Hemoflagellates (Teishmania & Trypanasoma). Trichomonas Vaginalis.

1. MEDICAL IMPORTANT PROTOZOA.
HEMOFLAGELLATES (LEISHMANIA and TRYPANASOMA).
PROTOZOA CAUSING INTESTINAL INFECTIONS.
TRICHOMONAS VAGINALIS.
BIOLOGICAL PROPERTIES, MEDICAL IMPORTANCE, EPIDEMIOLOGY,
PATHOGENESIS AND LABORATORY DIAGNOSTICS OF DISEASES, CAUSED BY
THEM.
THEORETICAL QUESTIONS:
1. Trypanasoma causing Chagas disease (American trypanasomosis): structure, life cycle,
pathogenecity for human. Epidemiology, pathogenesis and clinical manifestation of
Chagas disease. Laboratory diagnostics, therapy and prophylaxis of its.
2. Trypanasoma causing sleeping sickness (African trypanasomosis): structure, life cycle,
pathogenecity for human. Epidemiology, pathogenesis and clinical manifestation of
sleeping sickness. Laboratory diagnostics, therapy and prophylaxis of disease.
3. Leishmania causing cutaneous and mucocutaneous leishmaniasis. Biological
properties, epidemiology and clinical manifestations of disease. Laboratory diagnostics,
therapy and prophylaxis.
4. Leishmania causing visceral leishmaniasis (Kala-Azar). Biological properties,
epidemiology and clinical manifestations of disease. Laboratory diagnostics, therapy and
prophylaxis.
5. Entamoeba histolitica: biological features, epidemiology and clinical manifestations of
amebiasis. Laboratory diagnostics, therapy and prophylaxis.
6. Giardia (Lamblia) intestinalis: biological features, epidemiology and clinical
manifestations of diarrhea caused by Giardia. Laboratory diagnostics, therapy and
prophylaxis.
7. Balantidium coli: biological features, epidemiology and clinical manifestations of
balantidiasis. Laboratory diagnostics, therapy and prophylaxis.
8. Trichomonas vaginalis: biological features, epidemiology and clinical manifestations of
trichomoniasis. Laboratory diagnostics, therapy and prophylaxis.
The family Trypanosomatidae consists of many parasitic flagellate protozoans. Two genera,
Trypanosoma and Leishmania, include important pathogens of humans and domestic animals.
The diseases caused by these protozoa are endemic or enzootic in different parts of the world and
constitute serious medical and economic problems. Because these protozoans require hematin
obtained from blood hemoglobin for aerobic respiration, they are called hemoflagellates. The
digenetic (two-host) life cycles of both genera involve an insect and a vertebrate. The
hemoflagellates have up to eight life cycle stages which differ in the placement and origin of the
flagellum. Two stages the amastigote and the trypomastigote may occur in vertebrate hosts, and
three stages,the promastigote, paramastigote, and epimastigotein invertebrate hosts .

2. Structure: Trypanosoma cruzi is found in the peripheral blood as a 20 µm trypomastigote with a
large kinetoplast and a poorly developed undulating membrane. In the tissues (mainly
heart, skeletal and smooth muscle, and reticuloendothelial cells) the parasite occurs as
a 3 to 5 µm amastigote.
Multiplication and Life Cycle: In the vertebrate host, multiplication is carried out only by the
amastigote form, which divides inside cells or muscle fibers to form groups called
pseudocysts. Trypomastigotes, ingested when the insect takes a blood meal from an
infected host, transform into epimastigotes in the intestine (Fig.2). In the rectal sac
these attach by the flagellar sheath mainly to the surface of the epithelium on the rectal
gland, where they reproduce actively. In about 8 to 10 days, metacyclic trypomastigote
forms appear which are flushed out of the gut with the feces of the insect. These
organisms are able to penetrate the vertebrate host only through the mucosa or
abrasions of the skin; hence, transmission does not necessarily occur at every blood
meal. Within the vertebrate the trypomastigotes transform into amastigotes. After a
period of intracellular multiplication at the portal of entry, the amastigotes are
released into the blood as trypanosomes which may then invade other cells or tissues,
becoming amastigotes again.
