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Week 6 Micro TA review > non-worm parasites > Flashcards

non-worm parasites Flashcards

1
Q

Entamoeba histolytica morphology

A

Cyst and Trophozoite forms

Often see RBCs in trophozoite.

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2
Q

Entamoeba histolytica pathogenesis

A

Ingestion of cysts in food –> invasive colitis –> common GI colonization –> may spread beyond GI tract

E. Histolytica has a two stage life cycle

  • The cyst form is infective (1-4 nuclei)
  • the trophozoite is the reproductive/ invasive form (1 nuclei)
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3
Q

Entamoeba histolytica clinical presentation

A

Fecal oral transmission.

*Most infections result in asymptomatic carrier state, shedding cysts in stool*

-Hemorrhagic amoebic colitis – Bloody amoebic dysentery (“amoebic dysENTary” (blood, pus, and mucous in stool))

-Abcesses: –> Liver abscess (“anchovy paste” abcesses), Pulmonary, Brain

Aspiration of abscess may not always reveal trophozoites

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4
Q

Entamoeba histolytica diagnosis

A

Cysts/trophozoites in stool, abscess aspiration (may/may not reveal cysts), serology

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5
Q

Entamoeba histolytica epidemiology

A

50 million infections/year; 100,000 deaths. Humans = reservoir

Fecal oral transmission, Developing countries

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6
Q

Entamoeba histolytica treatment

A

Metronidazole (tx of choice) and Tinidazole, Iodoquinol (to kill cysts)

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7
Q

Free living amoeba species

A

Acanthamoeba, Balamuthia, Naegleria

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8
Q

Free living amoeba pathogenesis

A

Direct inoculation through the cribiform plate into the nares

Not responsive to therapy –> High Mortality; Usually kills Host

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9
Q

Free living amoeba clinical

A

Meningoencephalitis, skin lesions, keratitis

Acanthamoeba: can cause a severe Keratitis associated with contact lens uses

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10
Q

Free living amoeba diagnosis

A

Visualization of trophozoite in tissue biopsy or in CSF

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11
Q

Free living amoeba epidemiology

A

Fresh water sources (divers esp.)

No P2P transmission, Contact lens solution (keratitis), Neti-Pots

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12
Q

Free living amoeba treatment

A

Palliative;

various experimental treatments with no good results

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13
Q

Giardia Iambia morphology

A

Heart shaped trophozoite, flagellated.

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14
Q

Giardia Iambia pathogenesis

A

Ingestion of cysts in food or water

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15
Q

Giardia Iambia Clinical Presentation

A
  • Fatty diarrhea (steatorrhea) (blood and fever are rare) – often foul smelling stool due to fat malabsorption
  • Bloating, cramps, flatulence-Sulfur Burps
  • Can cause CHRONIC diarrhea (as well as intermittent)

–> non-invasive, inhibits sucrase and maltase, loss of brush border –> malabsorption

-Asymptomatic carrier state possible

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16
Q

Giardia Iambia Diagnosis

A

Cysts (4 nuclei)/Trophozoite (2 nuclei, 4 pairs of flagella) in stool

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17
Q

Giardia Iambia Epidemiology

A

Campers, Fecal-oral

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18
Q

Giardia Iambia Treatment

A

Metronidazole or Tinidazole

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19
Q

Trichomonas Vaginalis Morphology

A

Pyriform (PEAR-shaped) amoeboid shape (divides by fission), no cyst form

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20
Q

Trichomonas Vaginalis pathogenesis

A

Sexual transmission

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21
Q

Trichomonas Vaginalis clinical

A

Vaginitis, Cervicitis –> discharge (frothy yellow/green), pruritis, irritation

  • many are asymptomatic
  • associated with low birth weight and premature rupture of membrane

Men are mostly asymptomatic

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22
Q

Trichomonas Vaginalis diagnosis

A

Traditionally, Wet mount of vaginal discharge (highly motile); now do PCR

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23
Q

Trichomonas Vaginalis epidemiology

A

Associated with other STDs

High prevalence in those with multiple partners

24
Q

Trichomonas Vaginalis Treatment

A

Metronidazole or Tinidazole, must treat partner(s) too!!

