CHAPTER 1 parasite PROTOZOA mastigophora GIARDIA LAMBIA TRYCHOMONAS VAGINALIS AND HOMINIS TRYPNOSOMA CRUZI AFRICAN SLEEPING SICKNESS

2.  Mastigophora is a division of single-celled protozoans.
 There are approximately 1,500 species of Mastigophora.
 Their habitat includes fresh and marine waters.
 Most of these species are capable of self-propelled movement through the motion
of one or several flagella.
 The possession of flagella is a hallmark of the Mastigophora.

4.  In addition to their flagella, some mastigophora are able to extend their interior
contents (that is known as cytoplasm ) outward in an arm-like protrusion.
 These protrusions, which are called pseudopodia, are temporary structures that
serve to entrap and direct food into the microorganism.
 The cytoplasmic extensions are flexible and capable of collapsing back to form the
bulk of the wall that bounds the microorganism.

5. 1) Mastigophora replicate typically by the internal duplication of their contents flowed by a
splitting of the microbes to form two daughter cells.
This process, which is called binary fission, is analogous to the division process in bacteria .
2) some mastigophora can reproduce sexually, by the combining of genetic material from
two mastigophora. This process is referred to as syngamy.

7.  Giardia lamblia is a flagellated protozoan parasite that colonizes and reproduces in the small
intestine, causing giardiasis.
 The parasite attaches to the epithelium by a ventral adhesive disc, and reproduces via binary
fission.
 Giardiasis does not spread via the bloodstream, nor does it spread to other parts of
the gastrointestinal tract
 but remains confined to the lumen of the small intestine.
 Giardia trophozoites absorb their nutrients from the lumen of the small intestine, and
are anaerobes.
 Chief pathways of human infection include ingestion of untreated sewage, a phenomenon
particularly common in many developing countries contamination of natural waters also occurs
watersheds where intensive grazing occurs

8. HOST
 Giardia infects humans
 but is also one of the most common parasites infecting cats, dogs and birds

9. TRANSMISSION
 Giardia infection can occur through ingestion of dormant microbial cysts in contaminated
water, food, or by the fecal-oral route (through poor hygiene practices).
 The cyst can survive for weeks to months in cold water, so can be present in contaminated
wells and water systems.
 such as naturally occurring ponds, storm water storage systems, and even clean-looking
mountain streams.
 They may also occur in city reservoirs and persist after water treatment, as the cysts are
resistant to conventional water treatment methods, such as chlorination and ozonolysis.

10.  The giardia parasite can also spread through anal sex.
 Zoonotic transmission is also possible, so Giardia infection is a concern for people camping in
the wilderness or swimming in contaminated streams or lakes, especially the artificial lakes
formed by beaver dams (hence the popular name for giardiasis, "beaver fever").
 In addition to waterborne sources, fecal-oral transmission can also occur.

11. LIFE CYCLE

12. Intracellular metabolism
 Giardia relies on glucose as its major energy source and breaks glucose down into ethanol,
acetate and carbon dioxide.
 However, it can also use arginine as an energy source.
 B vitamins and bile salts, as well as glucose, are necessary for Giardia to survive.
 a low-carbohydrate diet was shown in mice to reduce the number of Giardia organisms
present

13. SIGNS & SYMPTOMS
 ITS usually appear one to three weeks after exposure.
 Watery, sometimes foul-smelling diarrhea that may alternate with soft, greasy
stools.
 Fatigue or malaise.
 Abdominal cramps and bloating.
 Gas or flatulence.
 Nausea.
 Weight loss.

14. RISK FACTORS
 Children. Giardia infection is far more common in children than it is in adults.
 People without access to safe drinking water.
 People who had anal sex.

15. COMPLICATIONS
 Dehydration. Often a result of severe diarrhea, dehydration occurs when the
body doesn't have enough water to carry out its normal functions.
 Failure to thrive. Chronic diarrhea from giardia infection can lead to malnutrition
and harm children's physical and mental development.
 Lactose intolerance. Many people with giardia infection develop lactose
intolerance — the inability to properly digest milk sugar. The problem may persist
long after the infection has cleared.

