flagellates - Leishmania tropica:
1. Leishmania donovani: Asia & Africa.
1. Leishmania braziliensis.
2. Leishmania infantum: Asia, Middle East. AETIOLOGY 2. Leishmania b. braziliensis.
 E vector: Phlebotomus argentipes (sandfly).
 E vector: Lutzomyia sp. (sandfly).
 Disease: Kala azar.
1. Leishmania donovani:
 Zoonosis: China – Dogs.
 In India it is not zoonosis.
EPIDEMIOLOGY  Not zoonosis.
2. Leishmania infantum: zoonosis.
 Many r asymptomatic. 1. Cutaneous leishmaniasis:
 There is rarely a local lesion because organisms r  E organism (L. tropica) multiplies locally,
rapidly eliminated at e site of infection. producing of a papule, 1-2 weeks after e bite.
 Dum – dum fever: very high fever accompanied by  E papule gradually grows to form a relatively
chills & sweating. painless ulcer whose center encrusts while
 Organ enlargement: satellite papules develop at e periphery.
1. Splenomegaly.  E ulcer heals in 2-10 months, even if untreated
2. Hepatomegaly. but leaves a disfiguring scar.
3. Lymphadenopathy.
PATHOLOGY  E disease may disseminate in e case of
 Skin develops hyperpigmented granulomatous area. depressed immune function.
 Post kala azar dermal leishmaniasis: 2. Mucocutaneous leishmaniasis:
 D/t incomplete treatment using antimony  Initial reaction is e same with cutaneous
compound. leishmaniasis.
 Viscerotrophic → dermatotrophic → treatment →  As disease progresses, it spreads to other
recover. mucoid tissues such as nasopharynx.
 If it becomes severe & untreated, results in death.  Mutilation of face: Espundia.
1. Early diagnosis: biopsy. 1. Biopsy ulcer.
2. Bone marrow. DIAGNOSIS 2. Parasite culture.
1. Antimony compound.
2. Miltefosine:
 Oral drug. TREATMENT  Antimony compound.
 Under trial in India.

LIFE CYCLE OF LESHMANIA

Leishmaniasis is transmitted by the bite of female phlebotomine sandflies.  The sandflies inject the infective
stage, promastigotes, during blood meals .  Promastigotes that reach the puncture wound are phagocytized by
macrophages and transform into amastigotes .  Amastigotes multiply in infected cells and affect different
tissues, depending in part on the Leishmania species .  This originates the clinical manifestations of
leishmaniasis.  Sandflies become infected during blood meals on an infected host when they ingest macrophages
infected with amastigotes ( , ).  In the sandfly's midgut, the parasites differentiate into promastigotes ,
which multiply and migrate to the proboscis .
 INTRODUCTION TO HELMINTHS
PROPERTIES DETAILS
 Multicellular (complex) & bilaterally symmetry.
 E integument:
 Hard, tough, & elastic.
 Resistant to digestion (of human).
 Acts as protection in nematodes & trematodes.
 Functions as food absorption in cestodes.
 Have spines, hooks, or cutting plates.
CHARACTERISTIC
 Have anticoagulant gland which functions to lyse e RBCs.
S  E digestive tract:
 Complete or partially loss.
 Environment is full of digested food.
 E reproductive system:
 Cestodes: monocious.
 Trematodes: monocious or hemaprhodites.
 Parthenogenesis: female egg production w/o male fertilization.
 Intestinal nematodes.
HABITAT  Blood flukes.
 Tissue cestodes.
1. Vector borne.
2. Contamination (trichuris).
3. Through eating: meat (taenia), fish (diphyllobothrium), or crab (paragonimus).
MODES OF
4. Skin penetration from soil (necator) or water (schistoma).
INFECTION 5. Autoinfection (enterobius).
6. Inhalation (enterobius).
7. Transmammary (trichinella).
1. Faeces: eggs or ova (intestinal worms).
2. Blood: microfilia (filariasis).
DIAGNOSTIC 3. Urine: eggs or ova (S. haematobium).
SPECIMEN 4. Sputum: eggs (paragonimus).
5. Duodenal aspirates: larva (strongyloides).
6. Biopsy: larva (trichinella & cysticercus).
 Nematodes - egg types:
1. Oviparous:
a. Ascaris: no segmentation of embryo.
b. Hookworm: early segmentation of embryo.
OTHERS c. Enterabius: with embryo.
2. Ovoviviparous: female adult releases egg with developed embryo which emerges larva (strongyloides).
3. Viviparous: female releases larva (brugia).
4. Parthenogenesis: larvae produced w/o copulation (strongyloides).

DIFFERENCES
NEMATODES TREMATODES PROPERTIES CESTODES ACANTHOCEPHAL
A
Round worms Leaf worms or flukes COMMON NAME Tape worms Thorny headed worms.
Cylindrical Flat (leaf like) SHAPE Ribbon like Thorny – round
Present None BODY CAVITY None None
Present None GUT None None
Monocious except
Dioecious
schistosomes SEXES Monocious Dioecious.

HEADS
Buccal cavity Suckers w/o hooks Suckers (may have hooks) Thorny proboscis.
(ANTERIOR)
 Ascaris lumbricoides Life Cycle of Ascaris lumbricoides
POINTS DETAILS
 Normal symptoms r mild, but intestinal blockage
 Probably earliest known worm.
can occur.
OVERVIEW  Also known as round worm (cacing gelang).
 Ectopic migration: pneumonitis ascariasis.
 Higher in cosmopolitan area.
 Disease: ascariasis.
 1.3 billion r infected all over e world: 22% of world population.
 73% Asian population r exposed.
EPIDEMIOLOGY  20,000 deaths per year in all over e world.
 Mode of infection: ingestion of infected eggs d/t contaminated food & water.
1. Adult worms:
 Size: male is 15 to 30 cm while female is 20 to 40 cm.
 3 oval lips around mouth with sensory papillae to suck in food.
 Male worm has a coiled tail with spicule (used as sex identity).
 Female worm produces 20,000 eggs/day/worm.
 In 2 months, become higher in no in e ileum.
 Live span is 1 – 2 years.
2. Eggs:
MORPHOLOGY  Measures 45 to 70 µm by 35 to 50µm.
 Unsegmented when passed.
 In 2 weeks: e eggs contain e infective larvae.
 Withstand adverse conditions such as in Sahara oasis & etc.
 Susceptible to desiccation, dryness, r destroyed by direct sunlight within 15 hours, & r killed by
temperature above 40oC.
3. Larvae:
 Egg hatches in duodenum → larvae penetrate intestine → sojoumin in lung for 5 to 10 days →
migrate up through esophagus → swallowed back.
2. Complications:
1. Clinical manifestations: a. Intestinal obstruction: commonest cause of
 Generally asymptomatic or only mild death d/t intestinal blockage in children.
symptoms. b. Ectopic migration: high fever &
 Larvae: anaesthesia.
 Cough & dyspnea. c. Adult worms migrate to unusual sites:
 Pneumonitis.  Invasion of bile ducts, gallbladder,
PATHOLOGY  Loeffler’s syndromes. liver, & appendix.
 Adult worms:  Migrate to peritoneal causing
 In small intestine. peritonitis.
 Symptoms depend on e worm load. d. E byproducts of living or dead worms may
 If > 26 worms can cause digestive rarely produce marked toxic manifestations
disorders & nutritional loss. in sensitized persons such as edema of e
 Vague abdominal pain is common. face, urticaria, insomnia, loss of apetite, &
weight loss.
1. Clinical manifestation: intestinal obstruction.
DIAGNOSIS 2. Parasitological diagnosis: eggs in stool.
3. Worm expulsion during treatment.
TREATMENT 1. Albendazole: single 400 mg dose.
2. Mebendazole: 100 mg twice daily for 3 days.
 3. Control: avoid contamination of fodd & water.

