nervous systems disease

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1.1.1. Streptococcus pneumoniae V/A : Has encapsulated virulent strain - caused it to resistance from phagocytosis, Produce pneumolysin ,Produce hydrogen peroxide M.O.T : Direct contact with droplets from nose or throat of infected person SYMPTOMS : High fever, Drowsiness, Vomiting, Severe headache , Stiff neck PATHOGENESIS : Bact, enter the host through direct contact with droplets from nose or throat of infected person and starts to colonize in nasopharynx before spreading to bronchi and alveoli. Bact. has polysccharide capsule which allow it to become resistance from phagocytosis. Its produce pneumolysin which induce cholesterol-binding toxin thus causing the damage of epithelial cells. Production of hydrogen peroxide by the bacterial has caused cell damage and inhibition of other bacteria. Inflammation occur in which cytokines are produced by the host alveolar macrophage. PREVENTION : Vaccinations, Avoid overcrowded places TREATMENT : Vancomycin antibiotics, Cephalosporin (cefotaxime or ceftriaxone)

1.1.2. Meningcoccal meningitis V/F : have pili that help in attachement at mucosal surface M.O.T :person to person SYMPTOMS : petechial rash ,high fever , neck stiffneee PATHOGENESIS cause infection by inhalation of water droplet contain of nesseria meningitidis . the bacteria replicate and colonize in nasopharyx by the adhesion of pili and spread to blood. make ways to meninges and grow rapidly PREVENTION : avoid overcrowding ,wear mask , avoid infected person TREATMENT : MenAfriVac , 3rd generation of cephalosporin

1.1.3. Hemophilus meningitis V/F : have pili that help in attachement at mucosal surface M.O.T : person to person SYMPTOMS : difficulty in sleep , fever, ear hearing difficulties PATHOGENESIS : cause infection by inhalation of water droplet contain of nesseria meningitidis, the bacteria replicate and colonize in nasopharyx by the adhesion of pili, spread to blood, make ways to meninges PREVENTION : avoid overcrowding, wear mask, avoid infected person TREATMENT :Hib vaccine


1.2.1. Listeria monocytes V/A : shed their cell wall and become L forms surrounded by only a plasma membrane M.O.T : foodborne transmission by improperly processed milk, cheese,meat and vegetables SYMPTOMS :fever, muscle ache ,diarrhea, other gastrointestinal symptom, High risk people (except pregnant women), stiff neck ,confusion , loss of balance PATHOGENESIS : Listeria monocytes transmitted by ingestion of improperly processed milk, cheese, meat and vegetables. Listeria bacilli shed their cell wall and become L forms and survive from phagocytosis. The causative agent able to cross the blood brain barrier and cause severe inflammation of brain PREVENTION : Wash raw vegetable and cooking raw food thoroughly, Reheating left over or ready-to-eat food until steaming hot, Spray cut surfaces of fruits with approved bacteriophage TREATMENT : Ampicillin, Gentamicin



2.1.1. Causative agent: Rabies virus, RNA rhabdovirus Virulent factor: Cell-to-cell spread, the rate of virus replication and the expression of the RV glycoprotein (G). Transmission: Passed on through saliva, to open wound or mucous membrane or through biting from an infected animal symptoms: Fever ,Headache , Anxiety , Hypersalivation, Hallucination Pathogenesis: 1) Transmitted thru bite or scratch from infected animals 2) Viral replicates rapidly in muscle cells and then moves into neurons Treatment and prevention: - Vaccination - Keep out from wild animals


2.2.1. Causative agent: togavirus Virulence factor: The viruses contain single-stranded RNA genome in which has higher rates of mutation. Transmission: Vector-borne (mosquito) diseases Signs and symptoms : Sudden high fever, Headache , Joint pain, Brain necrosis, Convulsions Pathogenesis: 1) The viruses are introduced into the body through bites of infected mosquitoes. 2) Virus multiply in skin and spread to lymph nodes. 3) Causing viremia which involves large number of viruses. 4) Then, they starts to invade the central nervous system thus causing shrinkage and lysis of neurons. Prevention: 1) Vaccination 2) Vector (mosquito) control 3) Personal hygiene measurement - Treatment: 1)Empirical therapy by using Acyclovir (zovirax) or Foscarnet (foscavir) 2) Steroids (dexamethasone) used to reduce brain swelling


