miscellaneous protozoa Flashcards

(62 cards)

1
Q

briefly explain the classification of miscellaneous protozoans

A

phylum: ciliophora
class: kinetofragminophorea
intestinal spp:
- Balantidium coli

phylum: apicomplexa
class: sporozoa
intestinal spp:
- Isospoa belli
- Sarcocystis spp
- Cryptosporidium parvum

tissue spp:
- Toxoplasma gondii

phylum: blastocystida
class: blastocystea
intestinal spp:
- Blastocystis hominis

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2
Q

the only ciliate to infect humans

A

Balantidium coli
- large and covered in cilia

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3
Q

diseases:
1. Balantidium coli
2. Isospora belli (Cystoisospora belli)
3. Sarcocystsis spp
4. Cryptosporidum parvum
5. Blastocystis hominis
6. Cyclospora cayetanensis
7. Microsporidia
8. Toxoplasma gondii
9. Pneumocystis jiroveci (Pneumocystis carinii)

A
  1. Balantidiasis (zoonotic infection)

2.
- Isosporiasis
- Human Coccidiosis

  1. Intestinal or Muscular Sarcocystosis
  2. Cryptosporidiosis
    • Blastocystis hominis infection
    • Blastocystis infection
    • Cyclospora cayetanensis infection
    • Cyclosporiasis
      ○ Very similar with cryptosporidiosis
      ○ Dierence is Cyclospora cayetanensis produces a longer duration of diarrhea
  3. Microsporidiosis
    • Toxoplasmosis
    • Congenital Toxoplasmosis
    • Cerebral Toxoplasmosis
    • Pneumocystosis (Atypical Interstitial Plasma Cell Pneumonia)
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4
Q

diagnostic and infective stage of
1. Balantidium coli
2. Isospora belli (Cystoisospora belli)
3. Sarcocystsis spp
4. Cryptosporidum parvum
5. Blastocystis hominis
6. Cyclospora cayetanensis
7. Microsporidia
8. Toxoplasma gondii
9. Pneumocystis jiroveci (Pneumocystis carinii)

A
  1. Diagnostic stage: trophozoites or cyst
    Infective stage: cyst
  2. Diagnostic stage: oocyst
    - unsporulated or partially mature oocysts in stool (acid-fast staining)
    Infective stage: mature oocyst
    - sporulated oocyst
  3. Diagnostic stage: oocysts or sporocysts in stool (intestinal form)
    Infective stage: sarcocyst in undercooked meat
  4. Diagnostic stage: thick walled sporulated oocyst
    - found in contaminated water or food
    - immediately infectiious when passed in feces
    Infective stage: thick- walled oocyst in feces
  5. Diagnostic stage: cyst
    Infective stage: cyst
  6. Diagnostic stage: unsporulated or immature oocysts
    Infective stage: sporulated oocysts

7.
Infective stage: spores

  1. Infective stage: oocyst
    *oocyst, tachyzoite, bradyzoite
    (- sporulated oocyst (cat feces)
    - tissue cyst (undercooked meat)
    - congenital (transplacental) transmission
    - blood transfusion / organ transplant)
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5
Q

life cycle of Balantidium coli

A
  1. Cyst is passed onto the stool of infected human
  2. Humans will acquire the infection of B. coli by ingesting cyst through contaminated food or water or vegetables
  3. In the intestine, the cyst undergoes excystation
    ○ Excystation – transformation of cyst to trophozoite; there will be a release of trophozoite
  4. Trophozoites will divide through binary
    fission
    ○ Asexual reproduction cycle of all protozoans
  5. Once done dividing, it will excyst as it passes down the colon and is excreted in
    the feces
    ○ Trophozoites – seen in loose stool
    ○ Cyst – seen in formed stool
  6. B. coli completes its life cycle in 1 host
    only
    ○ Infection is acquired from pigs and other animal reservoirs or from human carriers
    ○ Pig – reservoir host
    ○ Balantidiasis – zoonotic infection

