Micro CNS Infection – Flashcards
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| what are the layers of the head from the bone in |
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| periosteum epidermal space: filled with fat (only in spinal cord) dura mater subdural space: only space in pathology acrachnoid mater: connected to pia with CT subsrachnoid space: CSF pia mater: openings for vessels to get into the brain |
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| what are the three anatomical defenses of the CNS |
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| skill blood-CSF barrier BBB |
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| what are the 3 layers of the BBB, describe the composition of each |
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| vessels: tight endothelial cells Brain: tight parenchyma via pericytes, astocyte end feet, and miroglia BM: fibronectin, proteins |
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| what are the two types of junctions in the BBB, describe each |
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| adherin junctions: stablize cell-cell interactions in junctional zone complex tight junctions: interaction of transmembrane proteins (non-polar so restricts polar) |
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| what are the intracellular and extracellular enzymes associated with the BBB (6) |
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| monoamine oxidase (MAO) y-glutamyl transpeptidase (y-GT) alkaline phosphatase peptidase nucleotidases cytochrome P450 enzymes |
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| what are the six types of transport through the BBB |
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| receptor mediated transcytosis absorptive transcytosis influx carrier proteins efflux transporters transcellular lipophilic pathway paracellular aquous pathway |
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| what 4 substances are transported through the BBB in receptor mediated transcytosis |
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| LDL Leptin insulin transferrin |
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| what and how are things transported through absorptive transcytosis in the BBB |
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| cationization increases uptake of plasma proteins (like albumin) |
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| what uses carrier proteins to get through BBB (5) |
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| glucose AA purines nucleotides choline |
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| what uses and how do efflux transporters of the BBB work |
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| energy dependent transport of AZT (asidothymidine) |
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| what uses and how does the trancellular lipophilic pathway through the BBB work |
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| lipid soluble molecules cross lipid part of epithelium (despite non-polar complex tight junctions) this is how CNS drugs enter |
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| what uses and how does the paracellular aqueous pathway through the BBB work |
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| water soluble agents move between cells of BBB |
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| what cannot pass through the BBB (5) |
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| immune cells antibodies proteins toxins drugs |
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| what can pass through the BBB (7) |
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| oxygen ions glucose ETCH small lipid soluble molecules mannitol |
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| what are the 10 ways to acquire bugs that can infect the CNS |
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| hematogenous contagious infection congenital defect congenital infection across placenta congenital infection in birth canal trauma neurosurgery crawling up nerves ingestion and dissemination invasion |
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| define hematogenous entry, what places do bugs with hematogenous entry go to in the CNS (3) |
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| capillary to meninges choroid plexus, dural venous sinus, rarley cribiform plate |
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| what are the two modes of hematogenous entry to the CNS, give 5 examples of bugs that can do it |
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| macrophage transport and arthropod vector HIV, intracellular organisms like TB, listeria, salmonella, brucella |
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| what are 5 types of contagious infections that could lead to CNS contamination |
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| sinusitis, otitis media, dental work, mastoiditis |
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| what are three congenital defects that could lead to CNS contamination |
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| CSF shunt encephalocele (neural tube defect) meningomyelocele: posterior neural tube defet |
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| give examples of microbes that infect across the placenta (4 viruses, 2 bacteria, 2 plasmodiums) |
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| viruses: HSV, rubella, CMV, HIV bacteria: syphilis, listeria protozoa: plasmodium, toxoplasmosis |
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| give 4 examples of mirobes that infect during birth in the canal |
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| E. coli, GBS, listeria, HSV |
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| give 2 examples of microbes that crawl up nerves to the CNS |
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| HSV, rabies |
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| give three examples of microbes that are ingested and disseminate into the CNS |
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| T. solium, E. histolitica, echinococcus granluosus |
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| give 4 examples of microbes that direct invade the CNS |
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| acanthemoba, magleria, balmuthia, systemic fungi |