Epidemiology: Chagas disease is transmitted by cone-nosed triatomine bugs of several genera
(Triatoma, Rhodnius, Panstrongylus). Congenital and blood transfusion transmission
also can occur. Natural foci of Chagas disease exist among wild mammals and their
associated triatomines. Humans and domestic animals became involved in the
epidemiologic chain several centuries ago, when insects living under wild conditions
began adapting to households. Opossums, armadillos, and wild rodents are reservoirs
of the parasite, linking the wild and domestic cycles. Case of human trypanosomiasis
have been reported in almost all countries of the Americas, including the southern
United States, but the main foci are in poor rural areas of Latin America.
Clinical Manifestations: Chagas disease begins as a localized infection that is followed by
parasitemia and colonization of internal organs and tissues. Infection may first be evidenced by a
small tumor (chagoma) of the skin or, when the port of entry is the conjunctiva, by Romaña's
sign (unilateral bipalpebral edema). These typical inflammatory reactions are usually
accompanied by a swelling of the satellite lymph nodes that persists for 1 to 2 months.
Symptoms and signs include fever, general edema, adenopathy, moderate hepatosplenomegaly,
myocarditis with or without heart enlargement, and sometimes, in children, meningoencephalitis.
Laboratory diagnostics In the acute phase, the symptoms and signs described above suggest the
disease. Several methods are used to confirm disease:
Microscopy: In the early stages of the disease the parasite is demonstrated relatively easily by
direct microscopic blood examination or in the thin blood smears stained by Romanowsky-
Giemsa.
Xenodiagnosis - allowing clean, laboratory-reared insects to feed on a suspected victim and later
examining the insect feces
Culture method is reliable in early stage.

3. Serology. In the chronic phaset serologic tests [indirect hemagglutination, indirect
immunofluorescence, enzyme-linked immunosorbent assay (ELISA)] can be diagnostic.
African Trypanosomiasis (Sleeping Sickness)
Sleeping sickness (African trypanosomiasis) is caused by Trypanosoma brucei.
Structure: The two subspecies of T brucei are morphologically indistinguishable. They may be
pleomorphic, ranging from 12 to 42 µm long (mean, 30 µm), and have a small
kinetoplast and a well-developed undulating membrane. The posterior end is more
rounded than that of T cruzi.
Multiplication and Life Cycle : Trypanosoma brucei trypanosomes, unlike those of T cruzi,
multiply while in the blood or cerebrospinal fluid. Trypanosomes ingested by a feeding
fly must reach the salivary glands within a few days, where they reproduce actively as
epimastigotes attached to the microvilli of the gland until they transform into
metacyclic trypomastigotes, which are found free in the lumen. Around 15 to 35 days
after infection the fly becomes infective through its bite.
Epidemiology : Both forms of African trypanosomiasis are transmitted during the daytime by the
bite of infected tsetse flies (Glossina species), which inhabit the open savannah of
eastern Africa (T b rhodesiense) or riverine areas in western and central Africa (T b
gambiense). Wild game mammals (bushbuck, hartebeest, lion, hyena) as well as cattle
act as reservoirs of T b rhodesiense. Man-fly-man transmission is hence more common
in west and central Africa.
Clinical Manifestations: An initial chancre with regional lymphadenitis is frequently observed
in patients infected by Trypanosoma brucei rhodesiense but seldom in patients infected
by T b gambiense. The lesion persists for several weeks. After a period of local
multiplication, the trypanosomes enter the general circulation via the lymphatics, and
recurrent fever, headache, lymphadenopathy, and splenomegaly may occur. Later,
signs of meningoencephalitis appear, followed by somnolence, cachexia, coma, and
death. Enlargement of the posterior cervical chain of lymph nodes (Winterbottom's
sign) is more common in T b gambiense infection. The Rhodesian type of sleeping
sickness evolves more acutely to death and its neurologic effects are less characteristic.
