Protozoas of medical importance

1. Protozoa

3. Intestinal protozoa
• The World Health Organization (WHO) - diarrheal disease as the
2nd highest cause of morbidity and mortality in children in the
developing world.
• Intestinal protozoa are transmitted by the fecal-oral route.
• Life cycles consisting of a cyst stage and a trophozoite stage:
- the cysts consist of a resistant wall and are excreted in the feces,
its’ wall functions to protect the organism from desiccation in the
external environment
- trophozoite any stage which can ingest food, motile form

6. • EXCYSTATION occurs in the stomach and the duodenum
in the presence of acid and pancreatic enzymes
• In small bowel they multiply rapidly, with a doubling
time of 9-12 hours
• As trophozoites pass into the large bowel, ENCYSTATION
occurs in the presence of neutral pH and secondary bile
salts

7. • Assemblage A : A-I to A-IV:
• A-I has been reported in humans
and animals,
• A-II in humans
• A-III and IV exclusively in animals
• Assemblage B has broad host
specificity infecting humans and
animals.
• dogs and cats have been reported to
also carry Assemblages A-I or B:
zoonotic transmission ?
• Giardia lamblia is an enteric
protozoan pathogen found in a
variety of mammalian hosts,
including humans (isolated in 22
species of household stocks,
ranging from sheep, cows, goats,
to ducks: Sullivan 1988)
• seven genetic Assemblages of
Giardia duodenalis, named A-G
• humans are infected with
Assemblages A and B,
• dogs primarily with C and D,
• cats with F

8. Clinical:
-  90% of infected are asymptomatic carriers
- For symptomatic disease the incubation period is usually 3-20
days, but can be much longer
- Acute giardiasis includes diarrhea (90%), gas, anorexia, weight
loss: 10-15 pounds in adult (66%)
- Chronic giardiasis – Giardia inhibits the digestion
of fats by pancreatic lipase (malabsorption with diarrhea)
- Impaired absorption of carotene, folate, vit. B 12 and D-xylose
- Chief cause of growth retardation in infected children

9. Proposed mechanisms of pathogenesis include:
• occlusion of the mucosa by large numbers of the organisms,
• competition with the host for nutrients,
• epithelial damage,
• immune-mediated absorptive changes such as transient lactase
deficiency, altered mucus secretion, and alterations in motility.

10. Diagnosis:
- stool examination
- duodenal fluid (aspirate or string test)
- Giardia antigen detection in stool

11. In developed countries, giardiasis is considered a travel related disease.
(Germany >50% acquired indigenously- Espelage et. al. 2010).
Symptomatic cases are significantly more likely to be
immunocompromised than control persons from the general population.
Physicians should consider Giardia infections among patients with no recent
history of travel abroad, particularly if they have immune deficiencies.

12. Developing countries:
poor sanitary conditions,
poor water quality and overcrowding
Industrialized countries:
international travel and immigration
Populations at increased risk of autochthonous infection:
small children in day care centres, oral-anal sex practitioners, persons in
custodial institutions

13. Large community outbreaks
have been attributed to:
contaminated drinking water
Smaller outbreaks:
contaminated food
(eg. green salad)
contact with contaminated
recreational waters
(swimming and wading pools)

14. It is recommend boiling for 1 minute to allow for a margin of safety and so
users are clear that the water is truly boiling. Because the boiling point
decreases with increasing altitude, boil water for 3 minutes at altitudes
greater than 6,562 feet (>2000 m).
Microfilters with “absolute” pore sizes of 0.1–0.4 μm are usually effective
for removal of cysts and bacteria

15. Entamoeba histolytica
The only source: man (not a zoonosis)
Transmission: fecal-oral
Pathogenic amebas use three major virulence factors,
eg. proteases, for:
lyse,
phagocytose,
kill and destroy
cells and tissues in the host
Pathogenesis: - digests (liquifies) human host cells
(colon wall, neutrophils, liver cells, RBC’s)

16. About 40–50 million people develop clinical
amoebiasis each year, resulting on up to 100 000
deaths (Walsh 1988)
Risk factors:
• In tropics: crowded living conditions, poor sanitation
• High alcohol consumption
• Impaired immunity (eg. HIV infection)
• Recent travel to an endemic area
• Oral-anal contact :
invasive amebic diseases more prevalent in homosexuals

18. RUQ: The RightUpperQuadrant of the abdomen contains the liver and the gallbladder.

21. Vasa shape ulceration of intestinal (large intestine) mucosa

23. Balantidium coli-
balantidiosis
• Balantidiosis is a zoonotic disease and is acquired by humans via the
fecal-oral route from the pig
• Human-to-human transmission may also occur
• Balantidium's habitats in humans are the cecum and colon
• B. coli can become an opportunistic parasite in urban
environments, where pigs are not a factor in infection
• Areas of high prevalence include regions of Latin America, the
Philippines, Papua New Guinea Middle East (<1% to 29% in
endemic area)