16. MANAGEMENT
 Metronidazole is the most commonly prescribed antibiotic for this condition.
 In addition, an increasing incidence of nitroimidazole-refractory giardiasis has been reported,
particularly in travelers from India.
 Appropriate fluid and electrolyte management is critical, particularly in patients with large-volume
diarrheal losses
 Pregnant Patients:- necessary, paromomycin can be used as systemic absorption is poor.If the
patient is left untreated, adequate nutrition and hydration maintenance are paramount.
 Preventions:- drink purifying water , advise travelers to endemic areas to avoid eating uncooked
foods that may have been grown, washed, or prepared with contaminated water,
 Breastfeeding appears to protect infants from Giardia intestinalis infection. Breast milk contains
detectable titres of secretory IgA, which is protective for infants

17. TRICHOMONAS HOMINIS

18. HOST
 Humman

20. LIFE CYCLE

21. MANAGEMENT
 Metronidazole

22. TRICHOMONAS VAGINALIS

23.  Trichomonas vaginalis is an anaerobic, flagellated protozoan parasite and the
causative agent of trichomoniasis.
 It is the most common pathogenic protozoan infection of humans in
countries.
 it is a pear-shaped organism with a central nucleus and four anterior flagella and
undulating membrane extends about two-thirds of its length.
 It exists only as a trophozoite form, and measured 7-23μm long & 5-15μm wide.

24. HOST
Humans

25. TRANSMISSION
 Transmission usually occurs via direct, skin-to-skin contact with an infected
individual, most often through vaginal intercourse

26. LIFE CYCLE

27. SIGNS & SYMPTOMS
 It is a common cause of vaginitis in women
 men with this infection can display symptoms of urethritis.
 only 2% of women with the infection will have a "strawberry" cervix (colpitis macularis, an
erythematous cervix with pinpoint areas of exudation) or vagina on examination.
 This is due to capillary dilation as a result of the inflammatory response.
 Infection rates between men and women are similar with women being symptomatic, while
infections in men are usually asymptomatic.

28.  After introduction by sexual intercourse, proliferation begins which results in
inflammation & large numbers of trophozoites in the tissues and the secretions.
 The onset of symptoms such as vaginal or vulval pruritus and discharge is often
sudden and occurs during or after menstruation as a result of the increased vaginal
acidity.
 The vaginal secretions are liquors, greenish or yellowish, sometimes frothy, and
foul smelling.
 Infection in the male may be latent, with no symptoms, or may be present as self
limited, persistent, or recurring urethritis.

31. Dagnosis
 Classically, with a cervical smear, infected women have a transparent "halo" around their
superficial cell nucleus.
 It is unreliably detected by studying a genital discharge or with a cervical smear because
of their low sensitivity.
 T. vaginalis was traditionally diagnosed via a wet mount, in which "corkscrew" motility
was observed.
 Currently, the most common method of diagnosis is via overnight culture with a
sensitivity range of 75–95%.
 Newer methods, such as rapid antigen testing and transcription-mediated
amplification have even greater sensitivity but are not in widespread use.

32. COMPLICATIONS
 one of the complications of T. vaginalis in women include :-
 preterm delivery, low birth weight, and increased mortality as well as predisposing
to HIV infection, AIDS, and cervical cancer.
 T. vaginalis has also been reported in the urinary tract, fallopian tubes, and pelvis and
can cause pneumonia, bronchitis, and oral lesions.
 Condoms are effective at reducing, but not wholly preventing, transmission.
 T. vaginalis infection in males has been found to cause asymptomatic urethritis and
prostatitis.
 It has been proposed that it may increase the risk of prostate cancer.
 Contamination of the specimen with faeces may confuse T.vaginalis with T.hominis.

33. MANAGEMENT
 Infection is treated and cured with metronidazole or tinidazole.
 the alternate treatment recommended is 500 milligrams of metronidazole, twice
daily, for seven days if there is failure of the single-dose regimen.
 Medication should be prescribed to any sexual partner(s) as well because they
may be asymptomatic carriers.