Adult worms live in the lumen of the small intestine.  A female may
produce approximately 200,000 eggs per day, which are passed with the
feces .  Unfertilized eggs may be ingested but are not infective.  Fertile
eggs embryonate and become infective after 18 days to several weeks ,
depending on the environmental conditions (optimum: moist, warm, shaded
soil).  After infective eggs are swallowed , the larvae hatch , invade the
intestinal mucosa, and are carried via the portal, then systemic circulation to
the lungs .  The larvae mature further in the lungs (10 to 14 days),
penetrate the alveolar walls, ascend the bronchial tree to the throat, and are
swallowed .  Upon reaching the small intestine, they develop into adult
worms .  Between 2 and 3 months are required from ingestion of the
infective eggs to oviposition by the adult female.  Adult worms can live 1 to
2 years.
 Life Cycle of Trichuris trichiura

Trichuris trichiura
POINTS DETAILS
 Also known as whipworm.
 Seen in cosmopolitan areas where e weather r warm & humid.
EPIDEMIOLOGY  Presently e commonest intestinal helminth.
 Disease: trichuriasis.
 Infection is through e ingestion of embryonated eggs via hands, food, or drink.
 E female organism is 50 mm long with a slender anterior (100 µm diameter) & a
thicker (500 µm diameter) posterior end.
MORPHOLOGY  E male is smaller & has a coiled posterior end.
 E eggs r lemon or football (rugby) shaped & have terminal plugs at both ends.
1. Trichuriasis infection: 2. Rectal prolapsed:
 Infection often seen with Ascaris.  D/t worms damaging e muscles.
 Normally is “low worm burden”.  Straining to defecate.
 Normally asymptomatic.  Normally in children.
 Heavy infection:  Swollen mucosa: reflex
 Infection to rectum. peristalsis.
 Bowel irritation d/t poor water 3. Malnutrition:
resorption in colon.  Very heavy infection.
PATHOLOGY  Dysentery with blood &  Results in growth retardation &
mucus. stunting.
 Abdominal pain, headache, & 4. Finger clubbing:
anorexia.  Also known as kailonychia.
 Appendicitis.  Nail is convex.
 Hypochromic anaemia: 0.005  12% of heavy infection (in
mL blood/w/d. Malaysia).
 2o infection: E. histolytica, B.
coli, & Shigella. The unembryonated eggs are passed with the stool (1).  In the soil, the eggs
1. Clinical manifestation: rectal prolapsed with e worms seen. develop into a 2-cell stage (2), an advanced cleavage stage (3), and then they
DIAGNOSIS 2. Diagnostic eggs in e stool. embryonate (4); eggs become infective in 15 to 30 days.  After ingestion
1. Albendazole: single 400 mg dose & repeat treatment is required. (soil-contaminated hands or food), the eggs hatch in the small intestine, and
TREATMENT 2. Mebendazole: 100 mg twice daily for 3 days. release larvae (5) that mature and establish themselves as adults in the colon
3. Rectal prolapsed: revert rectum & give treatment for helminth.
(6).  The adult worms (approximately 4 cm in length) live in the cecum and
1. Treatment of infected individuals.
2. Sanitary disposal of human feces.
ascending colon.  The adult worms are fixed in that location, with the
PREVENTION 3. Washing hands before meals. anterior portions threaded into the mucosa.  The females begin to oviposit 60
4. Thorough washing & scalding of uncooked vegetable. to 70 days after infection.  Female worms in the cecum shed between 3,000
and 20,000 eggs per day.  The life span of the adults is about 1 year.
 HOOKWORMS Life cycle of Hookworms.
POINTS DETAILS
 Species:
1. Necator americanus: in Malaysia & South East Asia.
2. Ancylostoma duodenale: in subtropic areas.
EPIDEMIOLOGY 3. Ancylostoma ceylanicum: found in animal but lower in human.
4. Ancylostoma malayanum: in Malaysia.
 Disease: anchylostomasis.
1. Adults:
 Size: female is 9 to 11 mm while male is 7 to 9 mm.
 Male worms have spicule as copulatory organ.
 Live in 2nd & 3rd portion of jejunum & occasionally in duodenum.
 Have a large buccal capsule & cutting plate for damaging tissue to release blood.
 Also have one pair of anticoagulant gland to hold & suck in blood.
2. Eggs:
 E no. of e eggs is fairly constant with 3000 to 6000 eggs/day/worm.
 200 eggs at any one time.
MORPHOLOGY  4 to 8 cells when passed.
 Suitable condition for e eggs r warmth, shade, moisture, & sandy loam.
3. Larvae:
 Infective larvae in 5 days.
 Amongst upper at about 2 cm of soil (3 – 6 weeks).
 Killed by direct sunlight.
 Larvae penetrate soft tissues (A. duodenale: penetration swallowed).
 Lung migration is short, only 24 hours.
 Mature in 2 months.
 Live span is 1 to 14 years.
1. Larvae: Eggs are passed in the stool (1), and under favorable conditions (moisture, warmth,
a. Skin penetration (from e soil):
shade), larvae hatch in 1 to 2 days.  The released rhabditiform larvae grow in the
 Intense & ground itch (Local erythema, macules, & papules).
feces and/or the soil (2), and after 5 to 10 days (and two molts) they become become
 D/t cutaneous invasion and subcutaneous migration of larva.
b. Lung migration: filariform (third-stage) larvae that are infective (3).  These infective larvae can
 Brief symptoms: Loeffler’s syndrome (pulmonary bronchitis, pneumonitis, & survive 3 to 4 weeks in favorable environmental conditions.  On contact with the
eosinophilia). Cough & sore throat may present. human host, the larvae penetrate the skin and are carried through the veins to the
 D/t migration of larvae through lung, bronchi, & trachea. heart and then to the lungs.  They penetrate into the pulmonary alveoli, ascend the
PATHOLOGY 2. Adults: bronchial tree to the pharynx, and are swallowed (4).  The larvae reach the small
 Blood feeders which cause blood loss: light (3 mL) & heavy (100 mL). intestine, where they reside and mature into adults.  Adult worms live in the lumen of
 Anaemia: the small intestine, where they attach to the intestinal wall with resultant blood loss
a. Necator: normocromic normocytic. by the host (5).  Most adult worms are eliminated in 1 to 2 years, but longevity
b. Ancylostoma: hypochromic microcytic. records can reach several years. Some A. duodenale larvae, following penetration of
 Growth retardation. the host skin, can become dormant (in the intestine or muscle).  In addition, infection
 Anorexia, epigastric pain & gastro-intestinal hemorrhage d/t attachment of adult
by A. duodenale may probably also occur by the oral and transmammary route. N.
worms & injury to upper intestinal mucosa.
americanus, however, requires a transpulmonary migration phase.
 Diagnosis is made by identification of hookworm eggs in fresh or preserved feces.
DIAGNOSIS  Species of hookworms cannot be distinguished by egg morphology.
 Mebendazole, 200 mg, for adults & 100 mg for children, for 3 days is effective.
TREATMENT  Sanitation is e chief method of control: sanitary disposal of fecal material & avoidance of
 contact with infected fecal material.
Strongyloides stercoralis Life Cycle of Strongyloides stercoralis.
POINTS DETAILS
 Also known as threadworm.
 Disease: Cochin-China diarrhea.
 Widely distributed: 3 to 30 million cases (probably underdiagnosed).
EPIDEMIOLOGY  Female worms only r sufficient to maintain life cycle, this is known as
parthenogenesis: e production of progeny w/o female & male copulation.
 Strongyloides fulleborni is common in Africa & Asia.
 Modes of infection: skin penetration & autoinfection.
 E size of parasitic female is larger (2.2 mm x 45 micrometers) than the free-
living worm (1 mm x 60 micrometers).
MORPHOLOGY  E male worm is 2 mm but is rarely seen.
 E eggs, when laid are 55 micrometers by 30 micrometers.
 Light infections r generally asymptomatic.
 Skin penetration causes itching & red blotches.
 During migration, e organisms cause bronchial verminous pneumonia & in e
duodenum they cause a burning mid-epigastric pain & tenderness accompanied
by nausea & vomiting while diarrhea & constipation may alternate.
 Heavy, chronic infections result in anemia, weight loss & chronic bloody
PATHOLOGY dysentery.
 Secondary bacterial infection of damaged mucosa may produce serious
complications.
 Cell mediated immunity may become defective or immunologically deficient. If
there is steroid therapy or organ transplantation, disease will disseminate & can
lead to death d/t fulminating infection.
 E presence of free rhabditiform larvae in e feces is diagnostic.
DIAGNOSIS  Culture of stool for 24 hours will produce filariform larvae.
 Ivermectin or thiabendozole can be used effectively.
TREATMENT  Direct & indirect infections r controlled by improved hygiene & auto-infection
is controlled by chemotherapy.