The Gambian form tends to be more chronic and sometimes takes several years to
develop central nervous system (CNS) involvement.
Laboratory diagnostics. Microscopy of the thin blood or CSF smears stained by Romanowsky-
Giemsa. In the early stages of the disease, the parasites can be demonstrated in lymph nodes and
blood; later, they appear in the cerebrospinal fluid. In the Rhodesian type, lumbar puncture is
indicated because of early CNS invasion. Culture or laboratory animal inoculations can be
useful.
Serologic tests, such as indirect immunofluorescence, direct card agglutination, and indirect
hemagglutination, are used successfully for diagnosis.
Control : Tsetse fly populations have been reduced successfully by the use of insecticides or
traps with an attractant bait plus insecticide. No reliable vaccine is available, and the
variability in antigenic composition of the blood populations makes vaccination a
difficult goal. Drugs such as pentamidine and the arsenical suramin, are successful in
treatment, particularly in the early phase.
Leishmaniasis is a general term for diseases caused by species of the genus Leishmania,
which are transmitted by the bite of infected sand flies. The lesions of cutaneous and

4. mucocutaneous leishmaniasis are limited to the skin and mucous membranes. The
much more severe disease is visceral leishmaniasis, which involves the entire
reticuloendothelial system.
Cutaneous and Mucocutaneous Leishmaniasis
The main species in the Old World are Leishmania tropica, L. major, and L. aethiopica (causing
oriental sore); in the New World, L. mexicana (causing chiclero ulcer), L.
amazonensis, L. peruviana (causing uta), L. braziliensis, L. panamensis, L. guyanensis
(causing dermal leishmaniasis or espundia); other species occur in different
geographic areas.
Structure: All species of Leishmania parasitic in man are morphologically similar and appear
as intracellular amastigotes 3 to 6 µm long by 1.5 to 3 µm in diameter. Promastigotes
develop in the intestine of the sand fly.
Life Cycle: In mammalian hosts, amastigotes are phagocytosed by macrophages but resist
digestion and divide actively in the phagolysosome. Parasites ingested by a female sand
fly that sucks the blood of an infected person or animal pass into the stomach,
transform into promastigotes, and multiply actively. A paramastigote form also occurs
in sand flies.
Epidemiology: The vectors of Leishmania are sand flies of the genus Lutzomyia in the New
World and Phlebotomus in the Old World. Animal reservoirs are wild rodents, sloths,
marsupials, carnivores, and others. In the Old World, anthroponotic urban foci caused
by L. tropica are found, whereas L major and L. aethiopica are typically zoonotic,
involving rodents as reservoirs. In the New World, with the exception of L. peruviana,
all forms are zoonotic and mainly sylvatic. For L. mexicana, some rodents serve as
reservoir species, and the transmission is accomplished mainly by forest floor sand
flies.
Clinical Manifestations: Cutaneous leishmaniasis appears 2 to 3 weeks after the bite of an
infected sand fly as a small cutaneous papule. This lesion slowly grows, becoming
indurated and often ulcerated, and develops secondary infection. Secondary or diffuse
lesions may develop. The disease is occasionally self-limiting but usually chronic.
Leishmaniasis from a primary skin lesion may involve the oral and nasopharyngeal
mucosa. The patient presents single or multiple ulcers or nodules or nasal septum, may
develop, usually several years after the skin lesions have healed. In the panamensis type
mucosal lesions are uncommon and are less destructive than in the braziliensis type. In
the latter, the process sometimes extends from the palate to the pharynx and larynx.
These destructive lesions (constituting the condition called espundia) are common in
Brazil but are also observed in Sudan, produced there by L aethiopica, usually in a less
severe form. The diffuse type, characterized by disseminated plaques, papules, or
nodules, especially on the face or limbs, is observed in areas where organisms of the
mexicana and amazonensis types exist, as well as in some parts of Africa (L
aethiopica).
Laboratory diagnostics is based generally on microscopy. Parasites can be demonstrated in
scrapings of the borders of the lesions.
