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Pathophysiology Chapter 20: Diseases of the Nervous System and EyeI. Structure of the Nervous SystemA. Divided into 2 parts1. central nervous system (CNS)2. peripheral nervous system (PNS)B. CNS composed of brain and spinal cord1. brain has several main partsa. cerebrum - controls voluntary muscles, perception, thinkingb. cerebellum – controls many involuntary body movementsc. brain stem – controls breathing, heart rate, blood pressure2. spinal cord extends from brain stem through foramen magnum of skull down the back to lumbar region3. cauda equina – bundle of nerves extending from spinal cord below lumbar region4. skull, vertebral column, meninges protect an support brain and spinal cord-meninges - 3 layers of tissue surrounding brain5. cerebral spinal fluid (CSF)a. fluid circulating around brain/spinal cordb. shock absorberc. provides nutrients, O2, electrolytes, removes wasted. spinal tap-CSF removed from subarachnoid space surrounding cauda equinaC. Meninges of CNSa. dura mater -tough outer layer – next to skull-space below dura mater – subdural spaceb. arachnoid mater-thinner middle layer-space below arachnoid mater – subarachnoid space-web-like – full of blood vessels-blood vessel walls form blood/brain barrier through tight junctions-prevents microbes/large molecules from entering subarachnoid space-blood/brain barrier makes treating CNS infections difficultc. pia mater-very thin innermost layer – lies next to brainC. Structures of the Peripheral Nervous System1. nerves transfer commands from CNS to muscles and glands2. cranial nerves extend from brain through holes in the cranial bones3. spinal nerves extend from spinal cord through vertebral gaps4. 3 types of nervesa. sensory nerves – carry signals toward the CNSb. motor nerves – carry signals away from the CNSc. mixed nerves – carry signals toward and away from CNSD. Cells of nervous system1. 2 basic typesa. neuroglia-provide support, insulation, nutrients-phagocytize microbesb. neurons-carry nerve impulses-nucleus in region called cell body-ganglion - collection of many neurons’ cell bodies-dendrites and axons extend from cell body-each neuron has many short stubby dendrites – receive impulse and send to cell body-each neuron usually has 1-2 long axons – send impulse away from cell body-axonal transport - in cytoplasm of axon, cytoskeleton transports substances -cell membrane generates action potential (nerve impulse)-synapse – where nerve endings (axon terminals) form junctions with other nerves, glands, muscles, etc.-mediates transfer of nerve impulse (electrical signal)-synaptic cleft – space between axon terminal and postsynaptic cell, muscle, etc.-neurotransmitters – molecules released by axon terminals into synaptic cleft-facilitate the “jumping” of action potential (nerve impulse) across synaptic cleft-are inhibitory or stimulatory-inhibitory – blocks nerve impulse-stimulatory – causes nerve impulse to be producedE. Portals of infection of the CNS1. CNS a. an axenic environmentb. has no normal microbiota2. how pathogens can access CNSa. breaks in the bones and meningesb. medical procedures – spinal tapc. travel in peripheral neurons to CNSd. bacteria carried in blood or lymph cross blood-brain barrier-infects and kills cells of the meninges, causing meningitisII. Bacterial diseases of the nervous systemA. Bacteria cause disease in 2 ways1. infect cells of nervous systema. meningitisb. leprosy2. bacterial neurotoxins (toxins that affect neurons)a. botulismb. tetanusB. Bacterial meningitis1. signs and symptomsa. sudden high feverb. wbc in CSFc. severe meningeal inflammationpain, severe headache, nausea, vomiting, stiff neck, muscle control issuesd. behavioral changes-drowsiness, confusion, fretfulness, irritabilitye. if invades brain: deafness, blindness, encephalitis, coma, deathf. develops rapidly-can kill within 6 hours of initial symptoms2. pathogens and virulence factorsa. 