(Summary of life cycle:
Humans will ingest mature cyst → excystation in small intestine → trophozoites will colonize the cecum → binary fission → encystation in large intestine → cyst is passed into the feces that could either be as trophozoite or cyst)

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6
Q

reservoir host of Balantidium coli

A

pig

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7
Q

this is the largest protozoan

A

Balantidium coli

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8
Q

Balantidium coli
- shape
- motility
- nuclei
- structure

A

trophozoites:
shape
- Ovoid, sac-like; tapers at anterior end
motility
- Rotary, boring
nuclei
- Kidney-shaped macronucleus + small micronucleus
structure
- cilia (locomotion)
- cytostome (feeding)
- 1-2 contractile vacuoles, food vacuoles

cysts:
- double cyst wall
- cytoplasm is mostly granular
- only macronucleus usually seen as micronucleus may not be observed in wet or permanent prep
- may see cilia layer btwn cyst wall layers in young cysts
- usually found in chronic cases and carriers
- ingested through contaminated food or water and bcm a trophozoites in the large intestine

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9
Q

pathogenesis of
1. Balantidium coli
2. Isospora belli (Cystoisospora belli)
3. Sarcocystsis spp
4. Cryptosporidum parvum
5. Blastocystis hominis
6. Cyclospora cayetanensis
7. Microsporidia
8. Toxoplasma gondii
9. Pneumocystis jiroveci (Pneumocystis carinii)

A
    • produces flask-shaped ulcers
      (similar to E, histolytica but larger opening)
    • commonly found in colon region
    • can lead to perforation → peritonitis
    • usually no extraintestinal spread
    • asymptomatic
  1. Immunocompetent people (healthy immune system):
    - often asymptomatic
    - self-limiting watery diarrhea (may last ~2 weeks)
    - nausea
    - cramps
    - weight loss

Immunocompromised people (especially with AIDS):
- chronic
- profuse diarrhe
- malabsorption
- electrolyte loss
- may affect lungs/stomach → can be fatal.

*time from infection to symptoms: 2-14 days

    • often asymptomatic
    • diarrhea
    • abdominal cramps
    • nausea
    • prolonged watery diarrhea
    • fatigue
    • Chronic diarrhea (especially in HIV/AIDS)
    • Keratitis (ocular involvement)
    • Disseminated/systemic infections
    • Can involve biliary tract and respiratory tract

8.
*high fetal risk if pri infection during 1st trimester

    • Nonproductive cough, dyspnea, cyanosis
    • Rapid deterioration in AIDS patients
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10
Q

diagnosis
1. Balantidium coli
2. Isospora belli (Cystoisospora belli)
3. Sarcocystsis spp
4. Cryptosporidum parvum
5. Blastocystis hominis
6. Cyclospora cayetanensis
7. Microsporidia
8. Toxoplasma gondii
9. Pneumocystis jiroveci (Pneumocystis carinii)

A
  1. ● Stool examination
    - Trophozoites (in diarrheic stool)
    - Cysts (in formed stool)
    ● Biopsy
    - If stool is negative; identify trophozoites from ulcer scrapings.
  2. ● Stool oocyst detection (better with iodine wet prep or modified acid-fast stain)
    - stool samples may contain immature, partially mature, or fully mature oocyst
    ● Duodenal concentrates
    ● Entero test
    ● Sheather’s sugar flotation procedure
    *during diagnosis, oocyst appears transparent, may be difficult to recognize in saline wet prep
  3. ● To detect oocysts or sporocysts in fecal samples
    ● Muscle biopsy (PAS stain)
    -periodic acid schiff stain
  4. ● Stool
    ● Microscopy: use Modified Acid-Fast Ziehl-Neelsen stain → oocysts (can be mistaken as yeast) appear pink
    ● Molecular test: PCR (stool or biopsy) – highly accurate and highly sensitive
    ● Antigen detection: ELISA, indirect immunofluorescence (IFA)
    ● Biopsy (if stool test is negative): check small intestine tissue for merozoites or gametocytes
    • microscopy – culture (Jones medium)
    • PCR
    • modified acid-fast stain
    • UV autofluorescence
    • biopsy
    • Stool and biopsy of spores
    • Microscopy: modified trichrome stain, Gram-Chromotrope, or Kinyoun stain for stool/biopsy
    • PCR: stool or tissue samples
    • Electron microscopy: gold standard for identifying spores
    • serology (IgM, IgG)
    • double-sandwich ELISA
    • Sabin-Feldman dye test (gold standard).
  5. ● Gomori methenamine silver stain
    ● Bronchoalveolar lavage, biopsy
    ● “Honeycomb” lung appearance on X-ray
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11
Q