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| name the 9 CNS infections and where they infect |
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| osteomyelitis: skull or vertebral bone epidural abscess: epidural space intramedullary abscess: medullary column of spinal cord myelitis: infection of spinal cord ventriculitis: ventrical infection abscess: brain tissue infection epidural abscess: dural or skill encephalitis: brain tissue infection subdural and dural empyema: surdural or dural space infection meningitis: meninges infection |
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| what usually causes a brain abscess |
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| anaerobes or aerobes |
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| what is the reason epidural abscesses usually happen |
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| extension of local infection (like vertebral osteomyelitis) |
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| what is encephalitis, what are 2 symptoms |
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| brain tissue infection of the parenchyma seizures, obtundation |
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| what is a subdural or dural emphyema, why does it normally happen (4) |
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| infection of subdural space complication of meningitis in kids, complication of sinus infection, otitis media, mastoiditis in older kids and adults |
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| what is a subdural effusion |
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| sterile collection of fluid due to increased efflux or intravascular fluids from increased capillary wall |
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| what are the common causes of meningitis in adults and teens (2) |
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| s. pneumo, neisseria |
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| what are the 4 common causes of meningitis in the elderly |
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| S. pneumo, enterics, listeria, neisseria |
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| what are the signs of meningitis in an adult (11) |
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| headache, fever, coma, shock confusion, dissorientation, seizure, neck stiffness vomiting photophobia petechiae |
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| why is there vomiting in meningitis (3) |
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| brain stem irritation, increased IOP, inflammation |
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| what is the ddx for meningitis in the elderly, why |
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| bladder infection - also causes confusion and disorientation arthritis - causes stiff neck |
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| what are the 3 causes of meningitis in premes |
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| E. coli, listeria, GBS |
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| what are the 4 causes of meningitis at 1 mo |
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| GBS, E. coli, listeria, K. pneumo |
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| what are the 5 causes of meningitis at 1 yo |
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| GBS, E. coli, listeria, S. pneumo, neisseria |
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| what are the 8 signs of meningitis in kids |
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| lethargy insomnia poor feeding diarrhea afebrile cyanosis progressive (1-2 weeks) high mortality |
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| what are the common causes of acute meningitis |
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| virus, S. pneumo, neissiera, influenza (kids) |
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| what are the common causes of chronic meningitis (2) |
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| TB, fungi, virus, tubercle bacilli, syphilis others: B. burgdorferi, leptospira, coccidioides immitis (fungi), lymphoma, metastasis drugs: cyclosporine, NSAID |
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| why is chronic meningitis chronic |
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| causes are fungi, intracellular bacteria, mycobacteria, and viruses which are slower in disease progression |
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| why is acute meningitis acute |
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| the causes are bacteria and protozoans which have virulence factors (like cell walls), toxins, and cytokines allowing them to cause immediate infection |
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| what are some clues that someone has acute meningitis rather than chronic (5) |
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| progressed quickly lots of inflammatory markers fever irritability purlent exudate |
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| define aseptic meningitis, what is normally the cause, how is it determined |
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| no organism isolated usually caused by a virus usually have to determine with PCR or serology |
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| what are some of the common viruses that cause aseptic meningitis (4) |
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| enteroviruses: eosackie, ECHO Mumps LCM |
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| what is a clue an aseptic meningitis is caused by an enterovirus |
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| seen in late summer through fecal-oral route |
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| what are 4 clues someone has aspetic meningitis rather than acute or chronic |
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| mild self limiting low mortality increased lymphocytes |
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| what are the 4 causes of nosocomal meningitis or meningitis due to trauma |
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| S. pneumo, S. aureus, enterobacteriaceae, P. aerguinosa |
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| what is the most common cause of meningitis in a patient with diabetes |
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| GBS |
