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House Microbiology > Toxoplasmosis: Amoebic Meningitis > Flashcards

Toxoplasmosis: Amoebic Meningitis Flashcards

1
Q

Aetiology:

Toxoplasma gondii - A _______ _______

usually (asymptomatic or symptomatic?) infection in humans

A

tissue sporozoan

asymptomatic

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2
Q

Toxoplasmosis

Significant disease in _____________________,__________ patients and occasionally in ____________ individuals.

A

congenitally infected infants, immunodeficient

immunocompetent

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3
Q

Epidemiology of toxoplasmosis

T. gondii infection is a worldwide ______.

The organism infects ______,_______ and _________ animals, including ______.

A

zoonosis

herbivorous, omnivorous, and carnivorous

birds

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4
Q

Epidemiology of Toxoplasmosis

Mode of transmission:

Infection in humans most commonly occurs through
•the ________ of _______________ that contains _______

•the ________ of _________ contaminated with _______

•____________(________) transmission from a mother who acquired her infection during gestation

A

ingestion of raw or undercooked meat

tissue cysts

ingestion of water or food ; oocysts

transplacental (congenital)

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5
Q

Epidemiology of Toxoplasmosis

Less common transmission are:
– by _______ of _____________
–____________ of ___________
–___________ with contaminated needles
-exposing _________ or _____ surfaces to the parasite

A

transplantation of an infected organ

transfusion of contaminated blood cells.

Needle stick injury

open lesions or mucosal

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6
Q

Toxoplasmosis

The normal final hosts are strictly _____ and members of the family ______.

They play a significant role as powerful ______ of the infection in nature because the ______-producing (sexual or asexual?) stage of Toxoplasma develops in their ________.

A

cats; Felidae

amplifiers

oocyst; sexual

intestine

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7
Q

Life cycle of Toxoplasmosis

Organisms (either ________ from ________ or ________ from ________ cysts) invade the ________ cells of the ____________________, where they form ________ or ________________

After sexual fusion of the gametes, ________ develop, exit from the ________ into the ________ of the cat, and pass out via the ________.

In about __________, the environmentally (sensitive or resistant?) ______ are infective

When _______ are ingested by the cat, the parasites _______________. If oocysts are ingested by intermediate hosts such as certain birds, rodents, or mammals, including _______, the parasites can ____________ but reproduce only _________.

A

sporozoites ; oocysts

bradyzoites ; tissue

mucosal cells ;cat’s small intestine

schizonts ; gametocytes.

oocysts ;host cell

gut lumen ; the feces

48 hours; resistant ; oocysts

Oocysts; repeat their asexual and sexual cycle

humans; establish an infection

asexually.

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8
Q

Only members of the ____ family shed oocysts

A

cat

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9
Q

Life cycle of Toxoplasmosis

The oocyst opens in the human’s or animal’s ________ and releases the _______, which pass through the ______, circulate in the body, and invade various cells, especially _________, where they form ____________.

________ multiply, break out, and spread the infection to ________ and other organs.

A

duodenum ; sporozoites

gut wall; macrophages; trophozoites

Trophozoites ; lymph nodes

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10
Q

Trophozoites of toxoplasmosis

_________ are the actively proliferating trophozoites, which are observed during the (acute or chronic?) stage of infection

A

Tachyzoites

Acute

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11
Q

Life cycle of toxoplasmosis

The trophozites (rapidly multiplying _________ cells called ________ ) initiate the (acute or chronic?) stage of disease.

Subsequently, they penetrate _____ cells, especially of the _____ and _______, where they multiply (slowly or rapidly?) (as ______) to form ________ ——- cysts, initiating the (acute or chronic?) stage of disease.

The tissue cysts are infective when _________ (resulting in the intestinal ______ stage and _______ production); when they are eaten by other animals, more _________ are produced (_______).

A

crescentic ;tachyzoites

acute ; nerve

brain and eye

slowly ;bradyzoites

quiescent tissue ; chronic

ingested by cats ; sexual ; oocyst production

tissue cysts ;asexually

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12
Q

Tissue cysts of toxoplasmosis are found most commonly in the _____ and in __________________________ muscle but can occur in ______ organ

A

brain

skeletal and cardiac muscle

any organ

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13
Q

Pathogenesis of Toxoplasmosis 1

The tachyzoite directly ________ and has a predilection for ________ cells and those of the _______________ system.