treatment
1. Balantidium coli
2. Isospora belli (Cystoisospora belli)
3. Sarcocystsis spp
4. Cryptosporidum parvum
5. Blastocystis hominis
6. Cyclospora cayetanensis
7. Microsporidia
8. Toxoplasma gondii
9. Pneumocystis jiroveci (Pneumocystis carinii)

A

1.
● Oxytetracycline (Terramycin)
● Metronidazole
● lodoquinol

  1. ● Mild: Bland diet and rest
    - easily digestible
    - non-irritating foods
    ● Severe: TMP-SMX or Pyrimethamine + Sulfadiazine
    - trimethoprim-sulfamethoxazole
  2. ● TMP-SMX or Pyrimethamine + Sulfadiazine (intestinal infections only)
  3. metronidazole (if symptomatic)
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12
Q

prevention
1. Balantidium coli
2. Isospora belli (Cystoisospora belli)
3. Sarcocystsis spp
4. Cryptosporidum parvum
5. Blastocystis hominis
6. Cyclospora cayetanensis
7. Microsporidia
8. Toxoplasma gondii
9. Pneumocystis jiroveci (Pneumocystis carinii)

A
  1. ● Hygiene and sanitation
    ● Safe food and water handling
    ● Treat pigs as potential reservoirs

2.
● Hygiene, safe food and water practices
● Avoid oral-anal contact

3.
● Proper cooking of beef/pork
● Freezing meat at -5 °C for several days will kill the sarcocysts
● Hygiene around animal feces

  1. ● water sanitation
    ● hygiene

6.
● hygiene
● proper food washing
● safe wate

  1. ● Proper hygiene and sanitation
    ● Safe drinking water
    ● Early ART initiation in HIV-positive individuals

★ Balantidium coli = Boil water, proper hygiene, sanitation, treat pigs
★ Toxoplasma gondii = Avoid cat feces, cook meat well, wash hands/vegetables, blood screening
★ Cystoisospora belli = Safe food and water, hygiene, proper faecal disposal
★ Cryptosporidium parvum = Boil or filter water, hygiene, avoid contaminated recreational water
★ Cyclospora cayetanensis = Boil water, wash produce properly, hygiene
★ Sarcocystis spp. = Proper cooking/freezing of meat, safe water
★ Blastocystis hominis = Sanitation, water treatment, wash food properly
★ Microsporidia = Hygiene, safe water, initiate ART for immunocompromised

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13
Q

name all coccidia spp.

A
  • they mostly live in the intestines
  1. Isospora belli
  2. Sarcocystis spp.
  3. Toxoplasma gondii
  4. Cryptosporidium parvum
  5. Cyclospora cayetanensis
  6. Microsporidia
  7. Pneumocystis jirovecii
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14
Q

what are the similar characteristics between the coccidia spp.

