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Medically important parasites
PROTOZOA
Objectives
• Discuss the classification of medically important
protozoa.
1. Epidemiology
2. Morphology
3. Lifecycle
4. Pathogenesis
5. Clinical manifestations
6. Diagnosis
7. Treatment
8. Prevention and control
Methods of reproduction in protozoa
1. Asexual multiplication:
(a) Simple binary fission – in this process, after
division of all the structures, the individual
parasite divides either longitudinally or
transversely into two more or less equal parts.
• B) Multiple fission or schizogony – in this
process more than two individuals are
produced eg Plasmodia spp
• Diagram showing multiple fission
2. Sexual reproduction:
(a) Conjugation – in this process, a temporary
union of two individuals occurs during which
time interchange of nuclear material takes
place. Later on, the two individuals separate.
• Diagram of conjugation
• (b) Syngamy – in this process, sexually
differentiated cells, called gametes, unite
permanently and a complete fusion of the
nuclear material takes place. The resulting
product is then known as a zygote.
• Diagram of syngamy
Classsification of protozoa
AMOEBA
Entamoeba histolytica
Morphological features
(a) Trophozoites
• Motility is rapid, progressive, and
unidirectional, through pseudopods. In the
case of dysentery, RBCs may be visible in the
cytoplasm, and this feature is diagnostic for
E.histolytica.
(b) Cyst
• Round in shape, immotile.
Epidemiology
• E.histolytica has a worldwide distribution.
• The incidence is highest in tropical and
subtropical regions that have poor sanitation and
contaminated water.
• About 90% of infections are asymptomatic, and
the remaining produces a spectrum of clinical
syndrome. Patients infected with E.hisolytica pass
noninfectious trophozotes and infectious cysts in
their stools.
• Symptomatic amebiasis is usually sporadic. The
epidemic form is a result of direct person-to-
person faecal-oral spread under conditions of
poor personal hygiene.
Life cycle
• ingestion of a mature infective cyst, contaminated food or drink and also by hand
to mouth contact.
• It is then passed unaltered through the stomach, as the cyst wall is resistant to
gastric juice. In terminal ileum (with alkaline pH), excystation takes place.
• Trophozoites being actively motile invade the tissues and ultimately lodge in the
submucous layer of the large bowel. Here they grow and multiply by binary
fission.
• Trophozoites are responsible for producing lesions in amoebiasis. Invasion of
blood vessels leads to secondary extra intestinal lesions.
• Gradually the effect of the parasite on the host is toned down together with
concomitant increase in host tolerance, making it difficult for the parasite to
continue its life cycle in the trophozoite phase.
• A certain number of trophozoites come from tissues into lumen of bowel and are
first transformed into pre-cyst which secret a cyst wall and become a uninucleate
cyst. Eventually, mature cysts form which are the infective forms.
• Both mature and immature cysts may be passed in faeces. Immature cysts can
mature in external environments and become infective.
Life cycle of E. histolytica
Pathogenesis
• patients develop symptoms with invasive disease within 3
weeks of ingestion of the cysts
• amebic liver abscess formation takes about 3 months to
develop some patients apparently carry the organisms for
prolonged periods before developing significant clinical
manifestations
• Trophozoites divide and produce extensive local necrosis in
the large intestine.
• Invasion into the deeper mucosa with extension into the
peritoneal cavity may occur which can lead to secondary
involvement of other organs, primarily the liver but also the
lungs, brain, and heart.
• Amoebas multiply rapidly in an anaerobic environment,
because the trophozites are killed by ambient oxygen
concentration.
Clinical features
• The outcome of infection may result in a carrier state,
intestinal amebiasis, or exteraintestinal amebiasis.
• Diarrhoea, flatulence, and cramping are complaints of
symptomatic patients. More severe disease is
characterised by the passing of numerous bloody
stools in a day. Systemic signs of infection (fever,
leukocytosis, rigors) are present in patients with
extraintestinal amebiasis.
• The liver is primarily involved, because trophozoites in
the blood are removed from the blood by the portal
veins thus pain over the liver with hepatomegaly and
elevation of the diaphragm is observed.
Laboratory diagnosis
• Examination of formed or semiformed faeces
for cyst stage. (Cysts indicate infection with
either a pathogenic E.histolytica or non-
pathogenic E.dispar.)