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| what is the most common cause of meningitis in someone who is immune compormized (3) |
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| cryptococcus neoformans (transferred from pidgeons or other birds) cryptococcus gatti |
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| if the meningitis came from a respiratory infection, what are the 3 most likley causes |
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| S. pneumo, neisseria, influenza |
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| if the meningitis came from a GI infection what are the 3 most likley causes |
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| E. coli, strep agalactia, listeria |
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| what are the three physical exam test do to on a suspected meningitis patient |
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| neuro exam: sound, pain, and light responses brudzinski's sign: resistance to bending neck forward kernig sign: resist straightening bent knee |
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| what are the three contraindications to a LP |
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| tumor, impending herniation, brainstem changes |
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| how is a LP done |
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| CT first (to check for contraindications) insert needle between L3 and L4 take 3-4 tubes priority specimine to the lab |
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| where are the three LP tubes sent |
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| chemistry, microbiology, hematology |
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| what are the 4 things checked for in a chemistry LP tube, what are the normal values |
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| glucose: 2/3 BG, 40-70 in adult, 60-80 in kid protein: 15-45 lactic acid LDH: isoenzyme 3 is viral |
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| what are the 4 tests done on a micro LP tube |
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| staining capsule serology culture PCR |
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| what are the 6 stains done on a micro LP tube sample |
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| acridine orange gram stain AFB fungal stain lactophenol cottom blue (fungi) india ink (cryptococcus) |
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| what are the capsules you should check for in the capsule serology of a micro LP tube sample (10) |
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| S. pneumo HIV GBS neisseria A, B, C, Y W135 E. coli K-1 |
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| what three tests are done on a hematology LP tube |
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| cell count (normal: 0-5 wbc/dl) cell differential color |
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| what does red LP sample mean (3) |
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| hemorrhage, bad tap, tumor |
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| what does yellow LP sample mean (3) |
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| xanthoma, hemorrhage, bilirubin |
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| what are 4 finginds in a LP sample that suggest sepsis |
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| PMN increase glucose decrease protein leak out and increase lactic acid increase (anaerobic bacteria) |
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| what are 5 signs of a bacterial infection in a LP |
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| increased pressure, WBC, PMN, protein decreased glucose |
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| what are 3 signs of a viral infection in a LP |
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| normal pressure increased lymphocytes normal glucose |
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| what are 3 sgns of a fungal infection in a LP |
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| increased lymphocytes increased protein low glycose |
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| what are 3 signs of a TB infection in a LP |
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| increased lymphocytes increased protein low glucose |
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| explain how and why someone would become infected with meningococci (include 5 virulence factors in this story) |
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| viral URI stops cilia so meningococci can stick to the respiratory epitheloum wia fimbrae, pili, polysaccharide capsule, biofilms, and with the help of IgA protease |
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| explain how meningococci get from colonizing on the respiratory epithelium to the CNS |
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| 1. migrate through the epithelium to the blood 2. cause leaky capillaries, transport on macrophages, or move through endothelial cells to get into the blood 3. evade the immune system in the blood 4. enter CSF through transcytosis or through endothelial cells |
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| what are two microbes that just go through endothelial cells to get into the blood, not needing to cause leaky capillaries or use macrophages |
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| neisseria, listeria |
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| unlike other CNS infecters, listeria does not use transcytosis through endothelial cells to get into the CSF, what does it do |
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| uses listeriolysin O to get into the cytoplasm and move on actin |
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| what are 2 ways potential CNS infectors evade the immune system when they are traveling in the blood |
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| capsules inhibit opsonization by C3b and immunoglobulins (alternative and classic complement pathways) evade filtration by spleen and macrophages |
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| what are 4 microbes that have a capsule and can evade opsonization as they travel in the blood to the CNS to infect |
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| S. pneumo, influenza, neisseria, E. coli |