Humans are relatively (resistant or sensitive?) , but a (low or high?) -grade _______ infection resembling _____________ may occur.

When a _______ ruptures, releasing numerous _______, a local _______ may cause _______, _______ of blood vessels, and cell death near the ___________.

A

destroys cells ;parenchymal cells

reticuloendothelial system ; resistant

low; lymph node

infectious mononucleosis

tissue cyst ; bradyzoites

hypersensitivity reaction ; inflammation

blockage; damaged cyst.

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14
Q

Pathogenesis Of toxoplasmosis 2

Presence of ________ is the hallmark of active infection

They reside and multiply within ______ in their host’s cells, can infect virtually all __________ and _________ cell types, and multiply approximately every ______ to form __________.

Continuous multiplication leads to cell disruption and release of organisms that go on to invade nearby cells or are transported to other areas of the body by _______ and _______.

A

Tachyzoites; vacuoles

phagocytic and nonphagocytic cell types

6 to 8 hours ; rosettes.

blood and lymph.

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15
Q

Tachyzoites appear to (actively or passively?) and (slowly or rapidly?) migrate across epithelial cells and may traffic to distant sites while ____cellular.

A

Actively ; rapidly

extra

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16
Q

Pathogenesis Of Toxoplasmosis 3

T. gondii multiplies ______cellularly at the site of invasion (the _________ is the major route for and the initial site of infection in nature)

________ released from tissue cysts or ______ released from oocysts penetrate, differentiate to _______, rapidly multiply within __________ cells.

Organisms may spread first to the ______ lymph nodes and then to distant organs by invasion of ________ and _______

T. gondii tachyzoites infect virtually all cell types, and cell invasion occurs as a/an (active or passive?) process.

A

intra; gastrointestinal tract

bradyzoites ;sporozoites

tachyzoites; intestinal epithelial

mesenteric ; lymphatics and blood.

active

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17
Q

Pathogenesis Of Toxoplasmosis 4

Survival of tachyzoite is due to the formation of a ____________ that lacks _______ necessary for ______________

Active invasion of ______ by ______ does not trigger ________ mechanisms.

With the appearance of humoral and cellular immunity, only those parasites protected by ________ habitat or within ________ shall survive.

An effective immune response significantly reduces the number of _________ in ____ tissues

after the initial acute stages, _________ are (often or rarely?) demonstrable histologically in tissues of infected immunocompetent humans.

A

parasitophorous vacuole

host proteins ; fusion with lysosomes

macrophages ; tachyzoites

oxidative killing; intracellular habitat

tissue cysts; tachyzoites ; all

tachyzoites ; rarely

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18
Q

Clinical Features of Humans toxoplasmosis:

(Asymptomatic or Symptomatic?) in most immunocompetent humans

Congenital infection develops only when ___________ mothers are infected during pregnancy, is usually of (little or great?) severity

postnatal toxoplasmosis is usually much (more or less?) severe

A

Asymptomatic

nonimmune; great

Less

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19
Q

Clinical Features of Humans toxoplasmosis:

fulminating fatal infections may develop in patients with ______, presumably by alteration of a _____ infection to an ______ one.

Varying degrees of disease may occur in immunosuppressed individuals, resulting in _________ or ________ , _______ ,___________ , or various other conditions.

A

AIDS; chronic ; acute

retinitis or chorioretinitis

encephalitis, pneumonitis

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20
Q

Clinical features of toxoplasmosis

The major features of (acute or chronic ?) acquired _______ toxoplasmosis are those of meningoencephalitis, myocarditis, pneumonitis, lymphadenitis, rash, and occasionally ______

In rare instances in immunocompromised hosts ,———— may be a prominent clinical manifestation resembling _________

Marked ______,__________,_________, and __________s occur in such patients.

A

acute; disseminated ; hepatitis

polymyositis ; autoimmune polymyositis.

Marked myalgias, muscle weakness and swelling, and fasciculations

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21
Q

Clinical features of toxoplasmosis

Muscle biopsy specimens show ______ with destruction of muscle fibers, and _________ of Toxoplasma gondii can be found in areas of muscle that are __________

A

interstitial myositis

pseudocysts

free of inflammatory reaction

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22
Q

Clinical features of Toxoplasmosis

Congenital infection leads to ________, _________, _________ calcifications, _______ disturbances, and _________ or ________

Major cause of _______ and other congenital defects.