5 species cause 90% of bacterial meningitis cases-Neisseria meningitides-Streptococcus pneumonia-Haemophilus influenza-Listeria monocytogenes-Streptococcus agalactiaeb. virulence factors allow bacteria to resist phagocytosis and cause disease3. pathogenesisa. S. agalactiae acquired during birthb. Listeria transmitted via contaminated foodc. other species transmitted via respiratory dropletsd. bacteria spread to meninges from lungs, inner ear by way of the blood4. epidemiologya. S. pneumonia present in throat of 75% of humansb. not spread by casual contactc. N. meningitides causes meningococcal meningitis-spread by respiratory droplets-those most at risk are in close living quarters - such as barracks and dorms - allow it to spread rapidly-can become epidemic-100% fatality rate if untreated5. diagnosis, treatment, preventiona. diagnosis based on symptoms/culturing of bacteria from CSFb. treated with IV antimicrobial drugsc. vaccines available – meningococcal vaccine-S. pneumonia-H. influenzae type B-N. meningitidesd. individuals at risk for listeriosis should avoid high risk foodsC. Hansen’s disease (leprosy)1. signs and symptomsa. tuberculoid leprosy – nonprogessive – regions affected lose sensationb. lepromatous leprosy – progressive tissue destruction-more virulent form-regions affected lost – fingers, toes, facial features, etc.2. pathogen and virulence factors-Mycobacterium leprae is causative agent-gram+ bacillus with mycolic acid in cell wall-causes slow growth-protection from lysis-resistant to many antimicrobial drugs and drying out3. pathogenesisa. M. leprae grows best in cool regions of body-reproduces in neuroglia of peripheral nerve endings, cells of mucous membrane of nose,skin cells in fingers, toes, lips, and earlobesb. M. leprae can live inside infected cells for years-does so with no obvious signs-armadillo only other host4. epidemiology-transmitted by person to person contact or breaks in skin-takes years of intimate social contact-spread by inhaling respiratory droplets5. diagnosis, treatment, preventiona. diagnosis – signs and symptoms-confirmed by presence of acid-fast bacilli in samplesb. treated with multiple antimicrobialsc. prevention-BCG vaccine provides some protection-TB vaccine-prophylactic use of antibiotics when exposure occurs-limiting exposure to bacteriaD. Botulism -not an infection1. signs and symptomsa. ingest toxinb. affects synapses of PNSc. 3 forms-foodborne-weak, dizzy 1-2 days after ingestion-blurred vision, nausea, vomiting, abdominal pain, constipation, fixed/dilated pupilsprogressive paralysis-survivors recover slowly-infantcrying, constipation, failure to thrive-wound-grows in dead tissue2. pathogen and virulence factors-Clostridium botulinum – causative agent-different strains produce 1 of 7 neurotoxins-anaerobic-endospore forming-Gram+ bacillus-30g would kill everyone in US3. pathogenesisa. toxin blocks fusion of synaptic vesicles to axon terminal membrane-prevents secretion of ACh into synaptic cleftb. toxin never released c. synapse forever blockedd. muscles can’t contracte. flaccid paralysis4. epidemiologya. 50 cases of foodborne and wound botulism per year in USb. infant botulism most common form in US5. diagnosis, treatment, preventiona. diagnosis – culture from food, feces, wounda. 3 approaches to treatment-washing of intestinal tract-administration of botulism immunoglobulin (neutralizes toxin)-antimicrobial drugsb. prevention-destroying endospores in contaminated foodE. Tetanus1. signs and symptomsa. a.k.a. lockjawb. spasms and contractions of neck and jaw, drooling, grouchiness, bp fluctuations,arms/fists curl tightly, feet curl down and head goes back, back arches2. pathogen and virulence factors-Clostridium tetani – causative agent-obligate anaerobe with endospore – “lollipop”-found in soil, dust, intestines of animals-produce neurotoxin – tetanospasmin-toxin released when bacterial cell dies-toxin moves to CNS3. pathogenesisa. can acquire through break in skin or mucous membrane-doesn’t have to be deep puncture wound-staples, tacks, splinters, etc.b. distance of infection from CNS determines incubation pd.c. how neurotoxin tetanospasmin works:-blocks release of inhibitory neurotransmitter-nerve impulse