25
Intestinal-Spore forming Protozoa species
**Cryptosporidium**, Microsporidium, Isospora, Cyclospora
26
Intestinal-Spore forming Protozoa pathogenesis
Invades enterocytes, damaging epithelium of brush border
27
Intestinal-Spore forming Protozoa clinical presentation
- Mild **Watery** diarrhea in normal host - **Very SEVERE chronic Watery diarrhea** in AIDS/immunosuppressed (wasting syndrome - malnutrition)
28
Intestinal-Spore forming Protozoa diagnosis
**Acid fast** or DFA staining of oocysts in stool
29
Intestinal-Spore forming Protozoa epidemiology
**Water Parks**, Day care centers, Family settings, and Hospitals Outbreaks commonly associated with **public water supply and pools (protozoa are resistant to Chlorine)** AIDS patients, Immunocompromised
30
Intestinal-Spore forming Protozoa treatment
**Immune reconstitution and rehydration therapy** also: **TMP-SMX** can be used for Isospora and Cyclospora **Nitazoxanide** for Crypto (better to restore immunocompetence)
31
Intestinal-Spore forming Protozoa ## Footnote Cryptosporidium, Microsporidium, Isospora, Cyclospora differentiating factors
Cryptosporidium- AIDS Microsporidium: Obligate intracellular parasite (no mitochondria), can cause systemic infections in AIDS patients Isospora: endemic in Africa, S.America, and Asia among AIDS patients Cyclospora: Direct fecal oral transmission cannot occur, requires incubation outside of patients
32
Leishmania morphology
Non-flagellated **protozoan within macrophages**; kinetoplast (also exists in flagellated form)
33
Leishmania Pathogenesis
**Sandfly injects promastigotes (flagellated form) --\>** phagocytosed by macrophages as amastigote (non-flagellated form), spread through **reticuloendothelial system (RES)**
34
Leishmania Clinical
Large spectrum of clinical presentations that depends on species: * **L. mexicana, L. tropica- cutaneous**, painless ulcerated lesion at site of bite * **L. braziliensis- mucocutaneous**, erosive destruction of nose, oropharynx, larynx * **L. donovani- visceral (Dum dum fever, Kala Azar)**, incubates 3-8mo after ulcer, systemic symptoms (fever, **hepatosplenomegaly, dark grayish skin)** **\*Visceral form is the worst**
35
Leishmania diagnosis
**Visualize amastigotes on biopsy**, skin scrapings, culture, PCR, serology
36
Leishmania epidemiology
Reservoir = rats/rodents, canines. Found in Central and South America, Africa, Middle East, Southern Europe and Asia
37
Leishmania treatment
**Pentavalent antimonials, amphotericin B** --\> many toxic side effects **Miltefisone** (approved by FDA March 2014, but not widely available in US)
38
Trypanosoma cruzi morphology
Flagellated protozoa; kinetoplast
39
Trypanosoma cruzi pathogenesis
**Reduviid (kissing) bug leaves feces** (containing metacyclic trypomastigotes) on skin while taking blood meal, feces infect meal site or are brushed into mucous membrane = elicit **intense immune response** Can be self limiting or lead to **chronic infection --\> Chagas disease**
40
Trypanosoma cruzi clinical
Biphasic Acute- **Romana’s sign (unilateral edema of the eye)**, inflammation of various tissue, including heart and muscle, usually self-limiting Chronic- **megasyndromes = #1 cardiomegaly**, megaesophagus, megacolon
41
Trypanosoma cruzi diagnosis
Serology and PCR, Blood smear, xenodiagnosis and grown in culture.
42
Trypanosoma cruzi geography
Epidemiology: South America
43
Trypanosoma Cruzi vector
Reduviid (kissing) bug
44
Trypanosoma brucei morphology
Flagellated protozoa; kinetoplast;
45
Trypanosoma brucei pathogenesis
Undergo antigenic variation --\> cause waves of parasitemia Transmitted by the **Tsetse fly** Stage 1- proliferation at site of inoculation **(Winterbottom’s sign)**; spread to lymphatics and bloodstream- waves of parasitemia for months Stage 2- CNS invasion (months to years later)
46
Trypanosoma brucei clinical presentation
Sleeping Sickness * Stage 1- symptoms associated with **waves of parasitemia** = fever, lethargy, nausea, headache, facial edema. (\*Rhodesiense = more acute course- myocarditis, CHF, pulmonary edema, death often before CNS invasion) * Stage 2- headache, personality changes, **daytime somnolence**, seizures, tremors, ataxia, coma, death
47
Trypanosoma brucei diagnosis
Blood smear, visualize in CSF
48
Trypanosoma brucei epidemiology/geography
Gambiense- **chronic form**, Central and West Africa Rhodesiense- **acute form**, East Africa
49
Trypanosoma brucei treatment
Early disease: Rhodesiense - suramin, Gambiense - pentamidine, Late disease for both: melarsoprol
50
Toxoplasma Gondii morphology
Unicellular protozoa
51
Toxoplasma Gondii pathogenesis
**Cats = definitive host**; rats, pigs, sheep = intermediate hosts. **Ingested fecal oocytes** (infective stage) or tissue cysts transform into tachyzoites, localize in neural or muscle tissue, then develop into tissue cyst bradyzoites \*Tachyzoites can infect a fetus through the bloodstream
52
Toxoplasma Gondii Clinical presentation
**•Asymptomatic dormant infection = most common** •Reactivation in individuals with cellular immune deficiency: **encephalitis**, pneumonia --\> **“ring enhancing lesions on Brain CT”** •Acute infection in normal hosts: **mononucleosis-type illness**, lymphadenopathy •**Congenital infection (TORCHES disease):** (due to primary infection in a pregnant woman) usually subclinical, but may cause mental retardation, hydrocephalus, blindness --\> **classic triad: chorioretinitis, hydrocephalus, intracranial calcifications** \*Chorioretinitis: may complicate congenital or acquired infection
53
Toxoplasma Gondii Diagnosis
Serology, culture, PCR
54
Toxoplasma Gondii Epidemiology
**Immunocompromised, HIV patients, pregnant women**, normal hosts, cat feces
55
Toxoplasma Gondii Treatment
Pyrimethamine with Sulfadiazine (TMP-SMZ prophylaxis in immunocompromised)

Week 6 Micro TA review (3 decks)

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