Infection during the first trimester generally results in _________ or ________

Second- and third-trimester infections induce (more or less?) severe ______ damage

A

stillbirths, chorioretinitis

intracerebral; psychomotor

hydrocephaly or microcephaly

stillbirth or major CNS anomalies.

Less; neurologic

23
Q

Clinical features of Toxoplasmosis

Clinical manifestations of these infections may be delayed until _____, even beyond ______.

_______ problems or ______ difficulties may be caused by the long-delayed effects of late prenatal toxoplasmosis.

A

long after birth

childhood

Neurologic; learning

24
Q

Diagnosis of Toxoplasmosis
Direct detection of the organism is by
– ___________ assay,
– histopathology with immunoperoxidase staining,
-__________
–______ inoculation.

A

polymerase chain reaction (PCR)

tissue culture

mouse

25
Q

Diagnosis of Toxoplasmosis

Serologic assays

can help distinguish ______ from _______ infection and can identify patients at risk for __________
.

A

acute from chronic

reactivation

26
Q

Treatment of toxoplasmosis

Immunocompetent asymptomatic patients:____-

Immunocompromised patients: The therapy:

____________ plus ____________ plus ____________

OR

____________ plus ____________ plus either ____________ or ____________

OR

____________ ____________

A

no therapy

pyrimethamine plus sulfadiazine plus leucovorin

Pyrimethamine plus leucovorin plus either clindamycin or atovaquone

Trimethoprim sulfamethoxazole

27
Q

Treatment of Toxoplasmosis

______ are given only for clinically significant edema or mass effect, and _______ are given only after a seizure.

A

Corticosteroids

anticonvulsants

28
Q

Treatment of Toxoplasmosis

In pregnancy

less than 18 weeks: _______

Greater than 18weeks: ________+ ________

Congenital infection: ___________

A

spiramycin

pyremethamine + Folinic acid

pyremethamine

29
Q

Prevention of Toxoplasmosis

Avoidance of contact with _______ particularly for pregnant women with negative serologic tests.

pregnant women should avoid all contact with _____, particularly _____

daily changing of ______ and its safe disposal, since oocysts usually take ______ to become infective,

A

cat feces

cats; kittens

cat litter; 48 hours

30
Q

Prevention of Toxoplasmosis

Meat should be cooked very well to kill _______

Freezing meat at _____°C for ____ hours or heating to ___°C for _____ minutes will kill the organism.

A

tissue cysts

−20; 48hrs

50; 4-6mins

31
Q

Prevention of Toxoplasmosis

Kitchen cleanliness, ______ after touching raw meat .

Periodic serologic screening for ____________ antibodies to Toxoplasma is recommended.

Do not allow cats to eat __________ and ________

Wash hands thoroughly after outdoor activities

A

handwashing

immunoglobulin (Ig) G and IgM

wild rodents and birds

32
Q

prophylaxis of Toxoplasmosis

Immunocompromised patients: –_____-_____

–_______ + _______

A

TMP-SMX

dapsone; pyrimethamine

33
Q

Free-living amebae (FLAs) are (aerobic or anaerobic?) , __karyotic ____ that comprise several genera.

A

Aerobic

eukaryotic protists

34
Q

Free-living amebae (FLAs)

have ____ known insect vectors

Have ____ human carrier states of epidemiologic importance,

A

No

No

35
Q

Free-living amebae (FLAs)

(Little or Major?) relationship between poor sanitation and their transmission

Infection of humans with FLAs is an (frequent or infrequent?) but often _____ occurrence in both normal and immunocompromised individuals.

A

Little ; infrequent

fatal

36
Q

Free-living amebae (FLAs)

Central nervous system (CNS) invasion by __________,_________,__________ has been reported in hundreds of patients worldwide, with thousands of ____________________ cases described.

A

Naegleria fowleri, Acanthamoeba spp., and Balamuthia mandrillaris

Acanthamoeba keratitis

37
Q

Four distinct clinical syndromes are caused by the FLAs that infect humans

•_________________________(PAM)
•_____________________(GAE)
•_________________ disease
•______________ (AK).

A

primary amebic meningoencephalitis (PAM)

•granulomatous amebic encephalitis (GAE)

•disseminated granulomatous amebic disease

•Amebic keratitis (AK).

38
Q

Microbiology and Epidemiology of Free-living amoeba

The trophozoite stages of these organisms feed on _______ and ___________

Naegleria fowleri is widely distributed globally and has been isolated from _______, most commonly in (warm or cold?) environments.

