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Clinical Microbiology > Extraintestinal protozoa > Flashcards

Extraintestinal protozoa Flashcards

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Biology 101 flashcards
1
Q

Prevalence of malaria (Plasmodium species)

A

In 2016, 216 million cases of malaria occurred worldwide. 445,000 people died, mostly children in the African Region. There are 1,700 cases of malaria in the United States/year, mainly travelers and immigrants

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2
Q

Plasmodium species (5)

A
  1. Plasmodium falciparum – most common, most deadly (cerebral)
  2. Plasmodium vivax – 2nd most problematic (splenic rupture)
  3. Plasmodium ovale
  4. Plasmodium malariae
  5. Plasmodium knowlesi – most commonly in macaques, rare
    human infection
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3
Q

Malaria symptoms

A

Primary pathology is the result of RBC hemolysis. Symptoms: fever, sweats, chills, headache, fatigue, anemia, and splenomegaly. Paroxysm-intensification of the symptoms

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4
Q

Sporogony

A

The process of spore formation in parasitic sporozoans, which occurs in the intestinal tract of the mosquito. This is the mosquito portion of the plasmodium life cycle

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5
Q

Schizogony

A

Asexual phase of plasmodium, occurring in the human host

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6
Q

Infective stage of plasmodium

A

An infected mosquito inoculates the host with sporozoites when it takes a blood meal, and sporozoites infect hepatic cells (exoerythrocyte cycle). They mature into schizonts, which rupture and release merozoites. Merozoite invades RBC

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7
Q

Recrudescence

A

Treatment followed by parasite reappearance

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8
Q

Plasmodium falciparum

A

Most severe form; causes cerebral malaria, blocks capillaries, DIC, blackwater fever. RBCs lyse during malaria infection, causing the urine to turn black due to hemoglobin, which is what “blackwater fever” refers to. Infects any stage of RBC. 36-48 hour periodicity. Maurer’s dots are an identifying characteristic of P. falciparum. The number of merozoites in the shizont is 8-36

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9
Q

Maurer’s dots

A

A membrane-like vacuole or structure within the red blood cell. With P. falciporum, we see multiple rings within the RBC. The rings look purple within the RBCs during microscopy. The presence of the rings is an identifying characteristic of P. falciparum

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10
Q

Gametocyte

A

One and a half times the diameter of the erythrocyte, in length, seen with RBCs under a microscope. This is diagnostic for plasmodium falciparum

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11
Q

Plasmodium vivax

A

Only infects reticulocytes = low parasite burden. 48 hr periodicity. Trophozoites – amoeboid, Shuffner’s dots. Number of merozoites in schizonts 12-24

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12
Q

Plasmodium ovale

A

First identified 1922, similar to P. vivax. Only infected reticulocytes – low burden. 48 hour periodicity. Trophozoites with single chromatin dot
– Shuffner’s dots, fimbriation
* Number of merozoites in shizonts 4-12
– Smaller than P.vivax
– Elongated to oval shaped

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13
Q

Plasmodium malariae

A

Recrudescence for many years-symptoms from RBC forms. Infects mature RBC. 72 hour periodicity. Trophozoite is thicker than P. falciparum. Band formation during maturation. Zieman’s stippling. Number of merozoites in schizonts 6-12. Maybe arranged in rosette

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14
Q

2 hosts of plasmodium life cycle

A
  1. Intermediate- human
  2. Definitive- Anopheles mosquito
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15
Q

Plasmodium life cycle (9 steps)

A
  1. Female mosquito blood meal –
    sporozoites= infective agent for
    humans
  2. Sporozoites infect hepatic cells = schizonts
  3. Schizonts to merogony to form merozoites, to circulation ending the exo-erythrocytic cycle
  4. Plasmodium vivax and ovale species- dormant stage in the liver, relapses infection in weeks to years
  5. Erythrocytic schizogony (asexual multiplication within erythrocytes).
  6. Merozoites infect red blood cells- responsible for disease
  7. Mature to trophozoites may undergo schizogony to form schizonts, then merogony to release merozoites, infect red
    blood cells & continue the erythrocytic cycle.
  8. Trophozoites can mature into gametocytes
  9. The male gamete makes microgametocytes, and
    the female gamete makes macrogametocytes. Ingested by mosquito-infectious agent
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16
Q

Diagnosis of Plasmodium (5)

A
  1. Symptoms
  2. History
  3. Blood smear—finger stick or
    anticoagulant
  4. Giemsa or Wright’s stains
  5. Thick and thin smears
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17
Q

Babesia species

A

Causes Babesiosis, human infections are caused by B. microti, B. divergens, B. duncani, and a 4th un-named strain, but there are over 100 species. It can be confused with P. falciparum.

