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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
Q

Intestinal-Spore forming Protozoa species

A

Cryptosporidium, Microsporidium, Isospora, Cyclospora

26
Q

Intestinal-Spore forming Protozoa pathogenesis

A

Invades enterocytes, damaging epithelium of brush border

27
Q

Intestinal-Spore forming Protozoa clinical presentation

A
  • Mild Watery diarrhea in normal host
  • Very SEVERE chronic Watery diarrhea in AIDS/immunosuppressed (wasting syndrome - malnutrition)
28
Q

Intestinal-Spore forming Protozoa diagnosis

A

Acid fast or DFA staining of oocysts in stool

29
Q

Intestinal-Spore forming Protozoa epidemiology

A

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
Q

Intestinal-Spore forming Protozoa treatment

A

Immune reconstitution and rehydration therapy

also: TMP-SMX can be used for Isospora and Cyclospora

Nitazoxanide for Crypto (better to restore immunocompetence)

31
Q

Intestinal-Spore forming Protozoa

Cryptosporidium, Microsporidium, Isospora, Cyclospora differentiating factors

A

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
Q

Leishmania morphology

A

Non-flagellated protozoan within macrophages; kinetoplast

(also exists in flagellated form)

33
Q

Leishmania Pathogenesis

A

Sandfly injects promastigotes (flagellated form) –> phagocytosed by macrophages as amastigote (non-flagellated form), spread through reticuloendothelial system (RES)

34
Q

Leishmania Clinical

A

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
Q

Leishmania diagnosis

A

Visualize amastigotes on biopsy, skin scrapings, culture, PCR, serology

36
Q

Leishmania epidemiology

A

Reservoir = rats/rodents, canines.

Found in Central and South America, Africa, Middle East, Southern Europe and Asia

37
Q

Leishmania treatment

A

Pentavalent antimonials, amphotericin B –> many toxic side effects

Miltefisone (approved by FDA March 2014, but not widely available in US)

38
Q

Trypanosoma cruzi morphology

A

Flagellated protozoa; kinetoplast

39
Q

Trypanosoma cruzi pathogenesis

A

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
Q

Trypanosoma cruzi clinical

A

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
Q

Trypanosoma cruzi diagnosis

A

Serology and PCR, Blood smear, xenodiagnosis and grown in culture.

42
Q

Trypanosoma cruzi geography

A

Epidemiology: South America

43
Q

Trypanosoma Cruzi vector

A

Reduviid (kissing) bug

44
Q

Trypanosoma brucei morphology

A

Flagellated protozoa; kinetoplast;

45
Q

Trypanosoma brucei pathogenesis

A

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
Q

Trypanosoma brucei clinical presentation

A

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
Q

Trypanosoma brucei diagnosis

A

Blood smear, visualize in CSF

48
Q

Trypanosoma brucei epidemiology/geography

A

Gambiense- chronic form, Central and West Africa

Rhodesiense- acute form, East Africa

49
Q

Trypanosoma brucei treatment

A

Early disease: Rhodesiense - suramin, Gambiense - pentamidine,

Late disease for both: melarsoprol

50
Q

Toxoplasma Gondii morphology

A

Unicellular protozoa

51
Q

Toxoplasma Gondii pathogenesis

A

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
Q

Toxoplasma Gondii Clinical presentation

A

•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
Q

Toxoplasma Gondii Diagnosis

A

Serology, culture, PCR

54
Q

Toxoplasma Gondii Epidemiology

A

Immunocompromised, HIV patients, pregnant women, normal hosts, cat feces

55
Q

Toxoplasma Gondii Treatment

A

Pyrimethamine with Sulfadiazine

(TMP-SMZ prophylaxis in immunocompromised)

Week 6 Micro TA review (3 decks)

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