The Strongyloides life cycle is complex among helminths with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host.   Two types of
cycles exist: Free-living cycle: The rhabditiform larvae passed in the stool (1) (see "Parasitic cycle" below) can either molt twice and become infective filariform larvae (direct development) (6) or molt
four times and become free living adult males and females (2) that mate and produce eggs (3) from which rhabditiform larvae hatch (4).  The latter in turn can either develop (5) into a new generation of
free-living adults (as represented in (2)), or into infective filariform larvae (6).  The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) (6). Parasitic cycle: Filariform
larvae in contaminated soil penetrate the human skin (6), and are transported to the lungs where they penetrate the alveolar spaces; they are carried through the bronchial tree to the pharynx, are swallowed
and then reach the small intestine (7).  In the small intestine they molt twice and become adult female worms (8).  The females live threaded in the epithelium of the small intestine and by parthenogenesis
produce eggs (9), which yield rhabditiform larvae.  The rhabditiform larvae can either be passed in the stool (1) (see "Free-living cycle" above), or can cause autoinfection (10).  In autoinfection, the
rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the
filariform larvae may follow the previously described route, being carried successively to the lungs, the bronchial tree, the pharynx, and the small intestine where they mature into adults; or they may
disseminate widely in the body.  To date, occurrence of autoinfection in humans with helminthic infections is recognized only in Strongyloides stercoralis and Capillaria philippinensis infections.  In the
case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed
individuals
 Enterobius vermicularis Life Cycle of Enterobius vermicularis
POINTS DETAILS
 Also known as pinworm.
 Probably e commonest helminth infection.
 Difficult to diagnose.
 E worldwide infection is about 210 million. It is an urban disease of children in
crowded environment (schools, day care centers, etc.) with 1 – 12 years old is e
EPIDEMIOLOGY highest.
 Adults may get it from their children.
 Disease: enterobiasis.
 Modes of infection: autoinfection, inhalation, & toilet seats (family or institution
infection).
1. Adults:
 Female: 8 – 13 mm.
MORPHOLOGY  Male: 2 – 15 mm.
 Female worms produce 10,000 to 15,000 eggs/worm/one time.
2. Eggs: 60 µm x 27 µm r ovoid but asymmetrically flat on one side.
 Female worms go to e proximity of
 Mainly asymptomatic. genitals:
 Can lead to loss of appetite & sleep. 1. Pruritus vagiane.
 Pruritus ani: intense itching & 2. Mucoid discharge.
PATHOLOGY scarification. 3. Urinary or genital disturbances.
 Appendicitis: normally do not invade 4. Gravid female worms go to
tissues. fallopian tube: salphingitis
endometritis.
 Diagnosis is made by finding e adult worm or eggs in e perianal area, particularly
DIAGNOSIS at night.
 Scotch tape or a pinworm paddle is used to obtain eggs.
 Two doses (10 mg/kg; maximum of 1g each) of Pyrental Pamoate two weeks
apart gives a very high cure rate.
 Mebendazole is an alternative. E whole family should be treated, to avoid
TREATMENT reinfection.
 Bedding & underclothing must be sanitized between e two treatment doses. Eggs are deposited on perianal folds (1).  Self-infection occurs by transferring infective eggs to the
 Personal cleanliness provides e most effective in prevention. mouth with hands that have scratched the perianal area (2).  Person-to-person transmission can
also occur through handling of contaminated clothes or bed linens.  Enterobiasis may also be
acquired through surfaces in the environment that are contaminated with pinworm eggs (e.g.,
Diagnosis of soil transmitted helminths curtains, carpeting).  Some small number of eggs may become airborne and inhaled.  These would
be swallowed and follow the same development as ingested eggs.  Following ingestion of
1. Examination of fecal sample: simple, cheaper, & smelly.
2. Eggs: ascaris, hookworm, trichuris, strongyloides. infective eggs, the larvae hatch in the small intestine (3) and the adults establish themselves in the
Diagnosis 3. Larvae: strongyloides stercoralis. colon (4).  The time interval from ingestion of infective eggs to oviposition by the adult females is
4. Perianal swab: enterobius. about one month.  The life span of the adults is about two months.  Gravid females migrate
5. Concentration of eggs: Haroda Mori & Kato – katz. nocturnally outside the anus and oviposit while crawling on the skin of the perianal area (5).  The
1. Mebendazole: course for all intestinal worms. larvae contained inside the eggs develop (the eggs become infective) in 4 to 6 hours under optimal
2. Albendazole: stat dose for all except Trichuris trichiuria. conditions (1).  Retroinfection, or the migration of newly hatched larvae from the anal skin back
Treatment 3. Oxantel: pyrantel pamoate: stat dose except Trichuris trichiuria. into the rectum, may occur but the frequency with which this happens is unknown.
4. Thiabendazole: strongyloides.
5. Endemis areas: treatment twice a year & health education.
 FILARIASIS
POINTS DETAILS
 Common disease in tropical area.
 It involves 900 million cases in endemic areas & 90 millions r diseased.
OVERVIEW  It is a debilitating disease listed in WHO.
 One of Malaysia rural problem: 2.5 million in endemic areas.
1. Wuchereria bancrofti. 5. Loa loa.
2. Brugia malayi. 6. Acanthocheilonema perstans.
SPECIES 3. Brugia timori. 7. Acanthocheilonema streptocerca.
4. Onchocerca volvulus. 8. Mansonella ozzardi.
3. Habitat:
1. Microfilarial morphology: a. Adults (long, filiform, & viviparous):
 Oviviparous females → produce microfilaria →  Lymphatic: WB, BM, & BT.
prelarval form.  Subcutaneous tissue: OV, LL, AP, & AS.
 Important parts:  Peritoneal cavity: MO.
a. Microfiarial sheath: b. Microfilaria:
 Formerly was an egg shell.
 Blood: WB, BM, BT, LL, AP, & MO.
 Presence in blood microfilaria but absence
 Skin: OV & AS.
in skin microfilaria.
4. Periodicity:
b. Body of microfilaria.
c. Nucleus in e body for identification.  Periodicity is a biologic adaptation of e parasite to e
COMMON d. Tail nucleus for identification. time of maximum biting activity of e parasite vector.
FEATURES 2. Vectors & development:  E microfilaria r concentrated in e small blood
 Vectors: vessels of e lung during e day & r liberated into e
a. Mosquitoes: WB, BM, & BT. peripheral circulation at night & vice versa.
b. Chrysops: LL.  One stimulus which is increased oxygen pressure by
c. Simulium: OV. hyperventilation or exercise causes microfilaria to
d. Culicoides: AP, AS, & MO. leave e lung.
 Life cycle: L1 → L2 → L3 – infective stage (in  3 types of periodicity:
salivary gland of e mosquito) → Microfilaria. a. Nocturnal: WB, BM, BT.
 If there r too many microfilaria in e mosquito, it b. Diurnal: LL.
cannot fly because thorax muscles r damaged. c. Diurnal subperiodic: WB in South Pasific.
d. Nocturnal subperiodic: BM in Malaysia.