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| once the meningitis microbe gets into the aubarachnoid space and begins to multiply, what are the three main complications its presence causes |
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| immune activation cotytoxic edema vasogenic edema |
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| what are the 4 immune responses meningitis causes |
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| inflammation leukocytosis complements (C5a, C3a, IL-8) macrophage inhibitory proteins (MIP) |
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| how does meningitis cause cytotoxic edema |
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| water flows through BBB causing edema in the brain, increased pressure from water compresses vessels and causes ischemia ischemia decreases ATP causing Na to accumulate and thus water inside the cells causing swelling and Ca to accumulate activating phospholupases and releases arachidonic acid leading to ROS and infarction |
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| how does meningitis cause vasogenic edema |
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| endothelium increases in permeability and lets plasma proteins and water (not through AQP4) into ECF increased fluid displaces the brain and causes herniation usually follows or is a result of cytotoxic edema |
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| what microbes usually cause sepsis with meningitis (7) |
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| pyogenic encapsulated bacteria: S. pneumo, neisseria, infleunza, monocytogenes (kids and old ppl) nosocoma: enterobacteriaceae, S. aureus, S. pneumonia |
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| when microbes infect the CNS they cause and inflammatory response, what is activated (10) |
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| PMN lymphocytes astroccytes microgili cytokines: IL-1, 6, 8, TNF-a NO prostaglandins |
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| what does the immune response elicted by meningitis cause to happen in the brain tissue(6) |
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| necrosis thrombi bleeding edema increased IOP herniation |
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| how does the antibiotic treatment for meningitis effect the CNS |
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| antibiotic enters CSF and causes rupture of bacterium bacterial fragments stimulate even greater cytokine response increasing neutrophils, vessel leakage, and edema |
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| what are the two cryptococci that attack CNS, what type of patient |
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| immune compormised or HIV pt C. neoformans: comes from pidgeons and birds C. gatti |
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| neisseria meningitidis: shape, stain type, 3 adherence mechanisms, 5 virulence factors |
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| gram negative diplococci kidney shape adhere with pilli, opa, opc defent with IgA protease, porin protein (inhibits degranulation), capsule, endotoxins on LOS, bind to epithelium |
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| how is n. meningitidis transmitted / how is transmission helped out (5) |
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| aerosol enhanced by URI, stress crowding, confinment increase susceptability with complement defect |
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| what is the incubation time of n. minigitidis |
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| 1-3d |
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| what are the main symptoms of n. meningitis (5) |
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| headache, fever, disorientation, petechial rash (maculopapular), nucal rigidity |
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| besides the 5 main symptoms of n. meningitidis, what are the other 10 other symptoms |
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| vascular collapse shock pulmonary insufficiency waterhouse friderichsen deafness blindness speech loss mental changes gangrene 90% mortality in untreated and 10% in treated |
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| what is waterhouse friderichsen |
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| invasion of DIC, hemorrhage, and adrenal collapse and damage |
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| what microbes often cause waterhouse friderichen in meningitis (11) |
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| S. pneumo GAS n. meningitidis n. gonorrhea E. coli klebsiella influenza B salmonella pasturella acinetobacter plesiomonas shifelloides |
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| H. influenza: shape, stain type, 5 virulence factors |
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| gram negative rod encapsulated, polyribotol phosphate, pili, IgA protease, LPS |
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| how is H. influenza spread (3) |
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| URI epiglottitis translocation to blood |
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| how does H. influenza invade the immune system in the blood |
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| capsule |
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| what are the conditions only type B influenza causes (3) |
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| meningitis, epiglottis, bacteremia |
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| what are the conditions all types of influenza cause (4) |
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| otitis media, sinusitis, tracheobronchitis, pneumonia |
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| how is influenza treated |
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| it isnt, get the vaccine |
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| Strep pneumonia: shape, stain type, 5 virulence factors |
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| gram positive diplococci encapsulated, pneumolysin, teichoic acid, peptidoglycan, phosphotidal choline |
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| what microbe has phosphotidal choline, what does it do |
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| strep pneumo translocation assistance |