2.3.1. Causative Agent: Flavivirus Virulence Factor: Capsid Protein binds and protects viral RNA Transmission: Vector-borne disease Symptoms : High fever, Headache , Body aches, Skin rash, Swollen lymph nodes, Stiff neck, Sleepiness, Disorientation, Coma, Tremors, Convulsions, Paralysis Pathogenesis: 1. Infected mosquito bite the host. 2. Mosquito salivary components introduced at the site of infection in vertebrates modulate initial infection of target cells such as keratinocytes and skin-resident dendritic cells through several mechanisms including focalized suppression of immune effector cell trafficking to the site of inoculation. 3. Infected dendritic cells or keratinocytes migrate to draining lymph nodes from which a serum viremia is generated that then relays infection to visceral organs and potentially to the central nervous system. Treatment: IV fluids and stronger pain killers Prevention: No vaccine. Avoid from the mosquitos.


2.4.1. Causative Agent: Herpes simplex virus type 1 (HSV1) and Herpes virus 2 (HSV2) Virulence Factor: HSV-1 proteins, γ134.5 Transmission: Sexual contact or from an infected mother to her baby during childbirth. SYMPTOMS : Headaches, Fever, Neck stiffness, Sensitivity to light, Seizures, Trouble thinking clearly, Personality changes, Hallucination, visual and auditory PATHOGENESIS : 1. In primary phase, virus enters via cutaneous mucosal surfaces to infect sensory or autonomic nerve endings with transport to cell bodies in ganglia. 2. In latent phase, virus replicates in ganglia. 3. For the lytic phase, reactivation of Herpes simplex virus in trigeminal ganglion can result in spread to brain (temporal lobe) via meningeal branches of central nervous system. Infection may produce vesicular lesions, which contain fluid and infectious virions. Treatment: Antiviral acyclovir Prevention: Avoid making contact with infected person

2.5. Polyomavirus infection

2.5.1. C/A : BK virus M.O.T : transmit by respiratory fluid and urine V/F : Viral particles in the enlarged nuclei of oligodendrocytes produce myelin, lipoprotein that coats nerve fibers in the central nervous system. SYMPTOMS : onset is insidious with vision and speech impairment, Fever and headache absent, Mental deterioration, limb paralysis and blindness impairment. PATHOGENESIS : Polyomaviruses enter the body through the respiratary and gastrointestinal tract.Initial replication takes place in the cell the virus first enter.The viremia that follows allows the viruses to reach target organs such as kidney lungs, and brain. The viral particles in the enlarged nuclei of oligodendrocytes and produce myelin, the lipoprotein that coats nerve fibers in the central nervous system.Infected oligodendrocytes are observed to surround areas that lack myelin in the brains of patients dying from progressive multifocal luekoencephalopathy. TREATMENT :no effective drugs without toxicity PREVENTATION : antibodies to the BK virus are found by age 4.



3.1.1. Mycobacterium leprae M.O.T : through close extended contact with someone with leprosy. V/A : the bacteria invade into nerves of skin and multiply SYMPTOMS : muscle weakness, patches of skin decreased sensation, such as touch, pain, heat, the appearance of skin lesions that are lighter than normal skin and remain for weeks/months TREATMENT :no vaccine.Treatment includes depsone plus rifampin for months or year Clofazimine added for lepromatous disease. PREVENTION: take care of personal hygiene especially if you go somewhere with hot weathers and sick people. PATHOGENESIS: Invasion of small nerves of skin.Multiplication in macrophage ,Attack immune cell against infected nerve cell cause deformity. The bacteria destroyed bacterial tissue and lead to continuous bacteremia


3.2.1. Clostridium tetani V/A : Endospore M.O.T : Deep cuts and puncture wounds SYMPTOMS : Generalized muscle stifness, Spasm. Arched back, Clench lift and jaw (lockjaw) PATHOGENESIS : Bacteria usually enter body through wound. Due anaerobic condition, spore germinate and produce toxin. Toxin disseminate via blood and lymphatics. Its act at peripheral motor end plate, spinal cord, brain and symphatetic nervous system. Toxin interfere with the release of inhibitor neurotransmitters, lead to muscle contraction and spasm PREVENTION : Use sterile knive to cut the baby umbilical cord TREATMENT : Antitoxin, Antibiotic