Wuchereria bancrofti & Brugia malayi.

POINTS Wuchereria bancrofti Brugia malayi.
 Vectors: Mansonia uniformis (in paddy field).
 Vectors:
1. Culex quinquefasciatus: worldwide.  Restricted to South-East Asia.
2. Anopheles maculates: Orang asli.  2 types:
EPIDEMIOLOGY  Generally is an urban disease. 1. Not Zoonosis: nocturnally periodic (strictly human
parasites).
 Strictly human parasites.
2. Zoonosis: nocturnally subperiodic & difficult to
 Distributed in tropical areas worldwide.
control (found in man, monkeys, & cats).
 Adult female W. bancrofti found in lymph nodes & lymphatic channels are 10 cm x 250 µm whereas males r only
half that size.
MORPHOLOGY  Microfilaria found in blood r only 260 micrometers x 10 µm.
 Adult B. malayi are only half the size of W. bancrofti but their microfilaria r only slightly smaller than W.  bancrofti.
 These two organisms r very similar in e diseases they cause (signs & symptoms) but differ in e location of
elephantiasis.
 Factors in microfilaria transmission:
1. Many mosquito bites needed before transmission succeeded.
2. Mosquito susceptibility.
3. Mosquito with L3.
 Period after transmission:
1. Prepatent period: asymptomatic.
2. Patent period:
 B/w 3 month after transmission to 1 year.
 Microfilaria & eosinaphils r high in blood.
a. Acute:
 Lymphadenitis & recurrent high fever every 3 to 12 weeks, which lasts 3 to 7 days: indicate that
microfilaria r released.
PATHOLOGY  Lymphadenitis → recurrent lymphangitis (red streak) → edema of e limb (hand or leg).
b. Chronic:
 Also known as amicrofilarimic filariasis because microfilaria r absence in e peripheral blood.
 Edema is either pitting or non – pitting.
 Elephantiasis d/t 2o infection.
c. Tropical pulmonary eosinophilia:
 D/t hypersensitivity.
 Asthma like symptoms.
 Differences in e clinical manifestation of disease:
1. W. bancrofti:
 Edema is at above & below e knee which involves genital organs.
 Causes lymphuria, chyluria, & hydrocoele.
2. B. malayi: edema is below e knee & involvement of genital organ is not reported.
  Through examination of 60 cu mL of blood which is stained with Giemsa.
 Urine can also be used for W. bancrofti.
 Examine e microfilaria:
DIAGNOSIS 1. There r 2 isolated tail nucleases.
1. Tail nucleuses are separated in approximately same
2. Microfilarial sheath:
distance to each other.
a. Zoonosis: few or none emerge from e sheath.
2. Microfilarial sheath is present.
b. Non zoonosis: 50% – 70% leave sheath.
3. Microfilarial disposition is smoothly curves.
3. Microfilarial disposition is in sharp edge.
 Diethylcarbamazine (DEC) quickly kills e adults worms or sterilizes e female, but produces side effects.
TREATMENT  It is given 2 mg/kg orally for 14 days.
 Steroids & cooler climate help reduce e inflammatory reaction.

Life Cycle of Wuchereria bancrofti.

Different species of the following genera of mosquitoes are vectors

of W. bancrofti filariasis depending on geographical distribution. 
Among them are: Culex (C. annulirostris, C. bitaeniorhynchus, C.
quinquefasciatus, and C. pipiens); Anopheles (A. arabinensis, A.
bancroftii, A. farauti, A. funestus, A. gambiae, A. koliensis, A. melas,
Site A. merus, A. punctulatus and A. wellcomei); During a blood meal, an
infected mosquito introduces third-stage filarial larvae onto the skin
Symptoms of the human host, where they penetrate into the bite wound . 
They develop in adults that commonly reside in the lymphatics . 
The female worms measure 80 to 100 mm in length and 0.24 to 0.30
mm in diameter, while the males measure about 40 mm by .1 mm. 
Adults produce microfilariae measuring 244 to 296 μm by 7.5 to 10
μm, which are sheathed and have nocturnal periodicity, except the
South Pacific microfilariae which have the absence of marked
periodicity.  The microfilariae migrate into lymph and blood
channels moving actively through lymph and blood .  A mosquito
ingests the microfilariae during a blood meal .  After ingestion,
the microfilariae lose their sheaths and some of them work their way
through the wall of the proventriculus and cardiac portion of the
mosquito's midgut and reach the thoracic muscles .  There the
microfilariae develop into first-stage larvae and subsequently into
third-stage infective larvae .  The third-stage infective larvae
migrate through the hemocoel to the mosquito's prosbocis and
can infect another human when the mosquito takes a blood meal

Life cycle of Brugia malayi.