34. Prevention
 Both male & female sex partners must be treated to avoid reinfection
 Good personal hygiene, avoidance of shared toilet articles clothing.
 Safe sexual practice

35. TRYPANOSOMA BRUCEI COMPLEX

36.  T. brucei complex is composed of T. brucei gambiense and T. brucei rhodesiense .
 T. brucei group is etiological agent of African sleeping sickness.
 Two type of sleeping sickness
 1) The Gambian or west African sleeping sickness it is chronic from
 Found in west and central Africa
 2)the rhodesion or east African sleeping sickness it is acute form
 Found in east and south Africa

37.  Only epimastigote and trypomastgotes forms are exhibited by the T. brucei
complex.
 T. brucei trypomastgotes are polymorphic.
 They are minute, 14 to 33micro m in length and 1.5 to 3.5 micro m in width,
flattened, fusi form

38.  T. brucei is transmitted between mammal hosts by an insect vector belonging to the
species of tsetse fly.
 When testes fly, glossina spp., ingested blood from an infected host, the stumpy
trypomastgotes migrate to the posterior section of the gut and multiply .
 After 10 day the slender forms migrate in to the foregut, into the esophagus and pharynx,
then enters the salivary gland.
 Inside the salivary glands, they develop into epimastigote, multiply, and eventually
transform into the infective stages, the metacyclic trypomastgotes.
 The infective forms are inoculated during blood meal.
The complete cycle in the fly takes around 15 to 35 days .

39.  In humans T. brucei complex live in the blood in the reticular tissues of lymph and
spleen and the CSF .
 Its multiply by binary fission
 In chronic disease its involve CNS.
 As the disease progress the long slender forms develop into the stumpy non
dividing forms .

40. PATHOGENESIS AND CLINICAL MEDICAL
MANIFESTATION
 The earliest sign in African trypanosomiasis is the chancre a local , hard, painful,
lesion at the site of inoculation .
 ACTUTE STAGES :-
 Gambian trypnomiasis multiplying in blood and lymphatics during the first year
 The disease progress to the chronic sleeping sickness with the invasion of CNS .
 Incubation period is about 14 days

41. ACUTE STAGE
 Irregular fever
 Headache
 Joint and muscle pain
 Tachycardia
 Dizzinessdebility
 Rash
 A systemic phase is episodic, lasting from 1 to 6 days followed by an
asymptomatic period lasting several weeks

42.  In Gambian trypanosomiasis the posterior cervical lymph node enlarged,
Non tender and have consistency of ripe plums.
 Early systemic stage last from 1 to 6 months

43.  With cns invasion chronic disease, or sleeping sickness stage is initiated. Headaches
become more severe and there is increasing mental dullness and apathy.
 The [patient become alternately morose and excitable and lacks interest in work .
 Tremors hyperesthesia and inversion of sleep cycle my observed
 With progressive CNS involvement somnolence become more pronounced
 Prognosis is favorable if treatment is before cns involvement
 Untreated infections may progress to death or develop in to chronic or latent disease

44.  Rhodesian trypnomiasis is more rapid and fatal than Gambian trypnomiasis.
 Same clinical feature like Gambian type
 Onset of symptoms occur within a few days after a tsetse bite.
 Signs of CNS appear early and neurologic deterioration is rapid.
 Death occur within moth or week

45.  Trypanosomes are able to evade the immune response of the host through a
process called antigenic variation.
 This refers to the ability of the trypomastgotes to change its surface coat, which is
variant surface glycoprotein so that antibodies previously produce by the host can
not act on it resulting in recurrent wave of parasitemia

46. LIFE CYCLE

47. DIAGNOSIS
 Depends upon demonstration of trypomastgotes in giemsa stained blood, lymph
node aspirate, and CSF .
 Buffy coat concentration method can use
 Serologic test :-
 Indirect hem agglutination,
 Enzyme-linked
 Immunosorbent essay
 Immunofluorescences

48. TRATMENT
 Treatment of African sleeping sickness usually effective
 During blood lymphatic stage :-
 Pentamide
 Suramin
 Late stage disease with CNS involvement :- melarsoprol and tryparsamide

49.  Early or late stage of Gambian sleeping sickness :-
 Eflornithine
 Rhodesian sleeping sickness :-
 Difluromethylorntihine

50. Prevention
 Reduction of contact with teste's fly by using traps, screens, and insecticides.

51. TRYPANOSOMA CRUZI

52. TRYPANOSOMA CRUZI
This behavior causes disease or the likelihood of disease that varies with the organism: for
example, trypanosomiasis in humans (Chagas disease in South America and sleeping sickness in Africa).
 The triatomine likes the nests of vertebrate animals for shelter, where it bites and sucks blood for
food.
 Individual triatomine infected with protozoa from other contact with animals transmit trypanosomes
when the triatomine deposits its feces on the host's skin surface and then bites.
 Penetration of the infected feces is further facilitated by the scratching of the bite area by the human
or animal host.