to contract sent-muscles contract -muscles can’t relax – release of inhibitory neurotransmitter blocked-muscles stay contracted-contractions can be severe – can break bones4. epidemiology-mortality rate if untreated – ~50%-recovery depends on time it takes to grow new axon terminals5. diagnosis, treatment, and preventiona. diagnosis based on characteristic muscle contraction-at that pt. it is too late to save patientb. treatment - passive immunotherapy – immunoglobulins given – neutralize toxin- antimicrobials – kill bacteria-active immunization – forms AB-thoroughly clean woundc. vaccine availableIII. Viral Diseases of the nervous systemA. viruses more readily cross blood-brain barrier b/c they are smallerB. occur more frequently than bacterial and fungal infectionsC. include meningitis, polio, rabies, and encephalitisD. viral meningitis1. signs and symptomsa. similar to bacterial meningitis-fever, headache, stiff neck, drowsiness, confusion, nausea, vomitingb. usually milder than bacterial/fungal meningitis2. pathogens and virulence factors-90% caused by viruses in genus Enterovirus-positive single stranded RNA (+ssRNA)-can live in chlorinated water-common names for 3 enteroviruses causing meningitis-coxsackie A virus-coxsackie B virus-echovirus3. pathogenesisa. attack cells lining intestinal tract and lungsb. virus spreads to bloodstream – viremiac. damage to cells in meninges triggers meningitisd. incubation pd. – 3-7 dayse. complete recovery – 7-10 days after initial symptoms begin4. epidemiologya. more common than bacterial/fungal meningitisb. spread via respiratory droplets and feces5. diagnosis, treatment, and preventiona. characteristic signs/symptoms of meningitis in absence of bacteria in CSFb. no specific treatmentc. prevention-hand washing-avoid crowded poolsE. Poliomyelitis1. overviewa. stable for long pd. of time in pools/lakesb. ingested2. signs and symptomsa. asymptomatic infections – 90% of casesb. minor polio – nonspecific symptomsc. nonparalytic polio – muscle spasms/back paind. paralytic polio – produces paralysis-degree depends on :-infection dose-age of patient-health of patient-strain of virus involvede. complete recovery 6-24 monthsf. postpolio syndrome-30-40 years after original occurrence-occurs in 80% of prior polio patients-crippling deterioration in function of polio-affected muscles3. pathogen and pathogenesisa. poliovirus - causative agentb. transmitted most often by drinking contaminated waterc. species of Enterovirusd. replicates in cells of throat and small intestine-causes sore throat and nauseae. infects lymph nodesf. moves into bloodg. may progress to CNSh. paralysis develops-destroys motor neurons in upper spinal cord and brain stem4. epidemiology-exists only in central Africa and southern Asia5. diagnosis, treatment, and preventiona. diagnosis-virus in secretions and/or fecesb. treatment -none – manage symptomsc. prevention-vaccine-Jonas Salk-1995 – injectable, inactivated vaccine-Albert Sabin-1961 – live, attenuated, oral vaccineF. Rabies1. signs and symptoms-characteristic neurological signs if virus reaches CNS-initial symptoms-pain/itching at site of infection, fever, headache, malaise, anorexia-when reaches CNS-hydrophobia, seizures, disorientation, hallucinations, paralysis, death2. pathogen and virulence factors-rabies virus- negative ssRNA3. pathogenesisa. transmitted by bite or scratch from an infected animalb. virus attaches to skeletal muscle cellsc. virus replicates in muscle cells and moves into neuronsd. travels to CNSe. spinal cord/brain function degeneratesf. virus travels back to peripheral nerves/salivary glandsg. virus secreted in salivah. virus transmitted by bitei. can also enter through wounds, scrapes, and inhaled4. epidemiology-zoonotic disease – spread from animal reservoirs to humans5. diagnosis, treatment, preventiona. diagnosis by unique neurological symptomsb. postmortem detection of Negri bodies in brainc. treatment – human rabies immunoglobulin, vaccine, and cleansing site– human diploid cell vaccine (HDCV) – given on day 0, 3, 7, and 14 after exposured. prevented by controlling rabies in domestic animalsG. Arboviral Encephalitis 1. signs and symptomsa. 