A

bacteria and debris in the environment.

fresh water; warm

39
Q

Microbiology and Epidemiology of Free-living Amoeba

Acanthamoeba spp. are ubiquitous members of the environment and are found worldwide in ______ and ________.

Balamuthia mandrillaris is widely distributed and has been isolated from ____

A

soil and fresh water

soil.

40
Q

Clinical Manifestations and Diagnosis

N. fowleri typically causes a __________ ————- in healthy, immunocompetent young patients, in association with ______ in _______ water.

A

fulminant meningoencephalitis

swimming; warm fresh

41
Q

N. fowleri

The disease is nearly always fatal.

T/F

A

T

42
Q

Clinical Manifestations and Diagnosis
N. fowleri

The cerebrospinal fluid (CSF) profile of patients with N. fowleri primary amebic meningoencephalitis (PAM) is similar to that seen in ______ meningitis (____ white blood cell count, ____ glucose, ___ protein), but with a ____ Gram stain and culture.

(Motile or Non-motile?) trophozoites can sometimes be seen on wet mount of the CSF.

A

bacterial; high

Low; high ; negative

Motile

43
Q

Clinical Manifestations and Diagnosis

Neuroimaging studies in patients with PAM are usually (specific or nonspecific?).

A

nonspecific.

44
Q

Clinical Manifestations and Diagnosis

Acanthamoeba spp. and B. mandrillaris cause the ______ onset of focal neurologic deficits

mental status changes (_______________) are related to central nervous system ___________.

A

subacute

granulomatous amebic encephalitis [GAE]

mass lesions

45
Q

Clinical Manifestations and Diagnosis

Acanthamoeba is mostly seen in _________ and _________ individuals

Balamuthia occurs in _____________________ patients.

The case-fatality rate for these infections is also (low or high?).

A

immunocompromised and debilitated

both immunocompromised and immunocompetent

High

46
Q

Clinical Manifestations and Diagnosis

CSF studies of patients with GAE are usually (specific or nonspecific?) , and it is (common or rare ?) to isolate organisms from the CSF.

Neuroimaging studies generally reveal multiple _________ lesions in the brain, with or without contrast enhancement.

Biopsy of involved tissues (skin, brain, etc.) can be diagnostic, usually via histopathologic examination/immunohistochemical staining or polymerase chain reaction (PCR).

A

nonspecific; rare

space-occupying

47
Q

Clinical Manifestations and Diagnosis

Acanthamoeba spp. and B. mandrillaris can involve other sites ( _____,_______,_______, and skin).

Acanthamoeba spp. also cause _____ threatening ______ in otherwise healthy individuals in association with ______ use.

A

lungs, sinuses, adrenals

sight; keratitis; contact lens

48
Q

Diagnosis of free living amoeba

Diagnosis depends on a __________, in conjunction with IN VIVO ____ microscopy

Demonstration of Acanthamoeba in _____________

biopsy specimens by histopathologic examination, culture, or PCR.

A

high clinical suspicion

confocal

corneal scrapings

49
Q

Therapy for FLA

Therapeutic regimens for free-living amebic infections of humans are well defined

T/F

A

F

not well defined.

50
Q

Therapy for FLA

Treatment for N. fowleri PAM should include high-dose ______ amphotericin products; _______ amphotericin may also provide some benefit, and the addition of azoles, rifampin, miltefosine, or other antimicrobials should be considered.

Acanthamoeba keratitis should be treated with _______ _______ or ———- ————

adjunctive surgical therapy may also be necessary.

A

intravenous; intrathecal

topical chlorhexidine or polyhexamethylene biguanide

51
Q

Acanthamoeba GAE should be treated with ___________ regimens, possibly including ______,_______,________,_______, and ______.

However, the most efficacious regimen is _________________

A

Combination antimicrobial

pentamidine, an azole, a sulfonamide, miltefosine, and flucytosine

not currently known.

52
Q

B. mandrillaris GAE should be treated with ________ regimens, possibly including pentamidine, flucytosine, a sulfonamide, albendazole, an azole, a macrolide, amphotericin, and/or miltefosine.
However, the most efficacious regimen is _______________

A

combination antimicrobial

not currently known.

53
Q

_________________ may play an adjunctive role in the management of both forms of GAE( __________ and __________)

A

Surgical débridement

Acanthamoeba GAE

B. mandrillaris GAE

House Microbiology (93 decks)

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