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18
Q

Babesia distribution

A

Little known in malaria endemic
countries. In Europe, B. divergens is found in splenectomized patients. B. microti is found in most (Northeast and
Midwest), nonsplenectomized. Babesia duncani - found in Washington and California. MO-1 isolated from patients in
Missouri

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19
Q

Babesia symptoms

A

Can be asymptomatic (serology positive). Symptoms include fever, chills, sweating, myalgias, fatigue, hepatosplenomegaly, and hemolytic anemia. Incubation period is 1 to 4 weeks or greater. Disease can be severe in immunosuppressed, splenectomized, elderly. B. divergens has more severe symptoms (frequently fatal if not appropriately treated). In B. microti, clinical recovery usually occurs.

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20
Q

Babesia diagnosis

A

Smear – merozoite stage = maltese cross = pathognomonic
Diagnosis - serology, thick and thin blood smears, PCR

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21
Q

Trypanosoma brucei

A

Hemoflagellate, causes African sleeping sickness. Trypanosoma brucei subspecies rhodesiense (acute, rapid onset),
subspecies gambiense (chronic infection). Transmitted by the Tsetse fly.

22
Q

Trypomastigote

A

15 to 30um length
* Elongated body with posterior
flagellum
* central nucleus with
POSTERIOR kinetoplast
* Buffy coat smear best method
for diagnosis

23
Q

Babesia life cycle

A
24
Q

Trypanosoma life cycle

A
25
Q

African sleeping sickness symptoms (4)

A
  1. Gambian – neurologic deterioration
  2. Rhodesian - Rapid onset, leading to possible death.
  3. Recurring fever, lymphadenopathy, cervical lymph nodes involvement producing lesion = Winterbottom’s sign. – suggest brain involvement
  4. Sleeping sickness stage – invasion of CNS – behavior changes, apathy, fatigue,
    confusion, meningoencephalopathy, death
26
Q

Trypanosoma cruzi

A

South American trypanosomiasis – Chaga’s Disease. Caused by the Triatomid (reduviid) bug or “Kissing Bug”- they are nocturnal and feed on sleeping victims. trypomastigotes similar to
other species (nucleus & posterior kinetoplast), but found in form of a “C”. Reservoirs include dogs, rodents,
cats, pigs, opossums and raccoons- not found in other species. Can not eradicate

27
Q

Trypanosoma cruzi symptoms (5)

A
  1. Scratch at bite site, introduces feces into skin
  2. Acute infection – asymptomatic, unilateral periorbital swelling if feces rubbed into eye
  3. Chronic infection - amastigotes replicate in myocytes resulting in cardiomyopathy,
    congestive heart failure.
  4. Mega-syndromes – esophagus, colon
  5. End stage disease – heart transplant, surgery for organ removal (colon)
28
Q

Leishmania species (2)

A
  1. Primary Cutaneous Leishmaniasis- Leishmania donovani complex
    – donovani, infantum chagasi
  2. Cutaneous tropical sores – Old world (tropica complex)
    & New world (braziliensis & Mexicana complex)
    * Leishmania tropica complex
    * Leishmania mexicana complex
29
Q

Leishmania infective stage

A

Introduced by sandfly. Promastigote- regurgitation of parasite into the subcutaneous tissue as fly takes a blood meal. Enters into macrophage which subsequently ruptures releasing
parasite to disseminate and infect. Amastigote taken up by blood meal will transform in midgut of fly

30
Q

Leishmania symptoms

A

Visceral Kala-Azar - disseminated disease. Mild, self-limiting to sudden onset. Spiking fevers, anorexia, malaise. Chronic – abdominal pain, low-grade fever, hepato & splenomegaly,
anemia

31
Q

Primary Cutaneous Leishmaniasis-old world symptoms

A

Rash at site of bite progressing
over months to ulceration- raised, red margin, crusting, benign and self-healing. May cause deep-subcut infection. Possible disseminated disease

32
Q

Primary Cutaneous Leishmaniasis- new world symptoms

A

Aggressive, cutaneous ulcers with mucous membrane spread (oral, nasal, pharyngeal) = espundia

33
Q

Leishmania life cycle

A
34
Q

Leishmania diagnosis (4)

A
  1. Blood smear with:
    – Amastigotes within
    macrophage cells. Oval intracellular, 4-8um
  2. ELISA, NAAT
  3. IHC – parasites stain
    with H & E, Wright’s
    stain, NOT GMS
  4. Amastigotes have bar-like
    kinetoplast adjacent to
    nucleus. Helps to differentiate from Histoplasma capsulatum
35
Q

Trypanosoma diagnosis (4)