3-7 days incubation periodb. usually cause mild, coldlike symptomsc. if cross blood brain barrier-abrupt headache, high fever, weakness, nausea, vomiting, confusion, disorientationcoma, death-neurological effects may be permanentd. West Nile virus has most impact on human2. pathogensa. Eastern Equine Encephalitis – EEEb. Western Equine Encephalitis – WEEc. Venezuelan Equine Encephalitis – VEEd. St. Louis encephalitise. West Nile encephalitisf. California encephalitis3. pathogenesisa. arboviruses - arthropod-borne viruses-transmitted by blood-sucking arthropods (mosquitoes)b. produce viremiac. can cross blood brain barrier- if cross the blood-brain barrier mosquito-borne arboviruses can cause arboviral encephalitisd. West Nile virus can be transmitted between people by blood transfusion and transplanted organse. as zoonotic diseases, they rarely affect humans-mainly in horses, birds, chimps, cats, dogs, chimpanzees, alligators4. epidemiologya. normal host – bird (mostly sparrows) or rodentb. arbovirus seasonal – coinciding with mosquito activity4. diagnosis, treatment, preventiona. diagnosis based on signs and symptoms-confirmed by presence of arbovirus-specific antibodies in CSFb. treatment is supportivec. prevention-limit contact with mosquitoes-use netting-eliminate stagnant water-use insect repellants-vaccines for horses available against EEE, WEE, VEE, and WNVIV. Mycoses of the Nervous SystemA. Mycoses of the nervous system1. mycoses are fungal diseases2. spread from lungs to CNS by way of the blood3. mushroom toxins can produce hallucinations and neurological problems4. may also produce fungal meningitisB. Cryptococcal meningitis1. signs and symptoms-similar to bacterial meningitis-headache, dizziness, stiff neck, drowsiness, nausea, vomiting, irritability, confusion, loss of vision, coma2. pathogen and virulence factorsa. Cryptococcus neoformans (yeast) – causative agent-2 variants of yeast found worldwideb. produces melanin – helps it to resist phagocytosis by defensive cellsc. lives in soil, feces of birds, and sap of eucalyptus treesd. has predilection for CNS3. pathogenesis and epidemiologya. infections follows inhalation of spores or dried yeast cells-infects lung cells-moves into blood-infects meninges and brainb. commonly occurs in terminal AIDS patients and transplant recipients4. diagnosis, treatment, and preventiona. diagnosed by detection of fungal antigen in CSFb. treated with IV antifungal drugsc. prevention-threat to sick individuals-hospitals, nursing homes, etc. deter roosting of birdsV. Protozoan Diseases of the Nervous SystemA. Protozoan infections of the nervous system are rareB. 2 diseases caused by protozoa1. African Sleeping Sickness2. MeningoencephalitisC. African Sleeping Sickness1. signs and symptomsa. symptoms develop within months to ears of infections – depends on strain of protozoan involvedb. 3 clinical stages-site of bite becomes lesion-tissue dies-dead tissue full of rapidly developing parasites-parasites in blood create fever, lymph node swelling, headache-meningoencephalitis results when protozoa invade CNS-headache, abnormal neurological function, extreme drowsiness, loss of appetite,coma, deathc. cyclical waves of parasitemia (parasites in blood) occur every 7-10 days2. pathogen and virulence factorsa. caused by Trypanosoma bruceib. evades immune system by changing surface glycoproteins3. pathogenesis and epidemiologya. tsetse fly spreads protozoan by biting wild animals, sheep, cows, peopleb. some trypanosomes enter brain, spinal cord, and CSFc. others continue to circulate in blood – picked up by tsetse flyd. occurs in equatorial and subequatorial savanna and riverine areas of Africa4. diagnosis, treatment, and preventiona. diagnosed by microscopic observation of trypanosomes in blood, lymph, or spinal fluid-alternatively, tissue biopsy may be done b. treatment based on disease stagec. prevention - insecticide application can help reduce occurrenceD. Primary Amebic Meningoencephalopathy1. signs