53.  Trypanosoma is the etiologic agent of chaga`s disease or American trypanosomiasis.
 T. cruzi, unlike other trypanosomes is an intracellular parasite.
 It exhibit four all stages of development
 1) amastigote
 2) promastigote
 3) epimastigote
 4) trypomastgotes

54.  Trypomastgotes found in blood stream
 Amastigotes found in tissue cell
 In the triatomine bugs, the amastigote, epimastigote, and promastigote forms
occur in the midgut

55.  The long slender trypomastgotes are 16 to 20 micro m in length while the sort,
stumpy forms measure around 15 micro m .
 Posterior end is usually pointed.
 In stained specimens, trypomastgotes are look C or U or S shaped

56.  Amastigotes develop in muscles and other tissue .
 They are round or ovoid in shape and measure from 1.5 to 4 micro m. in diameter,
 Usually found in small group of cyst like collection in tissues.

57.  Trypomastgotes of T, cruzi do not multiply in bloodstream .

 Soon after their entry in the human host, the metacyclic trypanosomes are
engulfed by macrophages of the reticuloendothelial system and multiply through
binary fission as amastigotes

58.  Amastigotes develop in to trypomastgotes and cell erupts in 4 to 5 days
 The released trypomastgotes enter in blood stream, ready to replicate again once
they enter another cell or are ingested by an insect vector.
 These cell frequently invaded are the reticuloendothelial cells of he spleen, liver, as
well as cardiac, smooth and skeletal muscle cells.
 In some instances they can also infect the skin, gonads, intestinal mucosa, plecenta
.

59.  Trypomastgotes, ingested by the intermediate host, the triatomine bugs pass through the
posterior portion of the insects mid gut and become epimastigote.
 Epimastigote multiply by binary fission and transform in to the infective metacyclic
trypomastgotes.
 There's trypomastgotes appear in the insect`s rectum 8 to 10 days after infection.
 They are passed in the bug`s feces and may gain entrance in to the body through scratched
skin or through mucous membranes that are rubbed with fingers contaminated with the bug`s
feces

60. HOST
 The Trypanosoma cruzi life cycle starts in an animal reservoir, usually mammals,
wild or domestic, including humans.

61. TRANSMITION
congenital transmission,
blood transfusion,
organ transplantation,
consumption of uncooked food that has been contaminated with feces from infected
bugs,

62. PATHOGENESIS and Clinical manifestation
At the site of inoculation, a local inflammation is produced.
This is known as a chagoma a small painful, reddish nodule.
This is followed by acute and chronic phases.
Fever and generalized lymph adenopathy are features of the acute disease.
Trypanosoma's may enter in the conjunctiva of the eye and cause edema of eyelid
and a conjunctiva, a condition called roman`s sign.

63.  Chronic disease had no characteristics or manifestation up to 20 years or more
 Manifestation of chronic disease include
 Cardiomyopathy related to CHF
 Cardio spasm
 Mega esophagus
 Megacolon
THESE ALL CONDTION CAN LEAD TO DEATH.

64. LIFE CYCLE

66. DIAGNOSIS
Chagas's disease may be suspected when general cardiac symptoms are present in
patient .
 Electroencephalogram  Ventricular extra systole and atrial fibrillation.
 Trypanosomes in blood, CSF , fixed tissue or lymph.
 First two month of acute disease can T.cruzi ne seen by direct examination or thick
blood smears.
 Parasite concentration methods increase the probability of detecting parasitemia .

67. Low level of T.cruzi :- Blood cultures
xenodiagnoses
SEROLOGIC METHODS :- immunofluorescent antibody test.
complement fixation test
indirect hemaggluatination assay
ELISA test which are more sensitive and specific

68. epidemiology
 Chaga`s disease exists only in the American content.
 Prevalent is highest among the poor classes and rural areas
 Acute disease usually affected children and unrecognized
 Chronic is more common than acute disease
 Highest incidence occur at fifth decade of life more affected more than female

69. Prevention & control
vector control
screening sterilization of transfusion blood
health education
Controls of the vector of the disease has centered mainly on insectide spraying and
housing improvement to reduce breeding site of the triatomine bugs

70. MANAGEMENT
 Acute cases are treated with nifurtimox and benzonidazole, but no effective
therapy for chronic cases is currently known.