24. BALANTIDIUM COLI
• Form nests and necrotic ulcers of the large intestine (bigger than the
ulcer of E. histolytica)
• In acute infection explosive diarrhea may occur as often as every
20 min , with mucus, blood
•Perforation of the colon may also occur in acute disease, with life-
threatening consequences
• Chronic disease- intermittent diarrhoea alternating with constipation,
tender colon, anemia and cachexia- wasting syndrome

25. The trophozoites large
(typically > 50m )
vacuolated cytoplasm
classic dark “kidney-bean” shaped macro-nucleus

26. Balantidium coli
A Trophozoit ; B Cyst

27. Within the ulcer and intestinal mucosa, the large ciliated trophozoites
can be seen

28. Extraintestinal sites of infection
• the appendix but rarely, the liver
• the lungs, causing a pneumonia-like disease (in elderly or otherwise
immunocompromised )
• uterine infection, vaginitis, and cystitis, are thought to occur via
direct spread from the anal area (Balantidium coli in the urine
sediment -Maino et al. 2010)

29. • Cysts of Balantidium are large and would not be carried over great
distances, either on air currents or in water droplets. Thus, infection
by inhalation would require direct contact with aerosol droplets.
• Rats may be carriers of Balantidium, but it is not known if the rat
Balantidium species can infect humans.
• The cockroach, which has its own species of Balantidium, may serve
as a mechanical agent of transmission from feces to food

30. Protozoans of
uro- genital tract

32. TRICHOMONAS VAGINALIS
The most common non-viral human sexually transmitted pathogen
Flagelate of the lumen of the urogenital tract, prostate.
Only trophozoite stage known to exist i.e. absence of cyst stage.
Epidemiology: incidence is about 10 – 20% in women.
Higher among women with poor feminine hygiene.
Mode of transmission: sexual contact, direct contact with infected female,
contaminated toilet articles e.g. towels, toilet seats and infection acquired
in babies while passing the birth canal.

33. • Pathophysiology:
- causes degeneration and desquamation of local tissues; mechanism
unclear
symptomatic - vaginitis, prostatitis, urethritis
Epidemiology
- found in 3-5% of female population of N.A.
- increased in STD clinics (50%), prostitutes 50-75%
- only in humans; no animal reservoir
- sexual transmission
- can persist for 2 years in host

34. Treatment:
• Drug of choice:1 Metronidazole 2 g once
or 500 mg bid x 7d
• OR Tinidazole 2 g once 50 mg/kg once
(max. 2 g)

35. Pathology and Symptoms:
Incubation period 4 to 20 days
Symptoms: profuse, frothy, yellow-green or gray vaginal discharge
leucorrhoea, sometimes with bleeding, an unpleasant vaginal odor,
and vulvovaginal itching and discomfort. Painful and frequent urination,
vulvovaginal swelling, discomfort during sexual intercourse, and
abdominal pain
Granular – strawberry vagina.
In males, there may be urethritis

37. Between 15°N and 20°S
T.b gambiense T.b rhodesiense

40. African Sleeping Sickness
Gambian or Rhodesian tryponosomiasis
Congestive heart failure (CHF) occurs when the heart can no longer pump
blood efficiently, so the blood backs up in the body – particularly in the liver
EKG

41. Trypanosomiasis
The lymph node enlargement on the back
of the neck and head - known as
Winterbottom's sign.

42. Sleeping sickness

43. Diagnosis
- motile organisms on wet preparations of
fresh blood or CSF
- stained smears (Giemsa) may reveal
organism
- high levels of protein (IgG and IgM) in CSF
- lymphocytosis in CSF
-antigen capture or PCR

45. A zoonosis with reservoirs of
armadillo, opossums, raccoons;
transmitted to man
Epidemiology:
Transmission:by reduvid bug bite
vertical (in utero)
blood transfusion
12 million of people affected;
35 million at risk;
Central and South America.
Trypanosoma cruzi Chagas' Disease,
American
Trypanosomiasis

46. Triatoma infestans, Rhodnius prolixus
and Panstrongylus megistus.
The bug (Reduvidae bug) can live and be
infective for two years
Reduvid bug bites human while asleep and passes
feces containing parasite (trypomastigote form)
onto skin near the bite. Human rubs faeces and
parasite into wound or eye.

