Microbial Disorders Of The Nervous System PDF

MICROBIAL DISORDERS OF THE NERVOUS SYSTEM M E N I N G I T I S TO P O L I O Prepared by: BMS 150 Nick Inglis, Ph.D. BACTERIAL MENINGITIS Inflammatory bacterial infections of the meninges (particularly the two internal ones, the pia and arachnoid mater) Induces meningial swelling,...

MICROBIAL DISORDERS OF THE NERVOUS SYSTEM M E N I N G I T I S TO P O L I O Prepared by: BMS 150 Nick Inglis, Ph.D. BACTERIAL MENINGITIS Inflammatory bacterial infections of the meninges (particularly the two internal ones, the pia and arachnoid mater) Induces meningial swelling, restricting CSF flow and putting pressure on the organs, causing nausea, pain, vomiting, reduced brain function BACTERIAL MENINGITIS If the infection is in the spinal cord, muscles of the neck will become stiff and motor control will be reduced If the infection is in the brain (encephalitis), sensory perceptions are decreased, behavioural changes occur, and coma or death may result TESTING FOR BACTERIAL MENINGITIS Cloudy CSF; Positive meningitis test Lumbar puncture (aka spinal tap) Clear CSF; Negative meningitis test MANY BACTERIA CAN CAUSE BACTERIAL MENINGITIS: Opportunistic members of normal microbiota Staphylococcus aureus Steptococcus pyogenes Klebsiella pneumoniae Regular disease causing bacteria Streptococcus pneumoniae Haemophilus influenzae Constitute ~90% of cases Listeria monocytogenes of bacterial meningitis Neisseria meningitidis NEISSERIA MENINGITIDIS Causes meningicoccal meningitis Virulence factors include: fimbriae and polysaccharide capsules, Lipooligosaccharide (with Lipid A/Endotoxin), and various factors to prevent digestion in phagocytes BLEBBING OF N. MENINGITIDIS STREPTOCOCCUS PNEUMONIAE Leading cause of meningitis Virulence factors: capsule, secretory IgA protease, pneumolysin (inactivator of lysosomal enzymes) Primary virulence factor: phosporylcholine (attachment to cells of lungs, meninges, blood vessels – and triggers endocytosis) LISTERIA MONOCYTOGENES Gram +ve coccobacillus found in soil, water, and many animals (no endospores) Obtained through contaminated food/drink Causes meningitis in immunocompromised individuals, but only mild flu in healthy adults. Avoids immune system detection by dividing inside macrophages and epithelial cells Phagocytosis Listeria Newly infected cell Listeria Originally infected cell Pseudopod of cell 1 Pseudopod of cell 2 Phagocytosis Actin “tail” PATHOGENESIS OF BACTERIAL MENINGITIS N. meningitidis, H. influenzae, S. pneumoniae – inhaled in respiratory droplets Listeria – unpasteurized milk, cheese, meat Bacteria usually spreads to meninges from infections of lungs, sinuses, or inner ear Head or neck trauma may expose meninges directly Bacteria ferment glucose in CSF for energy PREVENTION Susceptible individuals should avoid undercooked veggies, unpasteurized milk, undercooked meat and all soft cheese People living in dormitories should receive vaccinations HANSEN’S DISEASE (LEPROSY) Causative Agent: Mycobacterium leprae Optimal growth – 30°C – so in the chilly parts of your body (peripheral nerve endings, earlobes, nose, tips of fingers and toes. Signs of disease may not be present for 10-30 years, but when the population becomes big enough, your immune system will aggressively attack them WHEN YOUR IMMUNE SYSTEM ATTACKS Not shown: nerve damage BOTULISM Causative agent: Clostridium botulinum toxin (note: NOT an infection) 3 types of botulism: foodborne, infant, and wound Foodborne/Wound Botulism symptoms: paralysis of all voluntary muscles, blurred vision, nausea (death from respiratory paralysis Infant botulism: not ingested, but C. botulinum can infect GI tract due to absence of microbiota HOW BOTULISM TOXIN ACTS AT A NEUROMUSCULAR JUNCTION TETANUS Causative agent: Clostridium tetani Portal of entry: endospores enter through breaks in skin Signs/symptoms: tightening of jaw and neck muscles, difficulty swallowing, fever, spasms Treatment: aggressive treatment of wound, antibiotics Prevention: Vaccination  Stimulating neuron Inhibitory neuron Inhibitory neurotransmitter counteracts the effect of stimulatory neurotransmitter Muscle not Stimulatory contracted neurotransmitter (relaxed) Nerve impulse inhibited Motor neuron Normal action of inhibitory neurotransmitter TETANUS TOXIN (TETANOSPASMIN)  Tetanospasmin Muscles fully contracted, cannot relax Ach Nerve impulse Tetanospasmin (tetanus toxin) blocks release of inhibitory neurotransmitter TETANUS TOXIN (TETANOSPASMIN) WEST NILE FEVER WEST NILE FEVER Absent from N. America until 1999! New York isolate identical to Israeli goose Virus infects 100s of bird, 37 mosquito, 18 other vertebrate (including humans/horses) species WEST NILE VIRUS TRANSMISSION CYCLE WNV - PATHOGENESIS Transmitted by mosquito bite Incubation period of 3-14 days 20-30% get flu-like illness called West Nile Fever 80% - NO symptoms 1/150 EXPERIENCE NEUROINVASION Headache Ocular manifestations Muscle weakness Cognitive impairment Polio-like flaccid paralysis 10% mortality WNV REPLICATIVE CYCLE IN HUMANS EPIDEMIOLOGY – US CASES EPIDEMIOLOGY – CASE FATALITY RATE WNV PREVENTION POLIOMYELITIS - POLIOVIRUS POLIOVIRUS PATHOGENESIS CD155 TRANSGENIC MICE POLIO STAINING IN MOUSE SPINAL CORD POLIO TIMECOURSE PATHOGENESIS OF POLIOMYELITIS Humans are the only known reservoir Spread by fecal-oral transmission Peaks during warm months in temperate climates Complication: post-polio syndrome 30-40 year interval 25-40% Not an infectious process POLIO EPIDEMIOLOGY EMERGENCE OF POLIO AS AN EPIDEMIC IN THE 1900S Polio has only minor symptoms for infants and adults (seems like a mild cold) Early in the 1900s, white, wealthy children starting getting paralytic polio Connection to modern plumbing, sewer systems, etc. POLIO EPIDEMIOLOGYZ 1988: 350000 cases; 2000s: ~1000 cases/year Americas/Europe: now “polio-free” THANK YOU! S E E YO U N E X T T I M E !