A

○ Intracellular parasites (Class: Sporozoa)
○ Life cycle includes Schizogony (asexual) and Sporogony (sexual)
○ Transmission mostly by ingestion of mature oocysts

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15
Q

definitive host of Isospora belli

A

humans
- catering both sexual and asexual reproduction
- does not have intermediate host

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16
Q

life cycle of Isospora belli

A
  1. A person becomes infected by swallowing or ingesting the mature sporulated oocyst through contaminated food or water
  2. Inside the small intestine, the oocyst releases sporozoites that emerge and begin infection by invading epithelial cells
  3. Sporozoites will have intestinal invasion most especially in epithelial cells
  4. In the intestinal invasion, will release sporozoite and invade epithelial cells of the intestines and enter host cells to begin multiplication
  5. The multiplication will start first at schizogony (asexual reproduction)
  6. Inside the intestinal cells, the sporozoites undergo schizogony and the sporozoites multiply to form many merozoites
    - sporozoites undergo asexual reproduction and form merozoites
  7. Merozoites can infect new cells that can continue the asexual cycle although there are some that transform into gametocytes
  8. Gametocytes are the sexual form wherein there will be a fertilization from the microgametes to the macrogametes and form zygote
  9. Zygote will mature into an oocyst
  10. Oocyst is passed into the feces and becomes the diagnostic stage
  11. If oocyst is sporulated in the environment, it becomes infective again, completing and repeating the cycle

(Summary of life cycle: Ingest mature oocyst (sporulated) → Sporozoites released → Intestinal invasion → Schizogony → Merozoites → Asexual or Sexual → Gametocytes (Micro and Macro) → Fertilization → Zygote → Oocyst formation and shedding → Passed to Feces)

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17
Q

habitat
2. Isospora belli
4. Cryptosporidium parvum
5. Blastocystis hominis
6. Cyclospora cayetanensis
7. Microsporidia
8. Toxoplasma gondii

A
  1. small intestinal epithelium
    • primarily inhabits the small intestine
    • may also be present in the stomach, large intestine, and lungs
  2. large intestine
  3. small intestine
    • intestinal epithelium
    • cornea
    • biliary tract
    • muscle

8.
- muscle tissue
- brain
- eyes

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18
Q

what spp has prolonged diarrhea in HIV/ AIDS patient

A

Isospora belli

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19
Q

clinical symptoms
2. Isospora belli
3. Sarcocystosis spp.

A
  1. ● Self-limiting to chronic diarrhea
    ● Pale, foul-smelling stool
    ● Weight loss, malabsorption
  2. ● Diarrhea, muscle tenderness (myositis)
    ● Muscle pain, fever, eosinophilia
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20
Q

Was first considered as member of the genus Isospora due to similar morphological characteristics

A

Sarcocystosis spp.
(S. hominis, S. huihominis, S. Lindemanni)

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21
Q

life cycle of Sarcocystosis spp.

A

ingestion of undercooked beef/pork containing sarcocysts → intestinal infection in humans (definitive host) → oocysts/sporocysts excreted in feces (diagnostic stage).

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22
Q

what is the intermediate host of Sarcocystis lindemanni

A

Humans
- parasite form cysts in muscles → this is called muscular sarcocystosis.

  • Symptoms:
    Muscle pain
    Fever
    Eosinophilia (increased eosinophils in blood – a sign of parasite infection)
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23
Q

Types of Sarcocystosis in Humans

A

★ Muscular sarcocystosis: S. lindemanni
[How it happens: Humans accidentally become intermediate hosts → parasite goes to muscles.]

★ Intestinal sarcocystosis: S. hominis and S. huihominis
[How it happens: Humans are definitive hosts, meaning the parasite stays in the intestines.
Infection comes from eating undercooked meat (beef for S. hominis, pork for S. suihominis).]

