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Unit 2 Micobio > L17: Tetanus+Botulism+Fungi > Flashcards

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
Q

Wound botulism

A

Follows entry by bacteria
anaerobic environment→ germination, reproduction→ neuroparalytic illness from toxin
Usually IVDU

26
Q

cryptococcus neoformans serotypes

A

A,D, A/D

27
Q

cryptococcus gattii serotypes

A

B, C

28
Q

cryptococcus morphology

A

Capsule: evade phagocytosis

Serotypes A-D

29
Q

cryptococcus epidemiology

A

Exogenous infections
Soil, bird droppings
NOT communicable

30
Q

Cryptococcus gattii epidemiology

A

originally goats, immunocompetent hosts, fatal

31
Q

of the 2 cryptococci, which one is more common

A

Cryptococcus neoformans

32
Q

Cryptococcus MOA

A

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
Q

Cryptococcus meningoencephalitis symptoms

A

Fever, HA, stiff neck, change in mental status, increased CSF amount and pressure, low glucose, lesions on tissue
FATAL

34
Q

Culture of cryptococcus can grow on

A

Grows at 37 C

canavanine glycine bromothymol blue (CGB) medium

35
Q

Direct exam of cryptococcus

A 
Encapsulated yeast (india ink)
Serology***: detection of capsule antigen in
36
Q

detection of cryptococcus in CSF or serum

A

latex agglutination test

37
Q

sabouraud dextrose agar, potato dextrose agar culture of cryptococcus

A

Creamy, mucoid colonies

38
Q

cryptococcus culture on bird seed agar/caffeic acid medium

A

Diphenol oxidase (laccase)
melanin from phenol containing substrates
(birdseed agar in mixed infections)

39
Q

Toxoplasma gondii transmission/epidemiology

A

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
Q

Toxoplasma gondii control

A

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
Q

Toxoplasma gondii life cycle

A

host for sexual stage is cats.

Other hosts involve birds, mice, livestock

42
Q

Toxoplasma gondii can be isolated from

A

CSF, difficult: Zoitocytes and trophozoites

43
Q

Toxoplasma gondii serology

A

ELISA: IgG or IgM in pregnant women

44
Q

Toxoplasma gondii molecular diagnosis

A

PCR: parasite DNA in amniotic fluid

45
Q

Toxoplasma gondii in immunocompetent

A

Asymptomatic/mild flu in immunocompetent hosts

46
Q

Toxoplasma gondii severe complication occur in

A

immunocompromised hosts, women newly infected in pregnancy

47
Q

Congenital toxoplasma gondii

A

damage is more severe the earlier infected in pregnancy→ blindness, epilepsy. Triad: chorioretinitis, hydrocephalus, intracranial calcifications

48
Q

Post-natal Toxoplasma gondii

A

fever, myalgia, blurred vision

49
Q

Naegleria fowleri cysts

A

single nucleate: arises from amoeboid form under harsh conditions

50
Q

Naegleria fowleri flagellate trophozoites

A

2 flagella, arises in minutes based on changes in ionic environment or lack of nutrients
Infectious form

51
Q

Naegleria fowleri epidemiology

A

Soil, freshwater free living: pools, streams, ponds
Summer months in southern states
No person-to-person, no drinking water

52
Q

Naegleria fowleri ameboid trophozoites

A

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
Q

Naegleria fowleri is a

A

Facultative environmental pathogen

54
Q

Naegleria fowleri mechanism

A

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
Q

Naegleria fowleri symptoms

A

Acute Meningoencephalitis:
Mimic bacterial meningitis +/- confusion, hallucinations, seizures
Rapidly fatal: death within 2 days

56
Q

Naegleria fowleri wet mount

A

motile amoeba

57
Q

Naegleria fowleri control

A 
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
Q

Naegleria fowleri tissue sections

A

trophozoites: atypical mononuclear cells

59
Q

Naegleria fowleri culture

A

Clearing zones on E. coli covered agar plates: drop of CSF→ clearing→ pick up amoeba, place in distilled water→ look for flagellated form

Unit 2 Micobio (9 decks)

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