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
Zygomycoses - diagnosis
- 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
Zygomycoses - treatment
amphotericin B
27
hyphae branching 90 degrees/right angles is?
Zygomycoses
28
Entamoeba histolytica can disseminate where?
brain or liver abcesses
29
Trypanosoma brucei causes?
sleeping sickness
30
Plasmodium falciparum causes?
cerebral malaria - coma and die
31
Opportunistic (Free Living) Amoeba - three genera? and found where?
- Acanthamoeba, Naegleria, and Balamuthia | - in warm fresh water
32
naegleria fowleri causes and presentation?
- -->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
Primary amebic meningoencephalitis (PAM) caused by and diagnosis?
- Naegleria fowleri | - observation of trophozoites in biopsy material or cerebrospinal fluid.
34
Primary amebic meningoencephalitis (PAM) - treatment?
-sometmies Amphotericin B helps
35
Acanthamoeba causes and presenation?
- 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
Balamuthia causes and presentation?
- 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
Granulomatous amoebic encephalitis (GAE caused by and diagnosis?
-Caused by Acanthamoeba and Balamuthia
38
Acanthamoeba keratitis - what is it? how do you get it? how do you treat it?
- 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
Toxoplasma gondii - causes what disease and what are sources of infection?
- 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
Toxoplasma gondii - symptoms? why worry about it?
- 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
Toxoplasmosis ocular infection
-asymptomatic lesions in eye
42
Toxoplasmosis in HIV/AIDS
- encephalitis - lesion in brain - ring looking | - most AIDS patients get this
43
Toxoplasmosis-caused by and disease presentation in normal vs immunodef
- 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
Toxoplasmosis diagnosis
- 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
Toxoplasmosis- prvention/control
- Cooking meat thoroughly. | - Avoid contact with cat feces: Pregnant & Immunosuppressed
46
Toxoplasmosis- treatment
- 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
Taenia solium is found where and transmission?
- PORK | - eating encysted larvae in undercooked meat
48
Taenia solium -extra-intestinal disease?
- 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
Taenia solium - diagnosis for Extra-intestinal
CT scan, MRI. Serology
50
Ascariasis-Ascaris lumbricoides
- 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
Visceral Larval Migrans - where do humans get this from?
-The infection of man by ascarid worms which normally infect and cause intestinal disease in dogs and cats
52
Toxocara canis and T. cati - transmission
-the accidental ingestion of eggs that are in dog and cat poop
53
Toxocara canis and T. cati - in humans:
- (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
Visceral Larval Migrans - symptoms:
- 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
eosinophilia seen in:
Toxocara canis and T. cati (ascardis) - Visceral Larval Migrans -
56
Visceral Larval Migrans - diagnosis
eosinophilia, clinical presentation, serology, history (pets)
57
Visceral Larval Migrans - treatment
can only treat symptoms - steroids - the worms will eventually die on their own