The typical vector for Brugia malayi filariasis are mosquito species
from the genera Mansonia and Aedes.  During a blood meal, an
infected mosquito introduces third-stage filarial larvae onto the skin of
the human host, where they penetrate into the bite wound .  They
develop into adults that commonly reside in the lymphatics .  The
adult worms resemble those of Wuchereria bancrofti but are smaller. 
Female worms measure 43 to 55 mm in length by 130 to 170 μm in
width, and males measure 13 to 23 mm in length by 70 to 80 μm in
width.  Adults produce microfilariae, measuring 177 to 230 μm in
length and 5 to 7 μm in width, which are sheathed and have nocturnal
periodicity.  The microfilariae migrate into lymph and enter the blood
stream reaching the peripheral blood .  A mosquito ingests the
microfilariae during a blood meal .  After ingestion, the
microfilariae lose their sheaths and work their way through the wall of
the proventriculus and cardiac portion of the midgut to reach the
thoracic muscles .  There the microfilariae develop into first-stage
larvae and subsequently into third-stage larvae .  The third-stage
larvae migrate through the hemocoel to the mosquito's prosbocis
and can infect another human when the mosquito takes a blood meal
 OTHER FILARIA
POINTS Onchocerca volvulus Loa loa Others
 Prominent in:
1. Africa: Sudan, Zaire, & Angola.
2. S. America: Colombia, Guatamala, & Brazil.  Common in Africa.
3. Middle East: Yemen & Saudi Arabia.  Disease: Calabar swelling – Nditot
 Disease: African liver blindness. skin.
EPIDEMIOLOGY  Vector – Simulium damnosum:  E worms can cross e conjunctiva.
 Breed in fresh stream.  One of zoonosis: found in monkeys.
 Not a zoonosis.  Vectors: Chrysops dimidiate.
 Pool feeder & day biting.
 Use e mouth part to lacerate e skin, so that
there is blood for microfilaria to enter.
1. Adults: 1. Other human filaria:
 Intricately coiled in subcutaneous nodule 1. Adults:
(onchocercoma).  Found in subcutaneous swelling.
A. perstans A. streptocerca M. ozzardi
 Size: male (2 -4 cm) & female (3 – 5 cm).  Non fibrous.
America & W.
 Life span: 16 years.  E worms & swelling r moving: Dist. Africa & America Africa
MORPHOLOGY 2. Microfilaria: called migratory nodules.
Indies
Subcutaneous
 In subcutaneous tissue. 2. Microfilaria: Mf habitat Peritoneal tissue Mesentry
tissue
 No sheath & periodicity.  Found in blood with sheath.
Vector Culicoides sp.
 Its cephalic part is enlarged like a spoon –  Diurnal periodicity.
Eosinophilia & Eosinophilia &
shaped (contains enzymes). Pathology Non - pathology
allergy allergy
1. Adults: Dx Blood Skin snip Blood
 Form fibrous nodules (immotile) called Rx DEC
onchocercoma:
a. Acute: soft & painful.
b. Chronic: harden & painless. 2. Animal filarial infecting man:
 Nodule position depends on e exposure & a. Dogs:
vector bite.  Dirofilaria immitis.
 Eosinophilia (10 % - 75%).  Adults:
1. Migration: in subcutaneous tissue  Dirofilaria tenuis.
PATHOLOGY  Presbyderma (aging skin) d/t e destruction of
& conjunctiva. b. Cats & dogs: Brugia pahangi.
elastic fibers & muscles.  No periodicity.
2. Eosinophilia: 60% - 90%.
2. Microfilaria:  Causes tropical pulmonary eosinophilia.
 In e skin, nodule, & eyes.
 Damage elastic fibers.
 Onchocercoma & lymph nodes r hang loose,
called hanging groin.
 In e eye: keratitis, photophobia, optic atrophy,
& blindness.
1. Calabar swelling in endemic area.
1. Skin snip: for microfilaria.
DIAGNOSIS 2. In blood if given DEC (50 mg).
2. Microfilaria ain blood.
3. Migration in e eye.
1. DEC. 1. DEC.
TREATMENT 2. Suramin. 2. Surgical removal with local anesthetics.
 Life Cycle of Loa loa Life Cycle of Onchocerca volvulus

During a blood meal, an infected blackfly (genus Simulium) introduces third-stage