47. Clinical:
• Acute: Seen mainly in children: local
inflammation at site of innoculation
(chagoma), lymphadenopathy,
hepatosplenomegaly, fever.
• Chronic: Seen mainly in adult life up to
several decades after acute stage
myocardopathy
• - heart failure, arrhythmias megaintestine
• - megaoesophagus, megacolon, megaureter

48. Romana's sign in acute Chagas' disease
Unilateral painless orbital oedema

49. Megacolon

50. Amastigota forms in
heart muscle
Cardiomegaly

51. CNS Protozoa

52. Naegleria sp. enters the body
through the nose while swimming
or participating in water sports.
Once inside the nose, the amoeba
makes its way to the brain.
There, it causes inflammation and
destroys brain tissue.
Naegleria infection is very rare.
Only 31 cases occurred in the
United States between 1989 and
2002. About 200 cases of
naegleriasis infection have been
reported worldwide.

53. Clinical Features:
Acute primary amoebic meningoencephalitis (PAM) is
caused by Naegleria fowleri.
• It presents with severe headache and other meningeal signs,
fever, vomiting, and focal neurologic deficits
• progresses rapidly (<10 days)
• frequently leads to coma and death.
Sources: the environment: warm water reservoirs, unchlorinated
groundwater, soil

54. Acanthamoeba spp. causes mostly subacute
or chronic granulomatous amoebic
encephalitis (GAE),
headaches, altered mental status, and focal
neurologic deficit,
which progresses over several weeks to death
cause granulomatous skin lesions
keratitis and corneal ulcers following corneal
trauma
(poor contact lens hygiene and exposure to
contaminated water may increase the risk among
contact lens users- coroneal trauma)

55. Immunocompromised patient.
skin lesion

56. corneal trauma

57. systemic parasites
tissues, body fluids:
blood, cerebro-spinal

60. • Diagnosis of Malaria
• a) clinical picture: - fever, chills
- travel history
- fever pattern
• b) examination of blood:
- thin
- thick smear
- PCR
- antigen capture (ELISA)

61. BLOOD examination
- thin smear for characteristics of
species
- use shape and size
of: trophozoite, schizont and
gametocyte
- % of RBCs with parasites (very
rarely over >1% parasitemia in
P. vivax, ovale or malariae)
- metabolic debris (pigment) in
RBC around parasite (called
Schuffner's dots in P. vivax
infection)
- size and age of RBCs which
contain parasites (P. vivax and
ovale infect younger (larger RBCs)

62. Severe Malaria: Common Clinical Manifestations
Pathogenesis Clinical Features
Cerebral Sluggish flow caused by sticky knobs on
parasitized red cells leading to stagnant
hypoxia and vascular damage.
Impaired level of
consciousness. Convulsions.
Generalized and localized
neurological signs.
Anaemia Destruction of parasitized and nonparasitized
red cells by immune complexes, bone marrow
suppression
Pallor and jaundice. High
output cardiac state.
Renal Acute tubular necrosis resulting from sluggish
blood flow and hypotension. Hemoglobinuria.
Oliguria. Haemoglobinuria.
Acute renal failure.
Gastro-
intestinal
Unknown. Diarrhoea.

63. Severe Malaria: Common Clinical Manifestations
Pathogenesis Clinical Features
Respiratory Increased pulmonary
capillary permeability.
Cough. Pulmonary edema,
bronchopneumonia.
Hepatic Unknown.? Partially due
to haemodynamic
changes.
Jaundice (mainly attributable to
haemolysis). Elevated serum enzyme
levels, impaired elimination of drugs,
prolonged prothrombin time, bleeding.
Fluid and
electrolyte
balance
Unknown.? Partially due
to inappropriate release of
antidiuretic hormone
(ADH).
Increased intravascular volume.
Electrolyte changes, hypoglycemia,
hyperkalemia and hemolysis.
Obstetric Sluggish blood flow in
placental vessels leading
to vascular damage.
Fetal death. Premature labour.

64. • ACUTE CLINICAL PICTURE COMPLICATIONS
• fever, headache, splenomegaly
• cerebral malaria (P.falciparum only)
• adult respiratory distress syndrome (ARDS)
(P.falciparum)
• black water fever (severe hemolysis) (P.falciparum
only)
• acute renal failure
• CHRONIC CLINICAL PICTURE:
- nephrotic syndrome (P. malariae only)
- big spleen syndrome (hypertrophic malarial
splenomegaly)

66. Nephrosis associated with malaria
Pigment in cerebral vessels (autopsy)

67. Entamoeba histolytica Giardia lamblia Balantidium coli

68. Trichomonas vaginalisTrichomonas vaginalis
Trichomonas vaginalis
Trichomonas vaginalis
Naegleria sp. Acanthamoeba sp.