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| what microbe has pneumolysin, teichoic acid, and peptidoglycan? what do they do |
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| strep pneumo damage cilia, kill inflammatory cells, enhance evasion, recruit inflammatory cytokines |
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| how is S. pneumo spread, who is it more likley to infect (5) |
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| routes from URI or LRTI (nosocomial pneumonia) asplenic, sickle cell, HIV, amaglobulinemia, and elderly patients |
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| what are the signs of s. pneumo meningitis (2) |
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| bacteremia high mortality |
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| how is s. pneumo meningitis treated |
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| it isn't, get multivalent vaccine |
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| listeria monocytogenes: shape, stain type, 3 virulence factors |
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| gram positive coccobacilli intracellular resistants escape from M cell phagosome via lysis into cytoplasm flagella |
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| how is listeria monocytogens transmitted, who does it infect most (3) |
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| contaminated food (unpasturized milk, lunch meat, fruits and veggies) infants, elderly, immune compormised |
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| how do we defent against listeria monocytogens, where does it like to go in the body |
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| liver and spleen then to blood CMI |
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| e. coli: shape, staining, how to identify it, 2 virulence factors |
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| gram negative rod lactose fermentor on MacConkey agar virulence: K1 capsule, type 1 fimbrae (in uropathogenic e. coli) allowing deep tissue invasion |
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| how is E. coli transmitted most often, to who |
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| contamination from colon to birth canal in premes and neonates |
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| what are our defenses against E. coli |
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| PMN do immature migration, diapedesis, degranulation, and killing |
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| [image] |
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| gram negatie rod E. coli MacConkey agar lactose fermentation |
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| [image] |
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| gram negative diplococci neisseria meningitidis |
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| [image] |
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| gram negative rod H. influenza |
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| [image] |
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| listeria monocytogens |
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| [image] |
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| peticheal maculopapular rash caused by neisseria meningitidis |
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| [image] |
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| strep pneumo alpha hemolysis mucoid colonies |
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| [image] |
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| strep pneumo diplococci anti phagocytic capsule |
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| [image] |
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| subarachnoid with inflammatory cells |
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| [image] |
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| neisseria meningitidis |
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| what are 4 cultures done on a LP sample |
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| optochin test bile salt susceptability quellung reaction india ink |
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| optochin test: how is it done, what does it test for, how can you tell, what test does it combine with |
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| similar to antibiotic susceptibility disc effusion standard for identifying strep pneumo other strep are resistant and will grow right up to the disc after do cAMP test to determine GBS presence |
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| what does the bilt salt susceptability test test for, how |
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| strep pneumo lyses quickly |
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| how is the quellung reaction done, what does it detect for |
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| mix anti serum with microbe causes capsules to swell |
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| what does india ink test for, how can you tell |
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| cryptococcus. capsule cannot be penetrated so there is halo effect |
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| what blood tests would you do on a suspected meningitis patient (4) |
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| CBC blood culture UA- antigen detection serology |
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| why is it difficult to make vaccine for microbes with a capsule |
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| T independent antigen. need more than polysaccharide to make vaccine because they are conjugated to a protein that needs T dependent response |
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| what illnesses does Cryptococcus begin with usually before meningitis |
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| respiratory infection causes acute meningitis |
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| what is a LOS, what microbe has it, what does it do |
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| N. meningitidis has one lipid oligosaccharide layer: same as LPS but with less carbs. has same endotoxin effects as LPS damaging capillaries and causing emboli |
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| what are the polysaccharide capsule serotypes for N. meningitidis, which are covered by vaccine |