The vector for Loa loa filariasis are flies from two species of the genus Chrysops, C. silacea filarial larvae onto the skin of the human host, where they penetrate into the bite wound
and C. dimidiata.  During a blood meal, an infected fly (genus Chrysops, day-biting flies) .   In subcutaneous tissues the larvae develop into adult filariae, which commonly
introduces third-stage filarial larvae onto the skin of the human host, where they penetrate reside in nodules in subcutaneous connective tissues .  Adults can live in the nodules
into the bite wound .  The larvae develop into adults that commonly reside in for approximately 15 years.  Some nodules may contain numerous male and female
subcutaneous tissue .  The female worms measure 40 to 70 mm in length and 0.5 mm in worms.  Females measure 33 to 50 cm in length and 270 to 400 μm in diameter, while
diameter, while the males measure 30 to 34 mm in length and 0.35 to 0.43 mm in diameter.  males measure 19 to 42 mm by 130 to 210 μm.  In the subcutaneous nodules, the female
Adults produce microfilariae measuring 250 to 300 μm by 6 to 8 μm, which are sheathed and worms are capable of producing microfilariae for approximately 9 years.  The
have diurnal periodicity.  Microfilariae have been recovered from spinal fluids, urine, and microfilariae, measuring 220 to 360 µm by 5 to 9 µm and unsheathed, have a life span
sputum.  During the day they are found in peripheral blood, but during the noncirculation that may reach 2 years.  They are occasionally found in peripheral blood, urine, and
phase, they are found in the lungs .  The fly ingests microfilariae during a blood meal .  sputum but are typically found in the skin and in the lymphatics of connective tissues
After ingestion, the microfilariae lose their sheaths and migrate from the fly's midgut .  A blackfly ingests the microfilariae during a blood meal .   After ingestion, the
through the hemocoel to the thoracic muscles of the arthropod .  There the microfilariae microfilariae migrate from the blackfly's midgut through the hemocoel to the thoracic
develop into first-stage larvae  and subsequently into third-stage infective larvae .  The muscles .  There the microfilariae develop into first-stage larvae and subsequently
third-stage infective larvae migrate to the fly's proboscis and can infect another human into third-stage infective larvae .  The third-stage infective larvae migrate to the
when the fly takes a blood meal blackfly's proboscis and can infect another human when the fly takes a blood meal
 LARVA MIGRANS
VISCERAL LARVA MIGRANS
CUTANEOUS
LARVA MIGRANS Toxocara cati
POINTS Anisakis marina Gnathostoma spinigerum Angiostrongylus cantonensis
(T. canis)
 Species:
1. Ancylostoma
caninum: dog.
2. Uncinaria sp.: dog.
3. Ancylostoma  Ascaris of seafish & mammals.
ceylanicum: cat.  Also known as herring disease.
4. Ancylostoma  Species:  Prevalent in:
malayanum. 1. Toxocara cati (cats). 1. Japan.  Visceral larva migrans.
 Pathology: 2. Toxacara canis (dog). 2. Europe.  Prevalent in:
1. Dermatitis. 3. USA. 1. Japan.  Visceral larva migrans.
 Visceral organ infection.
2. Intracutaneous  Life cycle: adult worms in fish gut 2. Thailand.  Prevalent in:
 Eosinophilic granuloma.
lesions. → human infection → severe:  Human infection: 1. Indonesia.
 Eye & brain infection.
3. Migration of partial obstruction of intestine.  Mode of infection: 2. Thailand.
 In cats & dogs, it is similar to 3. Philippines.
nematode larva in
Ascariasis in human.  Human infection: 1. Eating raw & marinated
animal: serpiginous  Zoonosis. fish such as somfak  There r cases in Sarawak.
 Human infection is by
migration.  Modes of infection: eating (Thailand) & Sashimi  Infection by eating raw snail &
contamination or accidential.
4. Modes of infection: infected raw fish & mammals (Japan). crab.
contamination of
PATHOLOGY  Infection is higher in youth & 2. From animal host such as  Increase in Achantina & Pila
with alcohols such as
beaches, play – pans, children.
Japanese sashimi. carnivors & paratenic host infection.
feet, & hands by  Life cycle: dog & cat (normal  Higher in adult males such as such as chicken & pigs.  A zoonosis.
cats’ & dogs’ feces. cycle) → mature egg in feces →  Complications:
fisherman removing guts of  Complications:
5. Results in infection in human → visceral fish. 1. Granulomatous recations  Eosinophilic meningitis:
erythematous tunnels migration → larva die in e organs  Man is accidental host. (swelling) d/t spines & recover after migration.
& intense itching such as brain & eyes.  Pathology: migration.  Eye, brain, & spinal cord
especially during e  Reinfection can be complicated & 1. Granulomatous reaction: 2. Allergic reaction. involvement.
night. causes allergic reaction such as eosinophilic. 3. Eye & spinal cord
6. Increased of asthma – like & increased 2. Gastric involvement: involvement in Thailand.
eosinophils. eosinophilia. pain, nausea, & vomiting.
7. Also leads to 2o  Control: eat only cooked food
infection. especially seafood.
 Treatment:
Thiabendazole topically
(at terminal end) or
orally.
 Clinical arounds: serology  Clinical based: increase
DIAGNOSIS (eosinophils).
 Clinical based.
eosinophils.
1. Symptomatic treatment.
TREATMENT  Thiabendazole.
2. Surgical.
 Symptomatic treatment.  Symptomatic treatment.
 Life Cycle of Toxocara canis.
Toxocara canis accomplishes its life cycle in dogs, with humans acquiring the infection as
accidental hosts. Following ingestion by dogs, the infective eggs yield larvae that penetrate the
gut wall and migrate into various tissues, where they encyst if the dog is older than 5 weeks. In
younger dogs, the larvae migrate through the lungs, bronchial tree, and esophagus; adult worms
develop and oviposit in the small intestine. In the older dogs, the encysted stages are reactivated
during pregnancy, and infect by the transplacental and transmammary routes the puppies, in
whose small intestine adult worms become established. Thus, infective eggs are excreted by
lactating bitches and puppies. Humans are paratenic hosts who become infected by ingesting
infective eggs in contaminated soil. After ingestion, the eggs yield larvae that 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 that are the basis of toxocariasis.
Life cycle of Ancylostoma braziliensis
Eggs are passed in the stool , and under favorable conditions (moisture, warmth, shade), larvae hatch in 1
to 2 days.  The released rhabditiform larvae grow in the feces and/or the soil , and after 5 to 10 days (and
two molts) they become become filariform (third-stage) larvae that are infective .  These infective larvae
can survive 3 to 4 weeks in favorable environmental conditions.  On contact with the human host, the larvae
penetrate the skin and are carried through the veins to the heart and then to the lungs.  They penetrate into
the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed .  The larvae reach
the small intestine, where they reside and mature into adults.  Adult worms live in the lumen of the small
intestine, where they attach to the intestinal wall with resultant blood loss by the host .  Most adult
worms are eliminated in 1 to 2 years, but longevity records can reach several years.
Some A. duodenale larvae, following penetration of the host skin, can become dormant (in the intestine or
