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Micro 7 > Fungal/Parasite of CNS > Flashcards

Fungal/Parasite of CNS Flashcards

1
Q

leading cause of fungal meningitis is?

A

cryptococcus

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2
Q

systemic fungi can can disseminate into the CNS?

A

Histoplasma, Blastomyces, Paracoccidioides, Coccidioides, and Cryptococcus

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3
Q

getting fungal meningitis starts how?

A

inhalation of fungal hyphae or spores - begins with pulmonary inf

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4
Q

what are dimorphic fungi? what this means

A
  • Histoplasma capsulatum
  • Blastomyces dermatitidis
  • Paracoccidioides brasiliensis
  • Coccidioides immitis
  • dimorphic fungi = filamentous molds in the environment; yeast in tissues during infection
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5
Q

only systemic fungi that is a yeast in the environment and a yeast in tissues?

A

cryptococcus neoformans (inda ink dude)

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6
Q

COCCIDIOIDOMYCOSIS - where is it found?

A
  • western hemisphere
  • San Joaquin Valley of California and in Southern Arizona
  • drought-rain-drought pattern
  • blown around in dust
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7
Q

Coccidioides immitis - organism info

A
  • dimorphic fungus
  • arthroconidia are easily airborne
  • Following inhalation the fungus converts into a SPHERULE
  • multinucleated structure
  • produces hundreds of single nucleated spores
  • In the environment, spores convert to the mold form; in tissues, they develop into new spherules
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8
Q

fungus that is a spherule in tissues?

A

coccidoides immitis

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9
Q

Coccidioides immitis - clinical/how it presents

A
  • 60% assymptomatic
  • Pulmonary disease=Mild to moderate influenza like syndrome: fever, cough, night sweats, malaise and chest pain
  • Most individuals spontaneously resolve the infection in 2 to 3 weeks
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10
Q

Coccidial meningitis - development

A

-develops slowly with increasing headache, fever, stiff neck, and other neurological signs. If untreated, the disease is frequently fatal.

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11
Q

Coccidial meningitis- diagnosis

A
  • Cultivation – rarely successful - wont really ever see the spherules - must rely on below two methods
  • Antigen detection in CSF
  • Serology
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12
Q

Coccidial meningitis - treatment

A

amphotericin B

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13
Q

Cryptococcosis - found where?

A

-everywhere –. BIRD POOP

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14
Q

Cryptococcosis - organism info

A

Cryptococcus neoformans= NOT A DIMORPHIC= IT IS AN Encapsulated yeast

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15
Q

Cryptococcosis - pulmonary disease - clinical/symptoms info

A
  • Pulmonary disease:
  • asymptomatic or a mild, spontaneously resolving, influenza like illness
  • little sputum production
  • little damage to the lung (granuloma or cavitation)
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16
Q

Cryptococcosis meningitis - presentation

A
  • develops slowly
  • intermittent bouts of headache, irritability, dizziness, and other CNS findings
  • Symptoms may present over weeks or months
  • Acute onset in immunodef (aids) –> RELAPSE IS COMMON AFTER TREATMENT
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17
Q

Cryptococcosis meningitis - diagnosis

A

-India Ink stain can reveal encapsulated yeast in spinal fluid, aspirates from skin lesions, sputum, and other clinical material
positive approximately 50% of the time
-Cultivation
-Serology

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18
Q

Cryptococcosis meningitis - treatment

A
  • Long term treatment (6-10 weeks)

- Amphotericin B and 5-fluorocytosine or fluconazole.

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19
Q

Zygomycoses

A
  • in fruits and breads
  • susceptibe are: immunosup, diabetes, and burn victims
  • not really seen in healthy indiv
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20
Q

Zygomycoses types

A
  • Rhizopus
  • Absidia
  • Mucor
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21
Q

Zygomycoses organism infor

A
  • Non-septate hyphae

- Sporangia bearing sporangiospores

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22
Q

Rhinocerebral zygomycosis - infects who most often?

A

diabetics

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23
Q

most common form of zygomycosis?

A

Rhinocerebral zygomycosis

24
Q

Rhinocerebral zygomycosis - presentation of disease:

A
  • Infection originates in the sinuses (inhalation of spores)
  • Extends to neighboring tissues (nose, adjacent sinuses, the hard palate, eye, and brain)
  • Initial symptoms include nasal congestion, blood-tinged rhinorrhea, tender sinuses, headache and fever
  • Progress to facial or periorbital edema and visual disturbances
  • Progression to the brain results in altered mental status, coma and death
25
Q

Zygomycoses - diagnosis

A
  • Observation of hyphal elements in clinical material
  • Culture confirmation.
  • In tissue section broad aseptate hyphae are frequently observed in blood vessels, frequently branching at right angels (90degrees)
26
Q

Zygomycoses - treatment

A

amphotericin B

27
Q

hyphae branching 90 degrees/right angles is?

A

Zygomycoses

28
Q

Entamoeba histolytica can disseminate where?

A

brain or liver abcesses

29
Q

Trypanosoma brucei causes?

A

sleeping sickness

30
Q

Plasmodium falciparum causes?

A

cerebral malaria - coma and die

31
Q

Opportunistic (Free Living) Amoeba - three genera? and found where?

A
  • Acanthamoeba, Naegleria, and Balamuthia

- in warm fresh water

32
Q

naegleria fowleri causes and presentation?

A
  • –>Primary amebic meningoencephalitis (PAM)
  • swimming in warm water (hot springs, heated pools, hot tubs).
  • southern US
  • associated with neti pots (used to irrigate nasal passages
  • gets in through: Intranasal inoculation.
  • The majority of cases are fatal within 1 week.
  • Symptoms begin as fever, headache, vomiting, and confusion, and rapidly progress to coma and death.
33
Q

Primary amebic meningoencephalitis (PAM) caused by and diagnosis?