A
  1. Blood smear– Trypomastigote, Amastigotes in somatic
    cells (myocytes)
  2. T. cruzi – circular
    trypomastigotes on blood
    smears, letter “C”
  3. Detailed history to
    differentiate from other
    infections.
  4. ELISA, NAAT, serology
36
Q

Toxoplasma gondii

A

Coccidia, worldwide distribution- most common human infections. Has a high prevalence. In France, transmitted by eating raw or undercooked meat. In Central America, the frequency of stray cats and climate favoring survival of oocysts and soil exposure. United States 22.5%,-seroprevalence among
women of childbearing age
(15 to 44 years) of 15%

37
Q

Toxoplasma gondii life cycle

A
38
Q

Acquired Toxoplasma gondii symptoms

A

Asymptomatic infection, benign and self-limited. 10% to 20% of patients have cervical lymphadenopathy and/or a flu-like illness. The clinical course is; symptoms usually resolve within a few weeks to months. In rare cases, ocular infection with visual loss can occur. Immunocompromised patients may experience CNS disease
– retinochoroiditis, pneumonitis, or other systemic disease,
AIDS=toxoplasmic encephalitis

39
Q

Congenital toxoplasmosis

A

An acute primary infection acquired by the mother during pregnancy. The incidence and severity of congenital toxoplasmosis vary with the
trimester during which infection was acquired. Immediate maternal treatment reduces the incidence of congenital
infection and reduce sequelae in the infant. Subclinical infection at birth will subsequently develop signs or symptoms of congenital toxoplasmosis.

40
Q

Toxoplasma gondii diagnosis (3)

A
  1. Observation of parasites in patient specimens - lymph node
    biopsy.
  2. Detection of parasite genetic material by PCR, especially in
    detecting congenital infections in utero.
  3. Serologic testing is the routine method of diagnosis
41
Q

Naegleria fowleri

A

Worldwide distribution, free-living amoeba. Found in soil and freshwater- ponds, streams, municipal tap- water, spas, air-humidifiers. Acute & lethal CNS disease– Primary amebic
meningoencephalitis (PAM). No cysts stage in human

42
Q

Acanthamoeba

A

Worldwide distribution, free-living amoeba. Found in soil and freshwater- ponds, streams, municipal tap- water, spas, air-humidifiers. Opportunistic pathogen, may cause corneal infections. If immunocompromised- granulomatous amebic
encephalitis (GAE)

43
Q

Acanthamoeba trophozoite

A

Infective stage – eye, nasal tissue, respiratory tract, broken skin. They are 10-25 μm, large prominent karyosome. Sluggish motility at 25°C, better at 37°C

44
Q

Acanthamoeba cysts

A

Have 2 walls- a wrinkled fibrous outer wall (exocyst) and an inner wall (endocyst) that may be hexagonal, spherical, star-shaped or polygonal. Cysts may be found in the brain, eyes, skin, lungs and other organs.

45
Q

Naegleria fowleri trophozoites

A

Infective stage – nasal tissue to brain. They are 8 to 15 um, large prominent karyosome. 1+ pseudopodia, active motility at 25 or 37°C. Ameboflagellate, only the former of which is found in humans. Trophozoites may get over 40 μm

46
Q

Naegleria fowleri and Acanthamoeba diagnosis (4)

A
  1. Examination of CSF
  2. Giemsa-stained smear
  3. Stained smears - brain tissue, skin, cornea biopsy
    or corneal scrapings trophozoites and cysts (Acanthamoeba only:
    HIGHLY resistant to chlorine)
  4. Real-Time PCR – CDC developed assay
47
Q

Trichomonas vaginalis

A

Tissue protozoa, worldwide prevalence among persons
with multiple sexual partners
or other venereal diseases. Incubation period is 5 to 28 days

48
Q

Trichomonas vaginalis symptoms- males

A

Asymptomatic infection most
common- occasionally, urethritis,
epididymitis, and prostatitis

49
Q

Trichomonas vaginalis symptoms- females

A

Symptomatic infection- vaginitis, purulent discharge, vulvar and cervical lesions, abdominal pain, dysuria and dyspareunia

50
Q

Trichomonas vaginalis life cycle

A
51
Q

Trichomonas vaginalis trophozoites

A

Pear-shaped (pyriform), 7-30μm long. Has five flagella: four anteriorly, one posteriorly along the outer membrane of the undulating membrane. Large nucleus at the wider, anterior end, chromatin granules, small
karyosome. Cytoplasm - granules, often not seen in Giemsa-stained specimens.

52
Q

Trichomonas vaginalis diagnosis

A

Wet prep of vaginal fluids - parasite motility, DFA, molecular
methods

Clinical Microbiology (19 decks)

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