• sigmoidoscopy
– lesions, aspirate, biopsy
• antigen detection
– histolytica/dispar
diagnosis cont’d
• Extraintestinal amoebiasis
• Diagnosed by the use of scanning procedures
for liver and other organs.
• Specific serologic tests, together with
microscopic examination of the abscess
material, can confirm the diagnosis.
Treatment
• Acute, amoebiasis is treated with metrondiazole
followed by iodoquinol, and
• asymptomatic carriage can be eradicated with
iodoquinol, diloxanide furoate, or paromomycin.
• The cysticidal agents are commonly
recommended for asymptomatic carriers who
handle food for public use.
• Metronidazole, chloroquine, and diloxanide
furoate can be used for the treatment of extra
intestinal amoebiasis.
• Prevention
• Introduction of adequate sanitation measures
and education about the routes of
transmission.
• Avoid eating raw vegetables grown by
sewerage irrigation
OTHER AMEBAE INHABITING THE
ALIMENTARY CANAL
• Entamoeba hartmanni-cosmopolitan in distribution.
Infection is similar to E.histolytica
• Entamoeba coli-lives freely in the lumen of large intestines
• Entamoeba polecki- common parasite in caecum and colon
of pigs
• Endolimax nana –found in lumen of large intestines
• Iodamoeba buetschlii:-lives in the lumen of large
intestines. The trophozoite feeds on enteric bacteria.
• Entamoeba gingivalis-Is a commensal in the gingival tissue
around the teeth.
• Blastocystis hominis
PATHOGENIC FREE-LIVING AMOEBAE
• Naegleria fowleri-Amoeboid forms with single pseudopodia and flagella
forms.
• -Amoeboid form is the invasive stage. Infection occurs by nasal
contamination during swimming in fresh water lakes, ponds and
swimming pools containing infective forms.
• Leads to primary meningoencephalitis
• Acanthameba species-
• Infection occurs through inhalation of dust particles containing
trophozoites and cyst
• -the trophozoite reach the lower respiratort tract then invade the Central
nervous system through the blood stream
• Infection may also be acquired through broken skin or ulcerated skin
• It causes granulomatous aamoebic enecephalitis in immunosuppressed
persons
Protozoa amoeba

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Protozoa amoeba

  • 2. Objectives • Discuss the classification of medically important protozoa. 1. Epidemiology 2. Morphology 3. Lifecycle 4. Pathogenesis 5. Clinical manifestations 6. Diagnosis 7. Treatment 8. Prevention and control
  • 3. Methods of reproduction in protozoa 1. Asexual multiplication: (a) Simple binary fission – in this process, after division of all the structures, the individual parasite divides either longitudinally or transversely into two more or less equal parts.
  • 4.
  • 5. • B) Multiple fission or schizogony – in this process more than two individuals are produced eg Plasmodia spp
  • 6. • Diagram showing multiple fission
  • 7. 2. Sexual reproduction: (a) Conjugation – in this process, a temporary union of two individuals occurs during which time interchange of nuclear material takes place. Later on, the two individuals separate.
  • 8. • Diagram of conjugation
  • 9. • (b) Syngamy – in this process, sexually differentiated cells, called gametes, unite permanently and a complete fusion of the nuclear material takes place. The resulting product is then known as a zygote.
  • 10. • Diagram of syngamy
  • 12. AMOEBA Entamoeba histolytica Morphological features (a) Trophozoites • Motility is rapid, progressive, and unidirectional, through pseudopods. In the case of dysentery, RBCs may be visible in the cytoplasm, and this feature is diagnostic for E.histolytica. (b) Cyst • Round in shape, immotile.
  • 13. Epidemiology • E.histolytica has a worldwide distribution. • The incidence is highest in tropical and subtropical regions that have poor sanitation and contaminated water. • About 90% of infections are asymptomatic, and the remaining produces a spectrum of clinical syndrome. Patients infected with E.hisolytica pass noninfectious trophozotes and infectious cysts in their stools. • Symptomatic amebiasis is usually sporadic. The epidemic form is a result of direct person-to- person faecal-oral spread under conditions of poor personal hygiene.