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24
Q

morphology of Sarcocystis spp

A

Oocysts:
2 sporocysts (10-18 um), each with 4 sausage-shaped sporozoites

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25
life cycle of Sarcocystis spp
1. Begins when the sporocysts and oocysts are passed in the feces coming from humans 2. Sporocysts and oocysts can contaminate grass and the cows and pigs can ingest them 3. In the intermediate host, the sporocysts rupture and release sporozoites which will invade the intestinal mucosa and reach the vascular epithelial cells where they undergo schizogony 4. Schizonts rupture and release merozoites 5. Merozoites will penetrate muscle cells and develop into cysts with bradyzoites 6. Cysts with bradyzoites ingested in undercooked meat for the sarcocystis 7. When the sarcocysts are ingested by humans (definitive host), the merozoites are released in the intestines and enter intestinal cells and develop into male and female gametocytes (microgametes and macrogametes) 8. Fertilization will happen and then zygote will develop into an oocyst 9. Oocyst contains 2 sporocysts which have 4 sporozoites 10. Oocysts are shed in feces and are ingested by intermediate host (cattle and pigs)
26
briefly explain S. hominis and S. lindemanni - how humans get it - human role - where it develops
S. hominis: (Intestinal form) - eating undercooked beef (cattle/pig) w sarcocysts - definitive host *cattle/ pig - intermediate host - intestines (Destroys the intestinal lining (epithelial cells) May cause mild intestinal symptoms like diarrhea or stomach pain.) S. lindemanni: (Muscular form / Extra-intestinal) - ingesting oocyst from animals - intermediate host *definitive host is unknown - striated muscle (muscular form) !! (Sarcocysts develop in skeletal or cardiac muscle (but usually not both). Causes: - Myositis (muscle inflammation) - Muscle pain - Allergic reactions (like swelling, fever, or rash) Diagnosis: - Muscle biopsy - Use PAS stain (special stain for detecting cysts) Treatment: No specific cure. Give supportive care (rest, pain relief, manage symptoms))
27
a zoonotic protozoan
Cryptosporidium parvum
28
distribution - Cryptosporidium parvum - Blastocystis hominis - Cyclospora cayetanensis - Microsporidia
Cryptosporidium parvum: ● Ubiquitous presence worldwide ● C. hominis: human-specific ● C. parvum: zoonotic (affects multiple mammals) Blastocystis hominis: ● worldwide Cyclospora cayetanensis: ● tropical and subtropical countries ● first reported in Nepal Microsporidia: ● worldwide (opportunistic infection, especially in AIDS patients)
29
morphology of Cryptosporidium parvum
● Roundish in shape; may resemble yeast ● Contains 4 sporozoites, but no sporocysts ● Surrounded by a thick cell wall ● May have 1-6 dark granules
30
infective form of Cryptosporidium parvum
thick-walled sporulated oocysts - which is responsible for autoinfection * resistant to chlorine and many disinfectants; ozone effective - water-borne transmission = hard to combat !! other forms (not commonly seen in clinical samples ) ● Schizonts with merozoites ● Microgametocytes and macrogametocytes
31
life cycle of Cryptosporidium parvum
1. Infective stage: humans ingest thick-walled sporulated oocysts through contaminated water or food - immediately infectious when excreted in feces 2. Excystation: in the small intestine, sporozoites are released from the oocyst. 3. Intestinal invasion: sporozoites enter the intestinal cells and become trophozoites. 4. Asexual cycle (schizogony): trophozoites multiply into meronts, which release merozoites to infect more cells. 5. Sexual cycle (gametogony): some merozoites develop into gamonts → microgametes (male) and macrogametes (female). Fertilization forms a zygote. 6. Oocyst formation: zygote develops into either: - thick-walled oocyst excreted in feces (Diagnostic stage; Infective stage) ○ Thin-walled oocyst → causes auto-infection inside the host
32
reservoir host of Cryptosporidium parvum
mammals birds
33
Cryptosporidium parvum: what happens to the intestines (Histopathology)
Villous atrophy: The finger-like projections (villi) in the small intestine get shorter. Crypt hyperplasia: The valleys between villi (crypts) get deeper and wider. Lymphocyte infiltration: White blood cells gather in the area (sign of inflammation).
34
this often considered as a commensal organism
Blastocystis hominis
35
morphology of Blastocystis hominis
4 forms - vacuolated (most common) - amoeboid - granular - cystic
