Diseases of The CNS
Blood- brain barrier
capillaries are built tighter- drugs must be lipid soluble. water soluble will not cross.
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Meningococcal meningitis (epidemic meningitis)
Transmission: respiratory aerosols, gets into CNS by injury, spinal tap, blood, etc.
Symptoms: caused by an endotoxin that is produced very rapidly and able to cause death within a few hours. There is a rash that does not fade when pressed. Fever, headache, stiff neck, nausea, vomiting. Can have gram - sepsis which leads to tissue damage and the person may need arm or leg amputation. Typically begins with a throat infection, leading to bacteremia and eventually meningitis. Usually occurs in children under 2 which causes residual damage such as deafness. Death can occur a few hours after onset of fever; however, antibiotic therapy has helped reduce mortality rate. People who survive may end up with some sort of neurological damage. Meningococcus occurs in 5 capsular serotypes. (A,B,C,Y and W-135) B,C & Y are most common in the U.S. Outbreaks occur among college students in dormitories and at one time in barracks. (epidemics) The vaccines are directed at the polysaccharide capsules of serotypes A,C,Y, & W-135. No vaccine against serotype B, which has a capule that is not immunogenic in humans.
Characteristics: aerobic, gram -, diplococcus, endotoxin, fastidious, polysaccharide capsule
Diagnosis: must be diagnosed quickly, spinal tap, gram stain and culture on blood agar. will be a STAT sample. latex- agglutination test.
Treatment: Vaccine, cephalosporin. Need to start treatment before definitive diagnosis because of 80% mortality rate
Streptococcus pneumoniae, and Haemophilus influenza.
Transmission: aerosols, complicating infections like head trauma in which soil gets in to brain, endogenous infections such as S.pneumoniae or throat infection can move up to meninges.
Symptoms: same as other meningitis. fever, headache, stiff neck, nausea, vomiting.
Characteristics: S. pneumonia is gram +, beta hemolytic, encapsulated diplococcus, and H. influenzae type B is gram -, coccobacillus, capsule, X,V factors, grows on blood agar.
Diagnosis: The capsule replicates in bloodstream and may enter CSF. Death can occur from shock and inflammation caused by release of endotoxins of gram - pathogens (H.influenzae) or the release of cell wall fragments of gram + bacteria (S.pneumoniae)
Requires a sample of CSF by lumbar puncture or spinal tap. Gram stain and culture on blood agar, prompt handling of specimens, can use latex-agglutination tests.
There are vaccines for S.pneumoniae (watch for resistance) and H.influenzae.
Gram +, encapsulated diplococcus, cocci in chains, beta-hemolytic.
Inhabited in nasopharyngeal region. 70% of population are healthy carriers. Most cases occur among children ages 1 month to 4 years with a mortality rate of 30% in children and 80% in elderly. Conjugated vaccine is recommended for children under 2, causes a decrease in otitis media. Watch for antibiotic resistance.
Haemophilus influenzae type B (Hib)
Common member of throat microbiota.
aerobic carbohydrate capsule, gram -, coccobacillus, diagnostic identification of pathogen uses speical media that determines X,V factors. Grows on blood agar. Hiv caused meningitis occurs mostly in children under age 4, especially at about 6 months. Causes about 45% of bacterial meningitis with a mortality rate of about 6%. Hib vaccine.
Leprosy (Hansen's disease)
Transmission: prolonged direct contact, lepromatous form by nasal secretions and the organism is in exudate of lesions. Young children are more susceptible because of weakened immune systems.
Symptoms: This is the least contagious transmittable disease and typically occurs if one has a compromised immune system.
Characteristics: Probably the only bacterium that grows in the peripheral nervous system, but it can grow in skin cells. It's an acid-fast rod, with a generation time of 12 days. It likes cooler areas on the human body such as extremities. It survives ingestion by macrophages and invades cells of the myelin sheath of the peripheral nervous system where is causes nerve damage from a cell mediated immune response. Armadillos are often a good way to culture the bacillus due to their colder body temperature. Transmission by contact with armadillos has been reported. The most efficient way of culturing is inoculation of footpads of nude mice. There are 2 main forms of leprosy. The tuberculoid form (neural form) is characterized by areas of skin that discolor and lose sensation with a boarder of nodules around them. This form occurs in people with good immune systems and there is often spontaneous recovery.
The lepromatous form (progressive form) often occurs in people with compromised immune systems. The skin cells become infected and there are disfiguring nodules all over body. This form likes cooler areas of body such as extremities, nose,
polio virus (picornavirus)
Transmission: Ingestion of water contaminated with feces containing the virus.
Symptoms: A cause of paralysis only affects less than 1% of cases. Great majority are asymptomatic or only exhibit mild symptoms such as headache, sore throat, fever and nausea. Respiratory muscles become paralyzed, and extremities become permanently crippled. Later in the 20th century development of the "iron lung" kept alive thousands with paralyzed respiratory systems. Maternal antibodies protected infants who were exposed which resulted in asymptomatic form and lifelong immunity. When infection is delayed until adolescence or early adulthood, the paralytic form of the disease appears more frequently. After ingestion, the virus multiplies in the throat and small intestine, which accounts for initial sore throat and nausea. Next it invades the tonsils and lymph nodes of neck and ileum. From lymph nodes the virus enters blood (viremia) Most cases, the infection does not progress. If the viremia is persistent, the virus penetrates the capillary walls and enters the CNS. Once in CNS virus attacks motor nerve cells in the upper spinal cord particularly, multiples, and the cells die resulting in paralysis. Death can occur from respiratory failure. During the 1980's many middle aged adults who had polio as children began showing muscle weakness called "postpolio syndrome". It may be that nerve cells that survived polio originally begin to die. Progression is slow.