Culture method: Culturing in blood agar media increases markedly the possibility of isolating
the parasite; material from direct puncture of the lesions' borders or lymph nodes or triturated
biopsy tissue is used. Serology: Various serologic tests (ELISA, immunofluorescent antibody)
are satisfactory for indirect diagnosis.

5. Allergic skin test: The Montenegro skin test, in which an indurated area appears at the site of
inoculation of the antigen after 48 to 72 hr, is usually positive after 2 to 3 months of infection
and remains so throughout the patient's lifetime.
Treatment and prophylaxis: Leishmaniasis transmitted in or near houses can be prevented with
insecticides, but this procedure is not practical for the forest tegumentary type. No
effective vaccine is yet available. Pentavalent antimonials, such as sodium antimony
gluconate (Pentostam) and meglumine antimoniate (Glucantime), are available for
treatment.
Visceral Leishmaniasis (Kala-Azar)
Kala-azar can be caused by at least three Leishmania species: Leishmania donovani and
L infantum are responsible for visceral leishmaniasis in the Old World; L chagasi and
L infantum (which may be the same organism) cause the disease in the New World.
Structure: The Leishmania species that cause kala-azar are similar in morphology and life cycle
to other members of the same genus.
Epidemiology : In India, transmission occurs in villages in an anthroponotic man-sand fly-man
cycle without nonhuman reservoir. In Europe and Africa, several rodents may act as
reservoirs. In rural semiarid zone of Latin America, both wild and domestic dogs enter
the epidemiological chain and the vector is a common anthropophilic and zoophilic
sand fly. The disease is more common in children in both Latin America and the
Mediterranean area.
Clinical Manifestations: Like cutaneous leishmaniasis, visceral leishmaniasis begins with a
nodule at the site of inoculation. This lesion rarely ulcerates and usually disappears
spontaneously in a few weeks or months. In contrast to cutaneous leishmaniasis,
symptoms and signs of systemic disease develop, such as undulating fever, malaise,
diarrhea, splenomegaly, hepatomegaly, lymphadenopathy, emaciation, anemia, and
leukopenia. In some areas of Europe and Latin America, L infantum may cause a
cutaneous form without apparent visceral involvement.
Laboratory diagnostics: Microscopy:The parasite usually can be demonstrated in stained or
cultured bone marrow or spleen material. Serologic tests (ELISA, immunofluorescent
antibody) are useful, particularly in surveys.
Therapy and control: The same insecticides and drugs that work for cutaneous leishmaniasis
are used for visceral leishmaniasis. Aromatic diamidines are also used.
Entamoeba histolytica
Amebas are unicellular organisms common in the environment: many are parasites of
vertebrates and invertebrates. Relatively few species inhabit the human intestine and only
Entamoeba histolytica is identified as a human intestinal pathogen.
Morphology: E. histolytica has a relatively simple life cycle that alternates between trophozoite
and cyst stages. The trophozoite is the actively metabolizing, mobile stage, and the cyst is
dormant and environmentally resistant. Diagnostic concern centers on both stages. Trophozoites
vary remarkably in size-from 10 to 60 µm or more in diameter, and when they are alive they may
be actively motile. The finely granular endoplasm contains the nucleus and food vacuoles, which
in turn may contain bacteria or red blood cells. The parasite is sheathed by a clear outer
ectoplasm. Nuclear morphology is best seen in permanent stained preparations. The nucleus has
a distinctive central karyosome and a rim of finely beaded chromatin lining the nuclear
membrane.

6. The cyst is a spherical structure, 10-20 µm in diameter, with a thin transparent wall. Fully
mature cysts contain four nuclei with the characteristic amebic morphology. Rod-like structures
(chromatoidal bars) are present variably, but are more common in immature cysts.
Multiplication and life cycle of E histolytica. Amebas multiply in the host by simple binary
fission. Most multiplication occurs in the host, and survival outside the host depends on the
desiccation-resistant cyst form. Encystment occurs apparently in response to desiccation as the
ameba is carried through the colon. After encystment, the nucleus divides twice to produce a
quadrinucleate mature cyst. Excystment occurs after ingestion and is followed by rapid cell
division to produce four amebas which undergo a second division. Each cyst thus yields eight
tiny amebas.