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| A, C, Y, W-136 (conjugate vaccune types) 8 (no vaccine but common in bug) |
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| what is the most common meningitis causing bug that causes maculopapular petechial rash |
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| N. meningitidis |
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| what microbes other than E. coli can show up on macConkey agar, why do they turn color |
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| klebsiella and enterobacteri lactose fermentation changes pH and turns on indicator |
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| define encephalitis |
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| inflammation of the cerebral cortex |
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| what is the most common cause of encephalitis in the US and how does it get into the CNS |
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| HSV-1 travels along CN5 |
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| what are the rhabdoviruses that cause encephalitis (3) |
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| lyssa rabies - sanskirt rhabas polio - myelitis |
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| what are the bacteria that cause encephalitis (3) |
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| borrelia burdgorferi - lyme treponema pallidum - syphilis leptospiral interrogans |
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| what are the ameoba that cause encephalitis (3) |
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| freshwater ameoba ancathamoeba/balmuthia - granulomatous encephalitis nagleria fowleri |
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| what are the parasites that cause encephalitis (6) |
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| toxoplasmosis gondii taenia - flat worms (cysticerosis) malaria - p. falciprum tryanosomiasis- African SS (T. brucei) echinoccus granulosus toxacara canis/cati |
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| what are the non-rhabdoviruses that cause encephalitis (12) |
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| HSV1, HSV2, VZV, CMV, HIB enterovirus: ECHO, pareco, cosackie arboviruses: west nile, california, EEE, WEE, St. louis |
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| what are the causes of brain abscess |
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| trauma or surgery infected emboli osteomyelitis from neighboring area (otitis, mastoiditis) bacteria - aerobe and anaerobe fungal opportunists |
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| what fungal opportunist likes to cause brain abscess |
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| zygomycetes: rhizopus |
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| what are the two types of zygomycetes: rhizopus, describe them |
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| septate: spores made in little colored sacs aseptate: one large sac with spores |
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| what are some general signs of encephalitis (4), which distinguish it from meningitis (3) |
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| headahce, neck pain, nausea, vomiting impaired conciousness, ABNORMAL BEHAVIOR, seizures (LESS than meningitis) |
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| when you suspect encephalitis, what labs should you do |
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| LP: lymphocytes, glucose, protein serology: acute and convalescent sera |
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| in general, what is the prognosis of encephalitis |
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| good with supportive treatment self limiting |
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| what is another name for lyssa virus |
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| greek for lud violent |
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| lyssa virus: shape, genome type, how to identify |
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| bullet shape -RNA may look like inclusions on EM |
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| what are two other names for rabies |
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| sanskirt rhabas to do violence |
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| what are 7 things that carry rabies which is the most common in us and in world |
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| Bats in US dogs in world cats, racoons, skunks, foxes, coyotes, cattle |
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| what does the fox say |
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| rabies rabies rabies.... |
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| how is rabies transmitted(3) |
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| saliva, inhalation, organ transplant (not a common screen and indetectably clinically in early stages) |
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| how does rabies cause damage |
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| binds to ACh in muscle ganglioside |
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| what does rabies do while it is incubating, how long can this occur |
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| weeks to years travels from site to dorsal root ganglion on nerve |
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| how long does it take for rabies to reach the brain, what parts does it go to first, what is this stage called when it arrives |
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| prodromal: 2-10 days cerebellum, purkinje, hippocampus then back to the peripherial nerves |
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| what symptoms arrive in the prodromal stage of rabies, why |
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| because at the end the virus travels back down the neaves (face first) and causes inability to swallow and spasms |
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| how long does it take for neurological symptoms of rabies to appear, what type of condition does it cause |
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| 2-7d encephalitis like |
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| what are 7 neurological symptoms of rabies |