36
life cycle of Blastocystis hominis
cyst ingestion → trophozoite replication (binary fission, sporulation)
37
morphologic form of Blastocystis hominis
1. Vacuolated Form ● Most common in stool specimens ● Has a large central vacuole with cytoplasm and nuclei pushed to the edge ● Reproduces by binary fission 2. Amoeboid Form ● Polymorphous, slightly larger than vacuolated ● Seen occasionally in feces ● Reproduces by sporulation 3. Granular Form ● 10-60 um in diameter ● Observed in old cultures 4. Cystic Form ● Smallest form ● Thick multilayered cyst wall ● Important for transmission and resistance
38
life cycle of Blastocystis hominis
1. Cyst and vacuolar forms are excreted or shed in feces - cyst – infective and diagnostic stage 2. Infection occurs via fecal-oral transmission by ingestion of contaminated food and water 3. Infectious stage is not yet confirmed but some articles support that the ingestion of cyst is the infective stage 4. Once ingested, the cyst reaches the small and large intestines where excystation will occur 5. Vacuolar form develops and multiplies that acts like a trophozoite - engages in nutrient update, undergoes binary fission, and may convert into other forms like granular, amoeboid forms 6. For the infection to continue, some vacuolar forms may encyst again and can be passed out in the feces, continuing the life cycle
39
which parasite shows polymorphism
Blastocystis hominis - polymorphism = many form *participates in sexual and asexual reproduction, and exhibits pseudopod extension and retraction
40
morphology of Cyclospora cayetanensis
sporulated oocyst (8-10 um, 2 sporocysts each with 2 sporozoites)
41
life cycle of Cyclospora cayetanensis
ingestion of sporulated oocysts → sporozoites infect intestine → asexual/sexual phases → unsporulated oocyst excreted
42
life cycle of Cyclospora cayetanensis
1. Begins during the excretion of unsporulated oocysts in the stool 2. Oocysts will contaminate and sporulate in the environment 3. Sporulated oocysts will enter the food chain (can be mixed with cilantro, basil, raspberries, water) 4. Humans acquire infection by the ingestion of food and water contaminated with sporulated oocyst 5. Excystation of the sporocysts will release sporozoites that infect the enterocytes of the small intestine where sexual and asexual phases will occur 6. Sporozoites will undergo asexual reproduction first forming meront I and meront II and then meront II will become a zygote 7. After the sexual phase, unsporulated oocyst develop and are excreted in the feces ● Summary of life cycle: ingestion of sporulated oocyst → excystation → release sporozoites → infect enterocytes in the small intestine → asexual → sexual → zygote from microgametes and macrogametes → unsporulated oocyst that will be shed in the stool
43
an opportunistic protozoan infection
Microsporidia
44
morphology of Microsporidia
spores (1-5 um) oval to cylindrical thick double-layered wall contain polar filament (tubule) that injects infective sporoplasm into host cells - infection will start by swallowing or breathing in spores
45
life cycle of microsporidia
1. Ingestion and inhalation of spores can happen from dirty water, contaminated food, or close contact with infected surfaces or people with Microsporidia 2. Once inside the body, the spores pops open and uses a special structure called polar filament 3. The extrusion of polar filament injects its content or sporoplasm into one of the body cells 4. Inside the cell, the parasites start multiplying by binary fission and new spores will be formed each with their polar filament ready to infect other cells - release of new spores can either be into the body or into the stool (ingestion or inhalation of spores → extrusion of polar filament → injection of sporoplasm → replication (binary fission) → release of new spores)
46
briefly explain the notable Microsporidia
1. Enterocytozoon bieneusi - Causes enteritis (intestinal infection) - Common in AIDS patients - Leads to diarrhea and malabsorption 2. Encephalitozoon spp. - Causes systemic infections (spreads to many organs) - Reported in transplant patients or through blood (donor-derived infections) 3. Pleistophora spp. - Infects muscle and other tissues - Seen in immunocompromised people 4. Microsporidium spp. and Nosema spp. - Can cause eye infections (especially corneal infections) - May also cause rare but serious systemic infections - Can be fatal in immunocompromised infants
47
morphology of Toxoplasma gondii