Epidemiology : Fecal-oral transmission occurs when food preparation is not sanitary or
when drinking water is contaminated. Contamination may come directly from
infected food handlers or indirectly from faulty sewage disposal. Endemic or
epidemic disease may result. The prevalence of amebiasis in underdeveloped
countries reflects the lack of adequate sanitary systems.
Clinical Manifestations The clinical manifestations vary with the extent of involvement.
Mucosal erosion causes diarrhea, which increases in severity with increasing area
and depth of involvement. Rectal bleeding is only slightly less common than diarrhea
and is usually, but not invariably, associated with diarrhea. Such bleeding may be
grossly apparent or may be occult and demonstrable only by chemical testing for
blood. Urgency, tenesmus, cramping abdominal pain and tenderness may be present.
Extraintestinal amebiasis begins with hepatic involvement. A focal amebic abscess in
the liver represents metastasis from intestinal infection. Symptomatic intestinal
infection need not be present.
Laboratory diagnostics: Microscopy: Amebic infections are diagnosed definitively by
identifying the ameba in stool or exudates. Amebas may be identified in direct
smears, but specific diagnosis usually depends upon obtaining a fixed stained
preparation.
Serologic studies may be useful, particularly when direct diagnosis is not possible. Such
methods include gel diffusion, immunoelectrophoresis, countercurrent
electrophoresis, indirect hemagglutination, indirect fluorescent antibody, enzyme-
linked immunosorbent assay (ELISA) and latex agglutination. In areas of high
prevalence a single positive antibody test is less significant. The physician rarely
observes the patient long enough to measure a rising titer as evidence of active
ongoing invasive infection.
Testing with monoclonal antibodies demonstrates ameba in the stool.
Allergic skin tests are rare used for diagnosis. Culture method: Amebas may be cultured
from the stool. It is essential for virulence testing.
Therapy and prophylaxis: Preventive measures are limited to environmental and
personal hygiene. Treatment depends on drug therapy, which in the case of some
abscesses must be supplemented with drainage, either open or by aspiration.
Effective drugs are available for liver abscess but intestinal infection is less
successfully treated. No single drug is completely effective in eradicating amebas
from the gut, so reliance is often placed on combination therapy. Acute intestinal
disease is best treated with metronidazole at a dose of 750 mg three times a day orally
for 10 day. In children the dose is 40 mg/kg/day divided into three doses and given
orally for 10 days. There are two choices for a drug to clear amebas from the lumen

7. of the gut: iodoquinol at an adult dose of 650 mg orally three times daily for 20 days
or diloxanide furoate at an adult dose of 500 mg orally three times daily for 10 days.
Giardia (Lamblia intestinalis)
Structure: The Giardia life cycle involves two stages: the trophozoite and the cyst. The G.
lamblia trophozoite is easily recognized under a microscope: it is about 12 to 15 µm
long, shaped like a pear cut in half lengthwise, and has two nuclei that resemble eyes,
structures called median bodies that resemble a mouth, and four pairs of flagella that
look like hair; these combine to give the stained trophozoite the eerie appearance of a
face. The flagella help these organisms to migrate to a given area of the small intestine,
where they attach by means of an adhesive disk to epithelial cells and thus maintain
their position despite peristalsis. The Giardia cyst - the form usually seen in the feces -
is ovoid, 6 to 12 µm long, and can often be seen to contain two to four nuclei at one end
and prominent diagonal fibrils.
Multiplication and Life Cycle: The trophozoite, or actively metabolizing, motile form, lives in
the upper two-thirds of the small intestine (duodenum and jejunum) and multiplies by
binary fission. Trophozoites that are swept into the fecal stream lose their motility,
round up, and are excreted as dormant, resistant cysts.