Rabies virus (Rhabdovirus) endemic in AK
Transmission: Bite from rabid animals, contact with saliva, blood or tissues, respiratory droplets and even corneal transplants. Bats, skunks, foxes. raccoons, dogs, cats.
Symptoms: Periods of calm and agitation. Early symptoms mimic other infections, mild symptoms such as headache and fever. Can cause a fatal form of encephalitis, affects cranial nerves associated with throat which causes it to close making swallowing difficult and painful, and the excess saliva flows out of mouth, the sight of water causes throat spasms. Paralysis sets in, and can cause brain and spinal cord damage. Incubation time is 30-50 days up to 6 years. There are 2 types. Furious rabies- "kujo" restless, than excitable and will snap at anything, and bite. and paralytic rabies in which there is minimal excitability and is common in cats. The animal remains quiet, and unaware of surroundings and might snap if handled.
Characteristics: This is a lyssavirus with characteristic bullet shape. Single strand RNA which mutates rapidly.
Diagnosis: Use immuno-fluorescent test on live patient and animal by culturing saliva, serum, or CSF. To diagnose after death, fluorescent antibody test is used on brain tissue.
Treatment: If bitten by a rapid animal, the person must undergo post-exposure prophylaxis (PEP).(HDCV) is a series of 5-6 injections at intervals during a 28 day period. (HRIG) human-rabies immunoglobin given with HDCV. Pre-exposure vaccines are availabl
Furious rabies vs. paralytic rabies
Furious rabies- "kujo" restless, than excitable and will snap at anything, and bite. and paralytic rabies in which there is minimal excitability and is common in cats. The animal remains quiet, and unaware of surroundings and might snap if handled.
Viral encephalitis or equine encephalitis
Eastern (EEE) and Western equine (WEE) viruses (togaviruses) and West Nile virus (flavivirus)
Transmission: Culex, Aedes, and Culiseta mosquito vectors. Reservoir are horses and birds mostly.
Symptoms: sub-clinical to very severe and even death. Chills, headache, fever can progress to mental confusion and coma. Survivors will have neurological problems. The Eastern equine encephalitis (EEE) is the most severe, mortality rate of above 30%, survivors have high rate of brain damage, deafness, etc.
Characteristics: These are all RNA, arboviruses short for arthropod-borne virus.
Diagnosis: Elisa tests or serological tests
Name means this is caused by a virus which means there are no bacteria present. Many viruses contribute: Coxsackie virus (Picornavirus), Echo viurs, mumps virus, adenovirus, Herpes simplex 1. Given the opportunity with a weak immune system, these viruses can enter into brain and cause meningitis.
Transmission: Usually complicating infection from something else; for instance an individual with HIV and Herpes Simplex 1, the virus can travel up to brain.
Symptoms: More common than bacterial meningitis. Tends to have milder symptoms in most cases. Common in children during late summer/ early fall. Symptoms are typical of meningitis, fever, headache, stiff neck, nausea, skin rash. Can also cause a form of "photo-phobia" or light sensitivity. Symptoms usually last less than 10 days and is self limiting.
Characteristics: RNA virus
Diagnosis: In order to diagnose, need to distinguish from septic or bacterial meningitis. Test CSF with spinal tap and stain. Look for absence of bacteria and normal glucose levels, along with the meningitis symptoms to suspect viral meningitis. If bacteria are in the CSF, they will use up glucose so glucose levels will be low.
Treatment: no treatment for viral meningitis. self limiting. just supportive care and pain meds if needed.
African sleeping sickness (trypanosomiasis)
Caused by Trypanosoma brucei gambiense (milder form, most common) or T. brucei rhodesiense (severe form). (Euglenozoa)
Transmission: tsetse fly bite
Symptoms: Takes weeks or months for symptoms to appear and 2-4 years for disease to run its course if not treated. Early on in disease the organism is in the blood, you have fever, headache, decreased physical activity and mental acuity. There are chills and anemia. As the disease progresses and the organism moves from bloodstream up to brain and CSF, there is sleepiness because the parasite gets into the part of brain that controls sleep habits, and affects that area, making the person fall asleep while doing anything. Can cause convulsions and if left untreated the host can go into coma and die.
Characteristics: The Rhodesiense form can cause death within a few weeks or months often from heart or cardiac problems. The Gambiense form is the cause of 97% of reported cases in which there are few symptoms for weeks or months. fever, headache, deterioration of CNS, coma, death.
Diagnosis: If a person has been in an area common for tsetse flies is one criteria. Early on in disease, take blood smear, stain it and look for the organism. Later on is disease, organism will not be in blood stream so you must take a sample from the CSF.
Classic Creutzfeldt- Jakob disease
Transmission: genetic, transplants or contact with body fluids
Symptoms: Plaques are formed in response to abnormal proteins, they destroy brain cells, looks like someone has poked holes in the brain. (Swiss cheese), may have dementia, fibrils, plaques and progressively death. CNS damage is very insidious, slow, aggressive, no fever, no inflammation
Characteristics: not a microbe, not cellular, not even a virus, simply a deviant protein.
Diagnosis: most dont get diagnosed until biopsy, ECG on brain, CSF protein test- look for CSF-1433
Treatment: NO treatment
Variant Creutzfeldt- Jakob disease
Transmission: contact, ingestion of mad cow disease, blood transfusions.
Symptoms: younger people seem to develop this after eating beef with mad cow disease. It has very distinctive psychiatric and behavioral changes because of damage to the brain. Late neurological symptoms can take up to 6-8 years to show up.
Characteristics: abnormal protein- only killed by denaturing them with intense heat, etc. Not by normal autoclaving measures.
Diagnosis: ECG on brain, autopsy, CSF protein test
Treatment: NO treatment
abnormally folded proteins that can change the shape of normal proteins, causing them to clump.