muscle).  In addition, infection by A. duodenale may probably also occur by the oral and transmammary
route. N. americanus, however, requires a transpulmonary migration phase.
 OTHER NEMATODES (NOT LARVA MIGRANS)
POINTS Trichinella spiralis Dracunculus medinensis Capillaria philippinensis
 Also known as Guinea worm; fiery
serpent of the Israelites.
 Not a larva migrant.
 Prevalent in:  Not a larva migrant.
 Worldwide distribution.
1. West India.  Prevalent in :
 Sources:
2. Pakistan. 1. Philippines.
1. E quality of pork &
3. Iran. 2. Thailand.
consumption of poorly
EPIDEMIOLOGY
4. Saudi Arabia.  History:
cooked meat.
5. Yemen. 1. 1963 onwards: malabsorption
2. Rats & bears: 40% - 50%
6. Middle Africa (belt). syndrome (mostly in males).
infected.
 Infection is linked to rural 2. 1967: many deaths.
 Autopsy surveys indicate about
community, ponds, wells, & other 3. 1980: a new epidemic in
2% of e population is infected.
water sources. Leyte (Luzon).
 E mortality rate is low.
 Associated with direct contact of
water.
 Life cycle: mucosa of small
intestine of birds, wild rats, &
1. Subcutaneous (adult worms): monkeys → eggs & larva →
1. Intestinal symptoms (d/t larval a. Inflammatory reaction. intestine of fish (in brackish) →
penetration): b. Sterile blister. raw fish eaten → human
a. Abdominal pain. c. Worm in tunnel. infection.
b. Diarrhea. d. Rupture causes abscess,  Clinical manifestation:
PATHOLOGY 2. Muscles (d/t larval ulceration, necrosis, & can 1. Abdominal pain.
calcification): lead to 2o infection. 2. Diarrhea.
a. Miositis. 2. Allergic manifestation: 3. Barborgymi.
b. Paralysis. a. Urticaria & pruritus. 4. Protein loosing enteropathy:
c. Epilepsy (rare). b. Vomiting & dyspnea. severe metabolic &
3. Worm removal: healing. nutritional imbalance.
 Complication: 25% mortality if
no treatment.
1. Eggs.
 Clinical based: increased 1. Local lesion.
DIAGNOSIS 2. Larvae.
eosinophils. 2. Examining blister fluid.
3. Adults.
1. Metronidazole for 1 week.
1. Steroids r used for treatment of
2. Removal of adults:
inflammatory symptoms.
a. Surgical.
2. Mebendazole is used to
b. Rolling out worms.
eliminate worms.
TREATMENT 3. Control:  Mebendazole.
3. Elimination of parasite infection
a. Avoid water contact.
in hogs & adequate cooking of
b. Boiling water: for Cyclops.
meat r e best ways of avoiding
c. 1981: WHO eradicable
infection.
disease.
 Life Cycle of Trichinella spiralis
Trichinellosis is acquired by ingesting meat containing cysts (encysted larvae) of Trichinella.  Humans become infected by drinking unfiltered water containing copepods (small
After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the
small bowel mucosa where they develop into adult worms (female 2.2 mm in length, males 1.2
mm; life span in the small bowel: 4 weeks).  After 1 week, the females release larvae that
migrate to the striated muscles where they encyst .  Trichinella pseudospiralis, however, does
not encyst.  Encystment is completed in 4 to 5 weeks and the encysted larvae may remain viable
for several years.  Ingestion of the encysted larvae perpetuates the cycle.  Rats and rodents are
primarily responsible for maintaining the endemicity of this infection.  Carnivorous/omnivorous
animals, such as pigs or bears, feed on infected rodents or meat from other animals.  Different
animal hosts are implicated in the life cycle of the different species of Trichinella.  Humans are
accidentally infected when eating improperly processed meat of these carnivorous animals (or
eating food contaminated with such meat).
Life Cycle of Dracunculus medinensis
crustaceans) which are infected with larvae of D. medinensis .  Following ingestion, the
copepods die and release the larvae, which penetrate the host stomach and intestinal wall
and enter the abdominal cavity and retroperitoneal space .  After maturation into adults
and copulation, the male worms die and the females (length: 70 to 120 cm) migrate in the
subcutaneous tissues towards the skin surface .  Approximately one year after infection,
the female worm induces a blister on the skin, generally on the distal lower extremity,
which ruptures.  When this lesion comes into contact with water, a contact that the patient
seeks to relieve the local discomfort, the female worm emerges and releases larvae . 
The larvae are ingested by a copepod and after two weeks (and two molts) have
developed into infective larvae .  Ingestion of the copepods closes the cycle
 Fasciola hepatica
POINTS DETAILS
 Geographical distribution:  Disease:
 Cosmopolitan.  Fascioliasis.
 Sheep & cattle – raising countries.  Primarily an animal disease.
 Human infection is common.  Modes of infection:
 Habitat: 1. Human infection:
EPIDEMIOLOGY  Proximal bile passage & gallbladder.  Ingestion of plants such as watercress.
 Occasionally ectopic sites.  Ingestion of water containing encysted
 Definitive hosts: metacercariae.
 Sheep, cattle, deer, & rabbits. 2. Herbivorous or omnivorous animal infection:
 Other herbivorous mammals: reservoir hosts. acquire e infection in e low damp pastures where e
 Rarely man. vegetation is infected with metacercariae.
1. Adults: 
 Adult Fasciola hepatica can reach lengths of 3 cm. 
 All of their major systems r branched, including e intestine, testes, & ovary.
2. Eggs: 
MORPHOLOGY  E eggs of Fasciola hepatica r large, 150 um in length. 
 E operculum often appears to be "too small" so that it doesn't fit quite right.
3. Life cycle: man ingests metacercariae → excysts in duodenum → penetrates liver → unembryonated egg in feces
→ enter e snail egg (embryonates in e water) → miracidium → sporocyst → redia (in water) → cercaria →
metacercaria (infective stage).
1. Liver root:
 Mechanical or traumatic lesions: d/t migration 5. Symptoms & signs:
of metacercariae which produces toxic effects.  1st evidence of infection: stabbing substernal
 Inflammation, necrosis, & fibrosis. pain & Rt. Upper quadrant pains.
2. Inflammatory & adenomatous changes:  With progression of infection:
a. Liver enlarged & tender.
PATHOLOGY  Mucosa of bile ducts, fibrosis, & obstruction.
b. Biliary colic & jaundice.
 Cholecystitis & cholelithiasis.
c. Generalized abdominal pain.
3. Migrating larvae in ectopic foci:
d. Digestive disturbance & diarrhea.
 Abscesses or fibrotic lesions.
e. Anemia.
 Lung, brain, orbits, & subcutaneous tissues. 6. Usually there is eosinophilia.
4. Halzoun: mechanical suffocation.
1. History.
2. Clinical pictures & prominent eosinophilia.
3. Direct methods:
 Finding characteristic eggs in stool.
DIAGNOSIS  False diagnosis: avoided by liver – free diet for few days before examination.
4. Indirect methods:
 Immunological based which is useful in early infection & ectopic fascioliasis.
 Intradermal (intracutaneous) test.
 Complement fixation test.
1. Dichlorophenol (bithionol).
Since both drugs r cardiotoxic, e patients should rest during therapy.
2. Dehydroemetine.
TREATMENT 3. Metranidazole.
4. Praziquantel: may be effective.
1. Snail control.
2. Treatment of infected sheep or cattle (reservoir hosts): main source of infection to e snail.
PREVENTION 3. Avoid eating raw vegetables before proper washing.
4. Water from possibly polluted sources should be boiled.
5. A safe water supply is important.