Epidemiology: Giardia infection occurs worldwide, with an incidence usually ranging from 1.5
to 20 percent. Higher incidences are likely where sanitary standards are low. Giardia infection is
acquired by ingesting cysts. The exposure of cysts to host stomach acidity and body temperature
triggers excystation, which is completed in the small intestine with the emergence of
trophozoites that promptly attach to host intestinal epithelium. Although people of all ages may
harbor these organisms, infants and children are more often infected than are adults. Carriers are
probably more important in the spread of these organisms than symptomatic patients because
cysts are less likely to be present in diarrheic stool. Like other diseases spread by the fecal-oral
route, giardiasis can be a problem in institutions, nurseries, and day-care centers.
Clinical Manifestations : Giardia infection may be asymptomatic or it may cause disease
ranging from a self-limiting diarrhea to a severe chronic syndrome. The length of the
incubation period, usually 1 to 3 weeks, depends at least partly on the number of cysts
ingested. Normal human hosts with giardiasis may have any or all of the following
signs and symptoms: diarrhea or loose, foul-smelling stools, steatorrhea (fatty
diarrhea), malaise, abdominal cramps, excessive flatulence, fatigue and weight loss.
Some patients with giardiasis develop a severe disease that is not self-limited. Signs
and symptoms may include interference with the absorption of fat and fat-soluble
vitamins, retarded growth, weight loss, or a celiac-disease-like syndrome.
Laboratory diagnostics: The symptoms of giardiasis are not pathognomonic. The patient's
history may indicate recent exposure to Giardia, but the infection is diagnosed, as in most
parasitic infections, by identifying the organism. Microscopy: In the case of giardiasis, cysts are
found in formed stool. Diarrheal specimens may also contain trophozoites. If still motile, the
trophozoites exhibit a typical "falling leaf" movement. When stools are negative, giardiasis can
be diagnosed by obtaining trophozoites directly from the small intestine by duodenal intubation.

8. Prophylaxis and therapy: Attention to personal hygiene is the key to preventing the spread of
giardiasis. Controlling the spread of Giardia in drinking water should be possible
where community water treatment methods (e.g., disinfection and filtration) are
available. For example, iodine and chlorine kill Giardia cysts under appropriate
conditions. Boiling promptly inactivates Giardia cysts and is the best solution.
The drug of choice for treating Giardia infections is quinacrine hydrochloride. Metronidazole
and furazolidone also may be used.
Balantidium coli
Balantidium coli, the only ciliate and by far the largest organism in this group, is a pathogen. The
trophozoites, which are ovoid, 40 to 70 µm or longer, and covered with cilia, live in the large
intestine of humans, swine, and perhaps other animals. The trophozoites divide by transverse
binary fission. They have a large, kidney-shaped macronucleus and a smaller ovoid
micronucleus; conjugation has been described. The cyst form is usually 50 to 55 µm in diameter.
Although the usual diet of B .coli is believed to be host intestinal contents (hence some infections
are asymptomatic), at times these organisms attack the host large intestine (aided apparently by a
boring action and the enzyme hyaluronidase) and cause ulcers. In contrast to E histolytica, B coli
does not invade extraintestinal tissues. Balantidiasis often is accompanied by diarrhea or
dysentery, abdominal pain, nausea, and vomiting. Diagnosis is made by demonstrating cysts or
trophozoites in stools or host tissue.
Balantidium infection is acquired by ingesting cysts in fecal material from another parasitized
host; water-borne epidemics have been reported. The precise relationship between human and
pig Balantidium strains is not clear. The organism is relatively rare in humans and common in
pigs. Tetracyclines are the most effective drugs for treating Balantidium infections.
Trichomonas vaginalis Of the three trichomonads that commonly colonize humans, only one, T
vaginalis, causes disease. T vaginalis inhabits the vagina in women, the prostate and seminal
vesicles in men, and the urethra in both sexes.
Structure: All the trichomonads are morphologically similar, having a pear-shaped body 7 to 23
µm long, a single anterior nucleus, three to five forward-directed flagella, and a single
posteriorly directed flagellum that forms the outer border of an undulating membrane. A hyaline
rod-like structure, the axostyle, runs through the length of the body and exits at the posterior end.

