L17: Tetanus+Botulism+Fungi Flashcards

1
Q

spores of clostridium tetani

A

Terminal spores: tennis racket appearance

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2
Q

tetanus diagnosis is

A

clinical

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3
Q

clostridium tetani reservoir

A

Contaminated soil

Human/animal feces

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4
Q

toxin production of clostridium tetani comes from

A

1 plasmid: all have 1 serotype

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5
Q

DTaP

A

4 doses starting at 6 weeks

→ booster: preschool/kindergarden

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6
Q

Td

A

booster q 10 years

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7
Q

neutralization treatment for tetanus

A

Human tetanus immune globulin (HTIG):

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8
Q

How do you get tetanus?

A

Trauma→ entry of spores
1. Bacteria remain localized
OR
2. Anaerobic conditions→ lowered oxidation/reduction potential→ multiply, release tetanospasmin (exotoxin) → absorbed by local nerve endings (or blood, lymph)→ transported through neurons→ disrupts central motor control

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9
Q

general tetanus symptoms (most common)

A

Lockjaw/trismus, risus sardonicus (grimace), HA, fever, sweating, difficulty swallowing, arching of back, flexion of arms, extension of lower extremities
+/- respiratory complication, cardiac complications → death

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10
Q

Tetanus in Neonates

A

infection of umbilical stump

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11
Q

Localized tetanus in

A

immunocompromised

Muscle spasms confined to are close to injury

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12
Q

Cephalic tetanus (least common)

A

Lesions on head/face, ear infections

Only facial muscles, but can progress

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13
Q

Clostridium botulinum spores

A

less swollen, heat resistance, give bacillus distended shape

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14
Q

Clostridium botulinum toxins

A

8 serologically distinct toxins: A-H

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15
Q

Clostridium botulinum toxins used in botox and human disease

A

A, B

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16
Q

Clostridium botulinum toxins that cause human disease

A

E, F

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17
Q

Clostridium botulinum toxins that cause animal disease

A

C, D, G

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18
Q

Clostridium botulinum is found

A

Spores in soil nad sediments worldwide, GI tracts of birds, fish mammals→ food poisoning

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19
Q

Clostridium botulinum toxin mechanism of paralysis

A

Toxin is neurotoxic on chromosome→ prevents acetylcholine release→ flaccid paralysis

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20
Q

Clostridium botulinum toxin can be isolated from _____ for diagnosis

A

fecal samples

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21
Q

Botulism symptoms

A

NO FEVER
Symptoms: double vision, difficulty swallowing, blurred vision, dry mouth, droopy eyelids, slurred speech, muscle weakness (descending from shoulders)

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22
Q

Type H botulism

A

most deadly substance ever:

Inhalation (13 ng) or injection (2 ng) → kill an adult, no antitoxin

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23
Q

Infant botulism

A

ingestion (honey) → germinate, colonize intestine, release toxin→ lethal systemic effects→ sudden infant death
<6 months (no established gut flora)

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24
Q

Foodborne botulis

A

improperly canned/processed/preserved foods→ GI disturbance, toxemia→ neuroparalytic illness

25
Wound botulism
Follows entry by bacteria anaerobic environment→ germination, reproduction→ neuroparalytic illness from toxin Usually IVDU
26
cryptococcus neoformans serotypes
A,D, A/D
27
cryptococcus gattii serotypes
B, C
28
cryptococcus morphology
Capsule: evade phagocytosis | Serotypes A-D
29
cryptococcus epidemiology
Exogenous infections Soil, bird droppings NOT communicable
30
Cryptococcus gattii epidemiology
originally goats, immunocompetent hosts, fatal
31
of the 2 cryptococci, which one is more common
Cryptococcus neoformans
32
Cryptococcus MOA
Immunodeficient: AIDS, lymphoma Inhalation of dessicated yeast cells→ pulmonary infection: asymptomatic or flu-like → resolve without intervention OR Skin/pulmonary infection→ progress to CNS→ meningoencephalitis
33
Cryptococcus meningoencephalitis symptoms
Fever, HA, stiff neck, change in mental status, increased CSF amount and pressure, low glucose, lesions on tissue FATAL
34
Culture of cryptococcus can grow on
Grows at 37 C | canavanine glycine bromothymol blue (CGB) medium
35
Direct exam of cryptococcus
``` Encapsulated yeast (india ink) Serology***: detection of capsule antigen in ```
36
detection of cryptococcus in CSF or serum
latex agglutination test
37
sabouraud dextrose agar, potato dextrose agar culture of cryptococcus
Creamy, mucoid colonies
38
cryptococcus culture on bird seed agar/caffeic acid medium
Diphenol oxidase (laccase) melanin from phenol containing substrates (birdseed agar in mixed infections)
39
Toxoplasma gondii transmission/epidemiology
Foodborne, zoonotic in soil (up to 1 year), congenital, blood transfusions/organ transplant (rare), inhalation from litter box Hot, humid climates No person-to-person
40
Toxoplasma gondii control
Cook meat thoroughly Wear glove during gardening, wash hands after Keep outdoor sandboxes covered Pregnant women should not: clean litter boxes, adopt new cats
41
Toxoplasma gondii life cycle
host for sexual stage is cats. | Other hosts involve birds, mice, livestock
42
Toxoplasma gondii can be isolated from
CSF, difficult: Zoitocytes and trophozoites
43
Toxoplasma gondii serology
ELISA: IgG or IgM in pregnant women
44
Toxoplasma gondii molecular diagnosis
PCR: parasite DNA in amniotic fluid
45
Toxoplasma gondii in immunocompetent
Asymptomatic/mild flu in immunocompetent hosts
46
Toxoplasma gondii severe complication occur in
immunocompromised hosts, women newly infected in pregnancy
47
Congenital toxoplasma gondii
damage is more severe the earlier infected in pregnancy→ blindness, epilepsy. Triad: chorioretinitis, hydrocephalus, intracranial calcifications
48
Post-natal Toxoplasma gondii
fever, myalgia, blurred vision
49
Naegleria fowleri cysts
single nucleate: arises from amoeboid form under harsh conditions
50
Naegleria fowleri flagellate trophozoites
2 flagella, arises in minutes based on changes in ionic environment or lack of nutrients Infectious form
51
Naegleria fowleri epidemiology
Soil, freshwater free living: pools, streams, ponds Summer months in southern states No person-to-person, no drinking water
52
Naegleria fowleri ameboid trophozoites
reproductive form which arises from flagellate form when conditions improve, only form in tissue and that feeds (on bacteria), phagocytose RBC, WBC, destroy tissue
53
Naegleria fowleri is a
Facultative environmental pathogen
54
Naegleria fowleri mechanism
Flagellate form enter nasal passages→ ameboid form→ migrates (lobopodia) along olfactory nerve to the brain → necrosis in olfactory bulbs and brain tissue by sucker apparatus, consumes brain cells → Primary Acute Meningoencephalitis
55
Naegleria fowleri symptoms
Acute Meningoencephalitis: Mimic bacterial meningitis +/- confusion, hallucinations, seizures Rapidly fatal: death within 2 days
56
Naegleria fowleri wet mount
motile amoeba
57
Naegleria fowleri control
``` Avoid swimming in stagnant ponds Do not disturb sediment in freshwater Keep head above water Distilled/purified water in neti pots Salination for decontamination (chlorine ineffective) ```
58
Naegleria fowleri tissue sections
trophozoites: atypical mononuclear cells
59
Naegleria fowleri culture
Clearing zones on E. coli covered agar plates: drop of CSF→ clearing→ pick up amoeba, place in distilled water→ look for flagellated form