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| seizure confusion headache fever hyperactivity paralysis degeneration of neurons |
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| how do you know when someone with rabies is infectious, what stage is this, how do they spread it |
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| neurological stage symptoms saliva and eyes are carrying virus |
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| why does someone with rabies usually die, how long does it take |
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| 0-14d cardiac failure, hypotension, secondary infection |
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| why does rabies move faster symptom wise in the prodromal phase than in incubation, what is the exception to this |
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| it can crawl faster on those nerves (200-400 mm/d vs 12-24 mm/d in periphery) if bitten on face it can get to CNS faster because it is closer |
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| what labs should you do on someone with suspected rabies |
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| saliva, serum, LP, brain, and skip biopsy testing PCR for RNA |
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| why can you do a skin test for rabies and where |
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| cutaneous nerves at base of follicles in cervical region may contain a few viruses |
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| what are two diagnostic signs for rabies |
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| negri bodies in purkinje cells on autopsy little antibody (hidden in nerves) |
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| how is rabies treated |
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| wash wound to reduce viral load passive immunization: hyper immune gamma globulin IM around wound killed diploid cell vaccine (5 doses over 28 d) |
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| why do we give someone the vaccine ..after.. they have rabies?? |
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| we cannot wait for active immune response. antibodies and CMI will be too slow |
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| how is polio transmitted |
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| fecal oral |
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| what are three general conditions polio causes |
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| initial GI infection meningitis/encephalitis causes neuro signs guillain barre |
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| what are the three ways polio presents neurologically |
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| paralytic polio: leg paralysis bilbar polio: respiratory muscle paralysis post polio: recourrance of paralysis years later due to slow deterioration of the nerves |
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| what is guillan barre |
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| autoimmune damage to myelin sheath following infection |
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| what are the two types of polio vaccines and what are they made of |
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| salk: killed vaccine sabin: live attenuated vaccine |
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| why would you use the sabin polio vaccine, why not |
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| better antibody response could revert to wild type, mild GI infection |
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| explain the clinical presentation of B. burdgorferi |
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| 1. erythema margins 2. dissemination to heart and brain (meningitis, neuritis) 3. autoimmune arthritis |
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| leptospira interrogans transmission |
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| animal urine gets into skin break |
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| leptospira interrogans pathogenesis |
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| toxicemia due to dying of bug and presence of endotoxin similar to more severe forms of endotoxicemia but shorter and less severe |
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| what are the initial symptoms of leptospira interrogans |
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| flu like abdominal pain jaundice |
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| what are the severe stage symptoms of leptospira interrogans |
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| meningitis wheil's disease |
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| what is wheil's disease, what causes it |
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| renal and liver failure caused in severe leptospira ictero infection |
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| where is granulomatous encephalitis found, where does it infect, prognosis |
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| well water can cause eye infection that have potential for encephalitis slow development, often fatal |
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| what infection does nagleria fowleri mimic, what is the prognosis |
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| bacterial like meningitis rapid progression, fatal in 1-2wks |
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| how is a brain abscess detected |
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| CT MRI |
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| how is a brain abscess treated |
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| antimicrobials drainage |
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| who does toxoplasmosis infect (3) |
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| congenital immune compormised old people |
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| how is toxoplasmosis transmitted (3) |
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| inhalation/ingestion of oocyte (reproductive form) ingestion of bradyzoite (cyst in food) congenital transmission of trachyzyoites |
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| what are 3 signs of non congenital toxoplasmosis |