A
  • Naegleria fowleri

- observation of trophozoites in biopsy material or cerebrospinal fluid.

34
Q

Primary amebic meningoencephalitis (PAM) - treatment?

A

-sometmies Amphotericin B helps

35
Q

Acanthamoeba causes and presenation?

A
  • Granulomatous amoebic encephalitis (GAE
  • Amoeba invade the brain, resulting in a slowly developing ulcerative lesion.
  • **-Course of disease is slower (1-2 weeks) than PAM.
36
Q

Balamuthia causes and presentation?

A
  • Granulomatous amoebic encephalitis (GAE
  • Amoeba invade the brain, resulting in a slowly developing ulcerative lesion.
  • **-Course of disease is slower (1-2 weeks) than PAM.
  • infections in AIDS patients may disseminate
37
Q

Granulomatous amoebic encephalitis (GAE caused by and diagnosis?

A

-Caused by Acanthamoeba and Balamuthia

38
Q

Acanthamoeba keratitis - what is it? how do you get it? how do you treat it?

A
  • Chronic infection of cornea.
  • Associated with contact lens use (85% of cases), and “homemade” or contaminated cleaning solutions or saline.
  • Corneal ulceration and ocular pain.
  • Topical treatment may be effective.
  • Corneal transplantation / Eye enucleation.
39
Q

Toxoplasma gondii - causes what disease and what are sources of infection?

A
  • cats, -birds and rodens–>GI infection and gets into the poop - Cysts –> to humans
  • pork/lamb/goats.. food born – cysts in that and we eat it undercooked.
40
Q

Toxoplasma gondii - symptoms? why worry about it?

A
  • most asymptomatic!
  • but issue bc it can be acquired congenitally = miscarriage or stillbirth OR blind, mental retardation, neurological disorders
  • ACUTE INFECTIONS ARE MOST DANGEROUS TO THE FETUS- thats when it can cross over to kid and start causing problems
41
Q

Toxoplasmosis ocular infection

A

-asymptomatic lesions in eye

42
Q

Toxoplasmosis in HIV/AIDS

A
  • encephalitis - lesion in brain - ring looking

- most AIDS patients get this

43
Q

Toxoplasmosis-caused by and disease presentation in normal vs immunodef

A
  • Toxoplasma gondii
  • Most infections are asymptomatic
  • Symptomatic disease – “flu like”: fever, headache, chills, lymphadenopathy, muscle aches
  • Following infection (ingestion) parasite goes through a process of differentiation and dissemination (muscle, brain).–>The immune system “walls off” bradyzoite filled cyst.
  • When the immune system is weakened reactivation can occur.
44
Q

Toxoplasmosis diagnosis

A
  • Diagnosis is generally made by serological testing.
  • Congenital infection may be tested by PCR analysis of amniotic fluid.
  • Maternal testing: IgM or rising IgG titer indicates acute infection
  • Newborn testing: IgM indicates congenital infection, however not all infected newborns are IgM positive.
45
Q

Toxoplasmosis- prvention/control

A
  • Cooking meat thoroughly.

- Avoid contact with cat feces: Pregnant & Immunosuppressed

46
Q

Toxoplasmosis- treatment

A
  • Most immunocompetent individuals do not require therapy
  • In pregnant mother, early treatment may reduce the severity of disease if transplacental transmission has occurred
  • Children with congenital disease should be treated for one year
  • Immunosuppressed patients may require prophylactic therapy to prevent reactivation
47
Q

Taenia solium is found where and transmission?

A
  • PORK

- eating encysted larvae in undercooked meat

48
Q

Taenia solium -extra-intestinal disease?

A
  • Ingested eggs hatch in intestine and release infectious larvae which enter the circulation and travel to various body sites where they encyst.
  • striated muscle, heart, brain, eyes
  • complications: Neurocysticercosis - seizure and neurological defects
49
Q

Taenia solium - diagnosis for Extra-intestinal

A

CT scan, MRI. Serology

50
Q

Ascariasis-Ascaris lumbricoides

A
  • the guys that we eat an egg it develops and gets up into lungs we clear throat and swallow and restart cycle
  • causes Visceral Larval Migrans
51
Q

Visceral Larval Migrans - where do humans get this from?

A

-The infection of man by ascarid worms which normally infect and cause intestinal disease in dogs and cats

52
Q

Toxocara canis and T. cati - transmission

A

-the accidental ingestion of eggs that are in dog and cat poop

53
Q

Toxocara canis and T. cati - in humans:

A
  • (Visceral Larval Migrans)
  • Humans ingest eggs, which hatch in the intestine releasing larvae.
  • Larvae enter bloodstream and migrate to numerous body sites.
  • Development is arrested in humans.
  • Granulomatous lesions develop. Commonly in the liver (hepatitis), spleen, lung (cough, wheezing), eye.
  • Eosinophilia
  • HUMANS DONT POOP THESE GUYS OUT - ONLY CATS AND DOGS
54
Q

Visceral Larval Migrans - symptoms:

A
  • FEVER and eosinophilia
  • Lesions in the brain can result in the development of epilepsy or encephalopathy
  • Eye infections are most common: “squinting” or a loss of visual acuity; retinal scarring; eye enucleation may be necessary
55
Q

eosinophilia seen in:

A

Toxocara canis and T. cati (ascardis) - Visceral Larval Migrans -

56
Q

Visceral Larval Migrans - diagnosis

A

eosinophilia, clinical presentation, serology, history (pets)

57
Q

Visceral Larval Migrans - treatment

A

can only treat symptoms - steroids - the worms will eventually die on their own

Micro 7 (6 decks)

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