and symptoms-same as meningitis and encephalitis caused by other microbes-headache, fever, stiff neck, altered mental state, vomiting, death within 7 days2. pathogen, pathogenesis, and epidemiologya. caused by Acanthamoeba and Naegleriab. amoeba lives in warm lakes, ponds, puddles, ditches, mud, moist soil, swimming pools,AC units,humidifiers, contact lens solution, dialysis unitsc. enter host through abrasions on skin or eyelid or inhalation of contaminated waterd. migrate to braine. usually fatal3. diagnosis, treatment, and preventiona. diagnosis-amoeba detected in scraping from covering of eye, CSF, biopsy of brain tissuea. treatment - drugs have ltd. successb. prevention - avoid possibly contaminated water supplies-forms cysts in environment – makes them very “hardy”-b/c of this, controlling them is difficultVI. Prion DiseaseA. Prion is infectious proteinB. Spongiform encephalopathies1. belongs to class of diseases called spongiform encephalopathies2. a class of diseases that includes scrapie (in sheep) and mad cow disease3. leave the brains of victims full of holes4. humans can contract prion by eating meat from infected cattleC. Variant Creutzfeldt-Jakob Disease1. signs and symptomsa. brain tissue destroyedb. cavities (holes) formedc. insomnia, weight loss, memory failure, act irrationally, progressive worsening of muscle control leads to the inability to speak, walk, maintain posture, death within 12 months 2. pathogen, pathogenesis, and epidemiologya. caused by abnormal form (structure) of prionb. how acquired-eating infected meat-medical procedures such as transplants, blood transfusions, using contaminated surgical instruments, injections of growth hormone derived from infected pituitary glandc. prions may remain dormant for up to 60 years 3. diagnosis, treatment, and preventiona. diagnosed by characteristic signs and symptoms-confused with other forms of dementia in elderly-tests on sample of CNS confirm presence of prion in brainb. no treatmentc. prevention- avoid prion contaminated meat-destroy infected animalsVII. Microbial Diseases of the EyeA. Microbial Diseases of the eye1. senses are important part of nervous system2. vision comprises almost half of function of cerebrum-considered part of brain and dura materB. Structure of Eye1. hollow ball about 2.5 cm in diameter2. white outer wall a. fibrous b. direct extension of dura materc. called sclera3. corneaa. clear b. covers front of eye4. conjunctiva- lines eyelids and covers sclera of eye except pupil5. humorsa. aqueous humor-watery fluid between cornea and pupilb. vitreous humor-gel-like fluid inside eye6. retinaa. back wall of eyeb. contains billions of sensory neuronsc. responds to light energyd. sends nerve impulses to brain via optic nerveC. Trachoma –1. signs and symptomsa. leading cause of nontraumatic blindnessb. caused by a sexually transmitted bacterium-may enter babies’ eyes as pass through infected birth canalc. conjunctiva and cornea are scarred by bacterial infection2. pathogen, pathogenesis, and epidemiologya. caused by Chlamydia trachomatis-multiplies in conjunctiva/kills cellsb. results in purulent (pus-filled) discharge - scars conjunctiva c. discharge also deforms eyelids-eyelids turn inward-eyelashes scratch, irritate, scar cornead. corneal scarring triggers invasion of blood vessels c. can lead to blindnessd. typically affects children infected at birth3. diagnosis, treatment, and preventiona. diagnosis- by identifying bacteria in cells at site of infection-bacteria obtained also by urethra/vaginal swabb. treated with surgery and antimicrobialsC. other microbial diseases of the eye1. bacterial infections of skin and reproductive tract can affect eyes2. sties-infections of sebaceous glands near the eye3. ophthalmia neonatorum-inflammation of conjunctiva and cornea of newborn-acquired as pass through infected birth canal4. conjunctivitis (pinkeye)-inflammation of the conjunctiva5. keratitis-inflammation of cornea6. treatment-antibiotics-no antiviral drugs available ................
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