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| eye isgns calcified ring lesions on MRI hydrocephalus |
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| what are 3 sigs of congenital toxoplasmosis |
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| blindness deafness retardation |
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| how is toxoplasmosis detected |
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| IgG/IgM IgM can be used for identification because few people have it |
question
| how is toxoplasmosis treated |
answer
| anti-parisitic |
question
| explain the two different ways T. solium can infect people |
answer
| consuming encysted larvae in undercooked meat and they mature in intestines ingest egg and larvae migrate to tissue and encyst (neurocysteriosis can be fatal) |
question
| what brain conditions can T. solium cause and why |
answer
| encephalitis: because of the neurocysteriosis abscess: the body cannot get rid of cyst so it walls it off with a lesion |
question
| what symptoms does T. solium cause (6) |
answer
| diarrhea, abdominal pain, weight loss, eosinophilia, neurocysteriosis, abscess |
question
| how is malaria falciprum transmitted |
answer
| female anopheles mosquito |
question
| how does falciprum cause problems |
answer
| RBC membrane becomes sticky and adheres to capillary walls |
question
| what are the two types of african sleeping sickness, their locations, and duration, their carriers |
answer
| trypanosome brucei gambinese: west africa. slow infection (mo - y). cow and human trypanosome brucirhiodesiense: east africa, rapid progression (wk-mo). sheep lion, cattle |
question
| what transfers african sleeping sickness between carriers |
answer
| tsetse fly |
question
| what does T. bruci do after the tsetse fly bites you |
answer
| enters blood then CNS |
question
| what are the 4 phases of african sleeping sickness and their signs |
answer
| initial: cancher at bite site haemolymphatic: fever, rash, headache winterbottom sign: large cervical nodes neurological phase: lethargy, confusion, convlusions, impaired speech |
question
| what is the tx and prevention for T. bruci |
answer
| perscription anti worm vector control no vaccine |
question
| toxacara canis/cati aka, once in body what does it do |
answer
| ingest egg, larvae migrate to brain and other organs dog/cat round worm |
question
| echinoccus granulosus: carriers, tranamission, what they do in body |
answer
| sheep and dog humans ingest egg and larvae migrate and form haydatid cyst which causes pressure and anaphylaxis |
question
| what three viral diseases cause slow neurological degeneration |
answer
| subacute sclerosing panecephalitis (SSPE) progressive multifocal leuco encephalopathy congenital rubella |
question
| what causes subacute sclerosing panencephelitis |
answer
| measles cause damage to myelin and cause encephalitis |
question
| what causes progressive multifocal leuco-encephalptathy, in who |
answer
| JC virus in compormised |
question
| what is a prion, what are some chemical characteristics |
answer
| PrPc is turned into PrPsc by PrPsc in cytoplasm (not cell surface) B pleated sheet (not alpha) globular disease causing fibrils protease resistant |
question
| what do prions do |
answer
| cause plaque in the brain |
question
| what are the 3 types of creutzfeldt jakob disease, what causes each |
answer
| familail: autosomal dominant mutation in PrP gene (long latency) sporadic V-CJD: acquired from eating cow with BSE (short laltency) |
question
| what is the cause of gerstmann straussler disease |
answer
| PrP gene mutation |
question
| what is the cause of fatal insonmia |
answer
| PrP gene mutation |
question
| how does c. tetani cause damage |
answer
| tetanospasmin toxin |
question
| how is C. tetani transmitted |
answer
| spores in soil get into open wounds |
question
| MOA tetaospasmin toxin |
answer
| blocks release of inhibitor neurotransmitters (GABA, glycine) |
question
| wat are 5 signs of toxoplasmin toxin |
answer
| muscle rigidity spasm lock jaw autonomic dysfunction |
question
| how is C. tetani prevented and treated |
answer
| active and passibe immunity no tx |
question
| how does C. botulinium cause damage |
answer
| botulism toxin |
question
| how is C. botulinium transmitted |
answer
| food, heroin, injections, soil, inhalation (terrorism) |
question
| what are 4 signs of botulism toxin |
answer
| vision issues speech issues restlessness paralsis difficulty swallowing |
question
| C. botulinium tx |
answer
| antitoxin |
question
| how do dinoflagellates cause damage |
answer
| ciguatera toxin |
question
| dinoflagellate transmission (4) |
answer
| snaller, groupr, sea bass, and barracuda hich eat dinoflagellates |
question
| ciguatera toxin MOA |
answer
| interfers with Na movement |
question
| 7 signs of ciguatera toxicity |
answer
| numbness around mouth, lips, arms, legs nausea vomiting muscle pain muscle weakness headache dizzy tachycardia |
question
| what does PANDAS stand for |
answer
| pediatric atoimmune neurophsychiatric disease associated with streptococci |
question
| what is the cause of PANDAS |
answer
| post strep caused cross reactivity to brain tissue (rheumatic hypersensitivity) |
question
| what are 7 signs of PANDAS |
answer
| emotional OCD depression agression disruptive behavior attention defcit tourettes |
question
| what are 6 mushrooms that cause CNS symptoms |
answer
| aminita fly agatic brain mushroom false moreles death cap destorying angel |
question
| what are 6 wild berries that cause CNS symproms, describe some |
answer
| poke weed /black night shade: leafted green shrub with purple berries on pink stems bittersweet: clusters of red orange betties lilley of the valley daphine belladonna |
question
| what are 9 house plants that cause CNS symptoms |
answer
| milstone philodendron pothos bulbs: tulips, narcissus, iris diffenbachia poinsettia easter lilly |
question
| image:890158|center} |
answer
| aseptate |
question
| [image] |
answer
| B. burdgorferi |
question
| [image] |
answer
| belladona |
question
| [image] |
answer
| lilly of the valley |
question
| [image] |
answer
| negri body |
question
| [image] |
answer
| negri body |
question
| [image] |
answer
| neurocysteriosis T. solium |
question
| [image] |
answer
| septate |
question
| [image] |
answer
| pokeweed blacknight shade |
question
| [image] |
answer
| T. brucei |
question
| [image] |
answer
| T. solium cysts |
question
| [image] |
answer
| T. solium |
