L17: Tetanus+Botulism+Fungi Flashcards
spores of clostridium tetani
Terminal spores: tennis racket appearance
tetanus diagnosis is
clinical
clostridium tetani reservoir
Contaminated soil
Human/animal feces
toxin production of clostridium tetani comes from
1 plasmid: all have 1 serotype
DTaP
4 doses starting at 6 weeks
→ booster: preschool/kindergarden
Td
booster q 10 years
neutralization treatment for tetanus
Human tetanus immune globulin (HTIG):
How do you get tetanus?
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
general tetanus symptoms (most common)
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
Tetanus in Neonates
infection of umbilical stump
Localized tetanus in
immunocompromised
Muscle spasms confined to are close to injury
Cephalic tetanus (least common)
Lesions on head/face, ear infections
Only facial muscles, but can progress
Clostridium botulinum spores
less swollen, heat resistance, give bacillus distended shape
Clostridium botulinum toxins
8 serologically distinct toxins: A-H
Clostridium botulinum toxins used in botox and human disease
A, B
Clostridium botulinum toxins that cause human disease
E, F
Clostridium botulinum toxins that cause animal disease
C, D, G
Clostridium botulinum is found
Spores in soil nad sediments worldwide, GI tracts of birds, fish mammals→ food poisoning
Clostridium botulinum toxin mechanism of paralysis
Toxin is neurotoxic on chromosome→ prevents acetylcholine release→ flaccid paralysis
Clostridium botulinum toxin can be isolated from _____ for diagnosis
fecal samples
Botulism symptoms
NO FEVER
Symptoms: double vision, difficulty swallowing, blurred vision, dry mouth, droopy eyelids, slurred speech, muscle weakness (descending from shoulders)
Type H botulism
most deadly substance ever:
Inhalation (13 ng) or injection (2 ng) → kill an adult, no antitoxin
Infant botulism
ingestion (honey) → germinate, colonize intestine, release toxin→ lethal systemic effects→ sudden infant death
<6 months (no established gut flora)
Foodborne botulis
improperly canned/processed/preserved foods→ GI disturbance, toxemia→ neuroparalytic illness
Wound botulism
Follows entry by bacteria
anaerobic environment→ germination, reproduction→ neuroparalytic illness from toxin
Usually IVDU
cryptococcus neoformans serotypes
A,D, A/D
cryptococcus gattii serotypes
B, C
cryptococcus morphology
Capsule: evade phagocytosis
Serotypes A-D
cryptococcus epidemiology
Exogenous infections
Soil, bird droppings
NOT communicable
Cryptococcus gattii epidemiology
originally goats, immunocompetent hosts, fatal
of the 2 cryptococci, which one is more common
Cryptococcus neoformans
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
Cryptococcus meningoencephalitis symptoms
Fever, HA, stiff neck, change in mental status, increased CSF amount and pressure, low glucose, lesions on tissue
FATAL
Culture of cryptococcus can grow on
Grows at 37 C
canavanine glycine bromothymol blue (CGB) medium
Direct exam of cryptococcus
Encapsulated yeast (india ink) Serology***: detection of capsule antigen in
detection of cryptococcus in CSF or serum
latex agglutination test
sabouraud dextrose agar, potato dextrose agar culture of cryptococcus
Creamy, mucoid colonies
cryptococcus culture on bird seed agar/caffeic acid medium
Diphenol oxidase (laccase)
melanin from phenol containing substrates
(birdseed agar in mixed infections)
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
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
Toxoplasma gondii life cycle
host for sexual stage is cats.
Other hosts involve birds, mice, livestock
Toxoplasma gondii can be isolated from
CSF, difficult: Zoitocytes and trophozoites
Toxoplasma gondii serology
ELISA: IgG or IgM in pregnant women
Toxoplasma gondii molecular diagnosis
PCR: parasite DNA in amniotic fluid
Toxoplasma gondii in immunocompetent
Asymptomatic/mild flu in immunocompetent hosts
Toxoplasma gondii severe complication occur in
immunocompromised hosts, women newly infected in pregnancy
Congenital toxoplasma gondii
damage is more severe the earlier infected in pregnancy→ blindness, epilepsy. Triad: chorioretinitis, hydrocephalus, intracranial calcifications
Post-natal Toxoplasma gondii
fever, myalgia, blurred vision
Naegleria fowleri cysts
single nucleate: arises from amoeboid form under harsh conditions
Naegleria fowleri flagellate trophozoites
2 flagella, arises in minutes based on changes in ionic environment or lack of nutrients
Infectious form
Naegleria fowleri epidemiology
Soil, freshwater free living: pools, streams, ponds
Summer months in southern states
No person-to-person, no drinking water
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
Naegleria fowleri is a
Facultative environmental pathogen
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
Naegleria fowleri symptoms
Acute Meningoencephalitis:
Mimic bacterial meningitis +/- confusion, hallucinations, seizures
Rapidly fatal: death within 2 days
Naegleria fowleri wet mount
motile amoeba
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)
Naegleria fowleri tissue sections
trophozoites: atypical mononuclear cells
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