  • 14. Life cycle • ingestion of a mature infective cyst, contaminated food or drink and also by hand to mouth contact. • It is then passed unaltered through the stomach, as the cyst wall is resistant to gastric juice. In terminal ileum (with alkaline pH), excystation takes place. • Trophozoites being actively motile invade the tissues and ultimately lodge in the submucous layer of the large bowel. Here they grow and multiply by binary fission. • Trophozoites are responsible for producing lesions in amoebiasis. Invasion of blood vessels leads to secondary extra intestinal lesions. • Gradually the effect of the parasite on the host is toned down together with concomitant increase in host tolerance, making it difficult for the parasite to continue its life cycle in the trophozoite phase. • A certain number of trophozoites come from tissues into lumen of bowel and are first transformed into pre-cyst which secret a cyst wall and become a uninucleate cyst. Eventually, mature cysts form which are the infective forms. • Both mature and immature cysts may be passed in faeces. Immature cysts can mature in external environments and become infective.
  • 15. Life cycle of E. histolytica
  • 16.
  • 17. Pathogenesis • patients develop symptoms with invasive disease within 3 weeks of ingestion of the cysts • amebic liver abscess formation takes about 3 months to develop some patients apparently carry the organisms for prolonged periods before developing significant clinical manifestations • Trophozoites divide and produce extensive local necrosis in the large intestine. • Invasion into the deeper mucosa with extension into the peritoneal cavity may occur which can lead to secondary involvement of other organs, primarily the liver but also the lungs, brain, and heart. • Amoebas multiply rapidly in an anaerobic environment, because the trophozites are killed by ambient oxygen concentration.
  • 18. Clinical features • The outcome of infection may result in a carrier state, intestinal amebiasis, or exteraintestinal amebiasis. • Diarrhoea, flatulence, and cramping are complaints of symptomatic patients. More severe disease is characterised by the passing of numerous bloody stools in a day. Systemic signs of infection (fever, leukocytosis, rigors) are present in patients with extraintestinal amebiasis. • The liver is primarily involved, because trophozoites in the blood are removed from the blood by the portal veins thus pain over the liver with hepatomegaly and elevation of the diaphragm is observed.
  • 19. Laboratory diagnosis • Examination of formed or semiformed faeces for cyst stage. (Cysts indicate infection with either a pathogenic E.histolytica or non- pathogenic E.dispar.) • sigmoidoscopy – lesions, aspirate, biopsy • antigen detection – histolytica/dispar
  • 20. diagnosis cont’d • Extraintestinal amoebiasis • Diagnosed by the use of scanning procedures for liver and other organs. • Specific serologic tests, together with microscopic examination of the abscess material, can confirm the diagnosis.
  • 21.
  • 22. Treatment • Acute, amoebiasis is treated with metrondiazole followed by iodoquinol, and • asymptomatic carriage can be eradicated with iodoquinol, diloxanide furoate, or paromomycin. • The cysticidal agents are commonly recommended for asymptomatic carriers who handle food for public use. • Metronidazole, chloroquine, and diloxanide furoate can be used for the treatment of extra intestinal amoebiasis.
  • 23. • Prevention • Introduction of adequate sanitation measures and education about the routes of transmission. • Avoid eating raw vegetables grown by sewerage irrigation
  • 24. OTHER AMEBAE INHABITING THE ALIMENTARY CANAL • Entamoeba hartmanni-cosmopolitan in distribution. Infection is similar to E.histolytica • Entamoeba coli-lives freely in the lumen of large intestines • Entamoeba polecki- common parasite in caecum and colon of pigs • Endolimax nana –found in lumen of large intestines • Iodamoeba buetschlii:-lives in the lumen of large intestines. The trophozoite feeds on enteric bacteria. • Entamoeba gingivalis-Is a commensal in the gingival tissue around the teeth. • Blastocystis hominis
  • 25. PATHOGENIC FREE-LIVING AMOEBAE • Naegleria fowleri-Amoeboid forms with single pseudopodia and flagella forms. • -Amoeboid form is the invasive stage. Infection occurs by nasal contamination during swimming in fresh water lakes, ponds and swimming pools containing infective forms. • Leads to primary meningoencephalitis • Acanthameba species- • Infection occurs through inhalation of dust particles containing trophozoites and cyst • -the trophozoite reach the lower respiratort tract then invade the Central nervous system through the blood stream • Infection may also be acquired through broken skin or ulcerated skin • It causes granulomatous aamoebic enecephalitis in immunosuppressed persons