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Flashcards related to microbial diseases of the nervous system
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Central Nervous System
The brain and spinal cord
Peripheral Nervous System
Cranial and spinal nerves
Blood Brain Barrier
Keeps toxins in blood from brain, capillaries wrapped by astrocytes, allows passage of lipid soluble substances
Encephalitis
Inflammation of the brain
Meningitis
Inflammation of meninges in brain
Meningitis Symptoms
Fever, headache, stiff neck, nausea, vomiting, convulsions, coma
Viral milder (meningitis)
Can be treated
Enterovirus (meningitis)
Attack guts, form of meningitis virus
Measles, mumps, influenza (meningitis)
Measles are the 1st infection
Historical Causes of Meningitis
Streptococcus pneumoniae, Haemophilus influenza, Neisseria meningitidis
Virulence Factors in Meningitis
Capsules and can replicate in the blood, travel to CNS
Haemophilus influenza type B (Hib)
Once most common, now nearly eliminated due to vaccine.
Neisseria meningititidis & Streptococcus pneumonia
80% of all cases 16+ years
Vaccines for S. pneumoniae
Has created herd immunity with 70% of the population as carriers
N. meningititidis
Without treatment it has an 80% mortality rate. 40% of the population acts as a reservoir carrying the bacteria in the throat.
Meningitis treatment
Develops quickly so broad spectrum of antibiotics are administered - usually cephalosporin. Once organism is identified, antibiotic treatment may change
Listeria monocytogenes
G+ rod, found in soil/water contaminated with animal feces. Mild in adults but can cause meningitis
Listeria monocytogenes virulence
Crosses placenta, causes still births. Grows in refrigerator temperatures. Transmission is food borne
Bacteriophage spray
Approved by the FDA as a spray preservative for deli meats
Antibiotic of choice for Listeria
Penicillin G
Clostridium tetani
G+, obligate anaerobe, spore forming rod. Tetanospasmin neurotoxin - toxin released from cell
Clostridium tetani infection
Bacteria do not spread, no inflammation
Lockjaw
First sign of Clostridium tetani infection, muscle contracts, not able to relax
Cause of death in Clostridium tetani infection
Spasms of respiratory system
DTaP
Diphtheria Tetanus acellular pertussis, a toxoid vaccine
Tetanus Immune Globulin (TIG)
Given formed antibodies
Debridement
Cut/remove necrotic tissue
Clostridium botulinum
Produces exotoxins in anaerobic environments. Blocks the release of ACh - flaccid paralysis
Clostridium botulinum infection
Death from respiratory or cardiac failure
Clostridium botulinum toxin
Toxin can be destroyed with heat, will not grow in acidic environments unless mold is present
Drugs of choice for Clostridium botulinum infection
Streptomycin and rifampin
Muktuk
Sliced flippers of seals and whales, tenderized in anaerobic jar until putrefaction, common among native Alaskans
Infant botulism
No honey for kids until 1 year old
Treatment for Botulism
Recovery slow, allowing time for nerve regeneration and may require respiratory therapy
Mycobacterium leprae & M. lepromatosis
Grows best at 30 degrees - periphery of body. Invades myelin sheaths of PNS
Generation time of M. leprae
12 days to go from 1 bacterium to 2
Culturing M. leprae
Will not grow on artificial medium - armadillos
Tuberculoid form of M. leprae
Creates lesions in skin, appear as light areas, loose sensation
Lepromatous form of M. leprae
Skin cells are affected causes formation of nodules, can cause destruction of peripheral body areas
Drugs of choice for M. leprae
Sulfone drugs and rifampin
Polio
Most asymptomatic or mild flu like, fecal oral transmission
Pathogenesis of Polio
Multiplies in the throat and small intestine - viremia - Blood - may enter the CNS
Polio Immunity
Antibodies cross the placenta - giving fetus natural protection
Polio Vaccine
Attenuated viruses
Rabies
Causes fatal encephalitis
Genetic Material of Rabies
SS RNA without proofreading abilities mutates
Transmission of Rabies
Saliva in bites but can be transmitted by skin abrasions, or cross mucous membranes
Pathogenesis of Rabies
Proliferate – travels to CNS (brain spinal cord), can replicate in skeletal muscle
Immune Response to Rabies
Immune system does not respond because of small # of viral particles. Multiplies in skeletal muscle
Rabies Incubation & Treatment
Incubation 30 days up to 6 years, post-exposure prophylaxis one successful & chance of recovering
Symptoms of Rabies
Agitation, fear of water cause spasms in pharynx causes death of neurons
Encephalitis
Mosquito borne virus. Symptoms range from mild to severe chills/headache/fever --> confusion/coma/death
Equine Encephalitis
Horse form of encephalitis
Cryptococcis
Fungal meningitis
African Trypanosomiasis
Trypanosoma brucei organisms, bite blood to CNS coma. TSE TSE FLY
Bovine Spongioform Encephalopathy
Prion (Infectious protein) = endemic (lives) in sheep. Neurological.