Fasciola gigantica
POINTS DETAILS
 It is a parasite of:
1. Cattle, water buffalo, camels, & wild hogs.
OVERVIEW 2. Herbivore.
3. Occasionally man in Africa, Asia, & Hawaii.
 E adult worm is distinguished from Fasciola hepatica by:
1. Greater length.
2. Shorter cephalic cone.
3. Larger ventral sucker.
MORPHOLOG 4. Borders r parallel.
Y 5. Medial branches of intestinal cecca r T or Y shaped.
6. > anterior position of e reproductive organs.
 Other differences:
1. Larger eggs.
2. Different snail or intermediate host species.
OTHERS  Habitat, life cycle, pathology, diagnosis, & treatment same as Fasciola hepatica.
 Life Cycle of Fasciola hepatica & Fasciola gigantica.

Immature eggs are discharged in the biliary ducts and in the stool .  Eggs become embryonated in water ,
eggs release miracidia , which invade a suitable snail intermediate host , including many species of the genus
Lymnae.  In the snail the parasites undergo several developmental stages (sporocysts , rediae , and cercariae
).  The cercariae are released from the snail and encyst as metacercariae on aquatic vegetation or other
surfaces.  Mammals acquire the infection by eating vegetation containing metacercariae.  Humans can become
infected by ingesting metacercariae-containing freshwater plants, especially watercress .  After ingestion, the
metacercariae excyst in the duodenum and migrate through the intestinal wall, the peritoneal cavity, and the
liver parenchyma into the biliary ducts, where they develop into adults .  In humans, maturation from
metacercariae into adult flukes takes approximately 3 to 4 months.  The adult flukes (Fasciola hepatica: up to 30
mm by 13 mm; F. gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host.  Fasciola
hepatica infect various animal species, mostly herbivores.
Clonorchis sinensis Life Cycle of Clonorchis sinensis.
POINTS DETAILS
 Hosts:
1. Definitive hosts:
 Also known as e Chinese or Oriental liver fluke.
a. Fish eating mammals.
 An important parasite of human in e Far East.
b. Man, dog, hog, & cat.
 Prevalent in: 2. Intermediate hosts:
1. Japan. a. 1st IH: snail of genera Alocima
2. China. & Parafossarulus.
3. South Korea.
EPIDEMIOLOGY 4. Formosa.
b. 2nd IH: fish of e family
cyprinidae.
5. Vietnam.
 Modes of infection:
 Habitat: 1. Usually by eating improperly
1. Mainly at distal biliary passages. cooked fish containing infectious
2. May be in e gallbladder. metacercariae.
3. Occasionally in e pancreatic duct. 2. Less often by ingestion of cysts in
drinking water.
1. Adults: size varies b/w 12 – 20 mm by 3 – 5 mm.
2. Eggs:
 Light-yellowish brown in color.
 Size: 29 µm by 16 µm.
 Have a thick shell & a pitcher shape.
MORPHOLOGY  At e smaller end, e operculum rests in a rim with distinct shoulders.
 At e thicker posterior end is a smaller protuberance.
 Content: fully developed miracidium.
3. Cercariae:
 Free – swimming with finned tail (lophocercous).
 Loses its tail to encyst & becomes metacercariae.
5. Fibrosis & destruction of liver: Embryonated eggs are discharged in the biliary ducts and in the stool . 
 Complications: function is impaired. Eggs are ingested by a suitable snail intermediate host ; there are more
1. Mechanical irritation of e distal bile ducts d/t 6. May predispose to hepatic & than 100 species of snails that can serve as intermediate hosts.  Each egg
toxic secretion. cholangiocarcinoma.
2. Slight leukocytosis & eosinophilia.  Clinical pictures:
releases a miracidia , which go through several developmental stages
3. Hepatomegaly: liver may become enlarged & 1. Might symptoms with light infection. (sporocysts , rediae , and cercariae ).  The cercariae are released
PATHOLOGY tender. 2. Indigestion, epigastric discomfort from the snail and after a short period of free-swimming time in water, they
4. E bile ducts: unrelated to meals, weakness, & loss come in contact and penetrate the flesh of freshwater fish, where they encyst
 Gradually thickens.\become dilated & of weight.
as metacercariae .  Infection of humans occurs by ingestion of
tortuous. 3. Heavy infections r complicated by
 Undergo adenomatous proliferation of cholethiasis & bouts of pyogenic undercooked, salted, pickled, or smoked freshwater fish .  After ingestion,
epithelium. cholangitis. the metacercariae excyst in the duodenum and ascend the biliary tract
4. Sign of liver failure.
through the ampulla of Vater .  Maturation takes approximately 1 month. 
1. Clinical signs in endemic areas with history of eating uncooked fish. The adult flukes (measuring 10 to 25 mm by 3 to 5 mm) reside in small and
DIAGNOSIS 2. Finding characteristic eggs in stool or biliary drainage: eggs require differentiation from those of
medium sized biliary ducts.  In addition to humans, carnivorous animals can
opisthorchid heterophyid flukes.
serve as reservoir hosts.
TREATMENT  Praziquantel.
PREVENTION 1. Good cooking of fish in endemic areas.
2. Refrigeration, salting, or e addition of vinegar or sauce do not kill e metacercariae.
3. Storage or addition of ammonia sulfate may affect e sterilization of human feces.
4. Molluscacides capable of destroying e snail may destroy fish & other aquatic life.
 Opisthorchis sp.
Opisthorcis viverrini POINTS Opisthorchis felineus
 Also known as e cat liver  Cats r e most important
fluke. reservoir hosts in highly
endemic areas.
 It is closely related to
Clonorchis sinensis.  Hosts:
 Geographical distribution: 1. Definitive hosts:
 Geographical distribution:
1. Thailand. a. Cats, dogs, foxes,
1. Eastern & southeastern
2. Laos. & hogs.
Europe.
 Definitive hosts: b. Man in endemic
2. Asiatic areas of e
1. People. areas.
2. Civet cat.
EPIDEMIOLOGY former USSR.
2. Intermediate hosts:
 Habitat:
3. Fish eating mammals. a. 1st IH: snails
1. Usually distal bile.
 Mode of infection: eating uncooked fish Bulinus (infected
2. Occasionally pancreatic
containing e infective metacercariae. by feces deposited
duct.
on sandy shores &
3. Sometimes gallbladder.
washed into
 Mode of infection: eating stream).
raw or insufficiently cooked b. 2nd IH: Cyprinoid
fish. fish.
1. Adults:
 It measures 7 – 12 mm by 1.5 – 3mm.
 Resemble Clonorchis sinensis.
 E ventral sucker is of e same size as e oral sucker.
 2 lobed testes obliquely situated.
 Adults:  Vitelline glands of follicles limited to middle third of e body
 Measures 26 by 13 µm. on either sides of intestinal ceca.
 Closely resemble that of Clonorchis
MORPHOLOGY 2. Eggs:
sinensis.  It measures 30 by 12 µm.
 Contain fully developed miracidium.
 Resemble those of Clonorchis sinensis but narrower & have:
a. More tapering ends.
b. Pointed terminal knob.
c. A less conspicuous opercular rim.
 There is striking association of this
parasite with cholangiocarcinoma.
 E annual rate of liver cancer or
cholangiocarcinoma is more than 100 &
35 – 40 per 100,000 in male & female
respectively.
 It has been hypothesized that biliary PATHOLOGY  Same as Clonorchis sinensis.
epithelium is already hyperplastic:
 From presence of worms.
 Stimulated by nitrosamines in foods.
 By nitrous compounds produced by
macrophages in chronically affected
tissue.
 E presence of characteristic eggs in stool
& duodenal drainage.
DIAGNOSIS  E presence of characteristic eggs in stool & duodenal drainage.

 Praziquantel. TREATMENT  Praziquantel.

1. Proper cooking of fish.
1. Proper cooking of fish.
2. Proper sanitary disposal of human PREVENTION 2. Proper sanitary disposal of human excreta.
excreta.
 Life Cycle of Opisthorchis sp

The adult flukes deposit fully developed eggs that are passed in the feces .  After
ingestion by a suitable snail (first intermediate host) , the eggs release miracidia ,
which undergo in the snail several developmental stages (sporocysts , rediae , cercariae
).  Cercariae are released from the snail and penetrate freshwater fish (second
intermediate host), encysting as metacercariae in the muscles or under the scales .  The
mammalian definitive host (cats, dogs, and various fish-eating mammals including humans)
become infected by ingesting undercooked fish containing metacercariae.  After ingestion,
the metacercariae excyst in the duodenum and ascend through the ampulla of Vater into
the biliary ducts, where they attach and develop into adults, which lay eggs after 3 to 4
weeks .  The adult flukes (O. viverrini: 5 mm to 10 mm by 1 mm to 2 mm; O. felineus: 7
mm to 12 mm by 2 mm to 3 mm) reside in the biliary and pancreatic ducts of the
mammalian host, where they attach to the mucosa.