1. Tachyzoites: rapidly divide and spread in tissues, causing initial damage. 2. Bradyzoites: form cysts in brain, muscles, eyes — may remain dormant for years ● Oocyst: 10-15 um x 8-12 um - similar to l. belli ● Tachyzoite: Crescent-shaped, 3-7 um ● Bradyzoite cyst: 12-100 um, clustered bradyzoite *All 3 forms are infectious to humans aside from oocyst
48
life cycle of Toxoplasma gondii
1. Starts during oocysts are passed out in feces of cats 2. The oocysts are ingested by rodents and follow life cycle to form tissue cysts 3. The definitive hosts which are the cats ingest tissue cysts present in the intermediate host 4. Oocysts ingested by other intermediate hosts such as sheep and pigs will follow life cycle and become tissue oocysts 5. Humans can acquire the infection and when they ingest uncooked meat containing tissue cyst or ingestion of oocyst via drinking contaminated water or eating unwashed fruits and vegetables 6. Humans can also acquire the infection via blood transfusion, organ transplant, or congenital infection
49
definitive host of Toxoplasma gondii
human
50
life cycle and transmission of Toxoplasma gondii
transes
51
how can humans get accidently infected by Toxoplasma gondii
- Cleaning cat litter boxes - Playing in sandboxes or soil contaminated with cat poop - Touching your mouth with unwashed hands after contact *Important: Fresh cat poop does not contain infectious oocysts. Oocysts need 1–5 days in the environment to become mature and infectious.
52
in Toxoplasma gondii, what happens after infections spread in the body
parasite becomes a tissue cyst. - resting (dormant) form that stays hidden in the body. - tissues found in: Brain Eyes Skeletal muscles Other organs *cysts can stay in the body for years, especially during the chronic stage of infection.
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Toxoplasma gondii - definitive host - infective host - MOT
Definitive host = Cats - both sexual and asexual reproduction in cats’ intestines. (Tissue cysts release zoites Asexual reproduction (schizogony) makes merozoites Some merozoites → tissue cysts Others → male (microgamete) and female (macrogamete) After fertilization → oocyst Oocysts are shed in feces and become infectious after sporulation in the environment.) - cats are the only animals that can shed oocysts in feces. Intermediate hosts = Humans, pigs, sheep, etc. - in these hosts, only asexual reproduction happens. - the parasite forms tissue cysts in organs like the brain, eyes, and muscles. (Humans ingest oocysts (from cat feces) or bradyzoites (from meat). In the intestines, they turn into tachyzoites (fast-replicating form). Tachyzoites spread through the blood to the: - Brain - Eyes - Muscles They form tissue cysts (bradyzoites), which stay dormant. If the person becomes immunocompromised, the cysts may reactivate and cause disease.) MOT: 1. Eating undercooked meat (especially pork or lamb) that contains tissue cysts. 2. Swallowing oocysts from contaminated: - Water - Food - Soil - Unwashed hands 3. Congenital transmission (mother to fetus): - Happens if the mother gets infected for the first time during pregnancy. - IgG antibodies can cross the placenta. 4. Blood transfusion or organ transplant from infected donors: - Involves tachyzoites (the active form). - Rare.
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this parasite is considered as fungus
Pneumocystis jiroveci
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morphology of Pneumocystis jiroveci
● Trophozoite: 2-4 um, ovoid - commonly seen form ● Cyst: 4-12 um, 4-8 intracystic bodies
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life cycle of Pneumocystis jiroveci
● Presumed: alveolar colonization → trophozoites multiply → cyst formation ● At-risk: immunocompromised patients (e.g., HIV/AIDS) ● Transmission: likely airborne
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Pneumocystis jiroveci MOT
likely airborne
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2 sporocysts, 4 sporozoites each, acid-fast, eosinophilia
I. belli
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Small acid-fast oocysts, no sporocyst
Cryptosporidium
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Slightly larger oocyst than Crypto, autofluorescence
Cyclospora
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Spores inject polar filaments
Microsporidia
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Fungus-like, causes deadly pneumonia in AIDS
Pneumocystis