9. Multiplication and Life Cycle: Trichomonads have the simplest kind of protozoan life cycle, in
which the organism occurs only as a trophozoite. Division is by binary fission. Because
there is no resistant cyst, transmission from host to host must be relatively direct.
Epidemiology: Trichomoniasis is a common, worldwide infection. Although sexual intercourse
is believed to be the usual means of transfer, some infections probably are acquired
through fomites such as towels, toilet seats, and sauna benches; the organisms may
spread through mud and water baths as well.
Clinical Manifestations: Although the incidence of T. vaginalis infections varies widely,
trichomoniasis is one of the commonest, if not the most common, of the sexually
transmitted diseases. More women than men are infected with T vaginalis. In both
sexes, most infections are asymptomatic or mild. Symptomatic infection is common in
women, rare in men. Trichomoniasis in women is frequently chronic and is
characterized by vaginitis, a vaginal discharge, and dysuria. The inflammation of the
vagina is usually diffuse and is characterized by hyperemia of the vaginal wall (with or
without small hemorrhagic lesions) and migration of polymorphonuclear leukocytes
into the vaginal lumen.
Laboratory diagnostics: A wet mount preparation of discharge from the patient should be
examined microscopically as a first step in diagnosing T vaginalis infection. The
presence of typical pear-shaped trophozoites, usually 7 to 23 µm in length, with
"bobbling" motility and, on careful examination, the wavelike movement of the
undulating membrane, are usually sufficient to identify T. vaginalis.
Culture method: Material that is negative by wet mount examination should be cultured because
culturing is a considerably more sensitive, although time-consuming, method of
diagnosis.
Therapy: A number of 5-nitroimidazole compounds are effective antitrichomonal agents. The
chemical in this group that is approved for treating trichomoniasis is metronidazole.
II.Students practical activities:
1. Microscopy of demonstrative smears prepared from blood specimens, feces and
vaginal discharge, study morphology and sketch the images.

10. Multiplication and Life Cycle: Trichomonads have the simplest kind of protozoan life cycle, in
which the organism occurs only as a trophozoite. Division is by binary fission. Because
there is no resistant cyst, transmission from host to host must be relatively direct.
Epidemiology: Trichomoniasis is a common, worldwide infection. Although sexual intercourse
is believed to be the usual means of transfer, some infections probably are acquired
through fomites such as towels, toilet seats, and sauna benches; the organisms may
spread through mud and water baths as well.
Clinical Manifestations: Although the incidence of T. vaginalis infections varies widely,
trichomoniasis is one of the commonest, if not the most common, of the sexually
transmitted diseases. More women than men are infected with T vaginalis. In both
sexes, most infections are asymptomatic or mild. Symptomatic infection is common in
women, rare in men. Trichomoniasis in women is frequently chronic and is
characterized by vaginitis, a vaginal discharge, and dysuria. The inflammation of the
vagina is usually diffuse and is characterized by hyperemia of the vaginal wall (with or
without small hemorrhagic lesions) and migration of polymorphonuclear leukocytes
into the vaginal lumen.
Laboratory diagnostics: A wet mount preparation of discharge from the patient should be
examined microscopically as a first step in diagnosing T vaginalis infection. The
presence of typical pear-shaped trophozoites, usually 7 to 23 µm in length, with
"bobbling" motility and, on careful examination, the wavelike movement of the
undulating membrane, are usually sufficient to identify T. vaginalis.
Culture method: Material that is negative by wet mount examination should be cultured because
culturing is a considerably more sensitive, although time-consuming, method of
diagnosis.
Therapy: A number of 5-nitroimidazole compounds are effective antitrichomonal agents. The
chemical in this group that is approved for treating trichomoniasis is metronidazole.
II.Students practical activities:
1. Microscopy of demonstrative smears prepared from blood specimens, feces and
vaginal discharge, study morphology and sketch the images.