3.3.1. Clostridium botulinum V/F :Toxin ( Botulism toxin),Endospore M.O.T : Foodborne, infant, and wound SYMPTOMS : Double vision ,Difficulty in breathing , No fever, Gastrointestinal disturbance PATHOGENESIS : Toxin enters bloodstream from mucosal surface or wound. Binds to peripheral cholinergenic nerve endings. Inhibits release of Acetylcholine (prevent muscle from contracting). Symmetrical, descending paralysis occur at beginning with cranial nerves and progressing downward. Can result from airway obstruction or paralysis of respiratory muscle. PREVENTION : Boiling home-canned food TREATMENT : Polyvalent antitoxin



4.1.1. Poliovirus Virulence factor: 1) Contain canyon on surface for attachment 2) Genome of the virus that act as mrna in cytoplasm of infected cells. Transmission: Person-to-person contact from making contact with the feces of infected person. Symptoms : Headache, Nausea, Paralysis, Meningitis Pathogenesis: 1) Usually begins with oral ingestion of the virus. 2) After oral ingestion, the virus multiplies in the alimentary mucosa, and possibly in the tonsils and Peyer’s patches. 3) The virus then moves into the blood stream (viremia) through the putative barrier(s) that virulent poliovirus strains cross more efficiently than attenuated strains. 4) The circulating virus invades the CNS and replicates in neurons, particularly motor neurons. Treatment and prevention: Inactivated poliovirus vaccine (IPV) and oral poliovirus vaccine (OPV).



5.1.1. Creutzfeldt-Jacob disease Causative agent : prions (lack of inflammatory response) Virulence factor : increase in size of astrocytes produces a large quantities of filamentous protein called amyloid Modes of transmission : exposal of contaminated harvested human brain product, corneal grafts, dural grafts, electrode implant, human growth hormone. SYMPTOMS : rapidly progressive dementia, memory loss ,personality changes , hallucination, Myoclonus (jerky movement), anxiety, depression, paranoia ,obsessive compulsive ,psychosis, physical problems -speech impairment, balance and coordination dysfunction,gait, rigid posture, pneumonia ,death of brain nerve's cell Pathogenesis 1. CFD prions promotes refolding of native prion protein. 2. Misfolded protein leads to large quantities of insoluble protein in cell and distrupts neuronal cell function and caused cell death. 3. Defective protein invade the brain and induce other prion protein to misfold in a sustaining feedback loop. Diagnosis 1. Electroencephalogram 2. Spinal tap 3. Magnetic resonance imaging Treatment : No specific treatment but opioids help with the pain, Clonazepam or sodium valproate help with involuntary movement Prevention : •Surgical instrument immediately destroyed after used



6.1.1. Trypanosoma brucei M. O. T. - vectoborne disease, Tsetse bugs PATHOGENESIS : Infeted tsetse bugs had blood meal on mammalian host. The parasite enter lymphatic system and past into bloodstream. Inside the host, they transform into bloodstream .Tryptomastigotes carried to other site of body, reach other body fluid and continue replicate by binary fission. SYMPTOMS : large sore at bite site, fever, headache, muscle n joint aches, some people develope rash, after a week infection without treatment, parasite invade central nervous system and cause mental deterioration and other neurologic problem Death ensues usually within a month PREVENTION : wear long-sleeved shirts n pants in neutral color, avoid bushes, use insect repellent, avoid travel to rural African area


6.2.1. Trypanosoma cruzi (parasite) M. O. T. - vectoborne disease, triatomine bugs V. F. - Tryptomastigotes in bugs feces PATHOGENESIS : Triatomine bugs infected with T.cruzi biting animal or human. This bugs takes a blood meal and release Tryptomastigotes in its feces near the site of the bite wound. Tryptomastigotes enter the host through intact mucosal membrane. Inside host Tryptomastigotes invade cell near the site of inoculation, they differentiate into intracellular amastigotes. Amastigotes multiply by binary fission, then released into the circulation bloodstream. SYMPTOMS : Acute - occur in few weeks or months - found parasite in blood - fever - swelling near the site inoculation - rarely, result in inflammation of the heart or brain Chronic - enter into a prolonged asymptomatic ( no sign n symptom ) - no parasite found in blood - life threatening medical problems Heart rythm abnormalities Dilated heart that doesn't pump well Dilated esophagus n colon Prevent n control 1. House at rural America area need spray insecticide 2. Screen blood donation 3. Prevent travel to rural America area.