| Question | Answer |
|---|---|
| What are the three routes of infection into the CNS | Blood Stream- principal route but difficult because of Blood Brain Barrier Nerves- pathogens such as rabies, hsv and tetanus toxin can enter via axon cytoplasm Direct Spread from adjacent infection- spread of infections along dura mater or through sinus |
| Most common cause of purulent CNS infections in newborns (less than 1 month old) | Group B Strep |
| Most common cause of putulent CNS infection in Infants and Children and Adults except adolescents | Strep Pneumoniae |
| Most common cause of purulent CNS infections in Adolescents | Nisseria Meningitidis |
| What are the three organisms that are the most common causes of ACUTE purulent meningitis | S. Pneumoniae, N. Meningitidis, and H. Influenza |
| What are the most common causes of Primary Acute VIRAL infections of the CNS not Purulent infections of the CNS | Enterovirus (major cause in USA), HIV, HSV, EBV and arhtropod borne viruses |
| Apart from common Purulent and Viral CNS infections what are the other potential infections should you consider for CNS infections | M. Tuberculosis, Deep Mycoses such as C. Neoformans and C. Immitis and protozoan infections such as T. Gondii |
| Why do you need to consider metabolic disturbances, toxic conditions, mass lesions and vascualr lesions when looking for CNS infections | They can mimic or mask CNS infections and should be considered in differential diagnosis |
| What are Purulent Meningitis, Chronic Meningitis, Aseptic Meningitis, Encehpalitis, Poliomyelitis, Acute polyneuritis, Reye's syndrome | Manifestations of NS infections |
| infection of meninges associated with marked acute inflammatory exudates and is usually caused by bacterial infection | Purulent MEningitis |
| What are the s/sx of purulent meningitis | fever, stiff neck, irritability, neurologic dysfunction, PMN large number |
| This CNS infection is makred by insidious onset and progression of the disease over weeks g | Chronic Meningitis |
| what are the two common and one occasional causes of chronic meningitis | common mycobacteria and Fungi (that cause granulamatous inflamation) Occasionally can be protozoa |
| Meningeal inflammation associated with increase of cells (pleoctosis), Primarily lymphocytes and other mononuclear cells in the CSF. -abscence of cultivable bacteria or Fungi -often associated with viral infections |
Aseptic Meningitis |
| What are the sypmtoms of aseptic meningitis | fever, headache, stiff neck or back, nausea and vomiting |
| What can syphilis and other spirochets presence of drug or radioopaque substances in CSF Tumors or bleeding involivng meninges or subarachnoid spaces cause |
Aseptic Meningitis |
| What is it called when patient may not show signs and symptoms of meningitis and CSF finding are compatible with Aseptic Meningitis but you also have seizures, paralysis or disordered mentation | Encephalitis |
| What are the common causes of encephalitis | virus infection, acute of chronic demyelinating disease |
| Selective destruction of anterior motor horn cells in the spinal cord and or brainstem manifested by weakness or paralyis of muscle groups and in severe cases respiratory insufficiency, Asymmetric flaccid paralysis | Poliomyelitis |
| What is the cause of poliomyelitis | polio Virus (most common) and coxsackie virus type A7 and other enteroviruses |
| Inflammatory disease of peripheral nerve with SYMMETRIC flaccid paralysis of muscles | acute polyneuritis |
| Most cases are of unknown cause and may be associated with C. Diphtheriae, enteric bacterial pathogen, cytomegalovirus, EBV | Acute polyneuritis |
| This is characterized by encephalopathy with fatty infiltration of viscera usually encounterd in childhood | Reye's Syndrome |
| What are the manifestations of Reye's syndrome | Systemic viral illness followed by cebreal edema, hepatic dysfunction, hyperammonemia |
| What is the pathogenesis of Reye's syndrome | precise mechanism is unknown, Influenza A and B and Varicella have been implicated along with Aspirin treatment during illness |
| If you have a suspected CNS infection what is your first step to confirm infection | Get a lumbar puncture, |
| What are you looking for in the CSF collected from lumbar puncture | measure pressure during procedure, protein count, glucose content, and direct staining and culture of CSF samples |
| Apart from testing CSF what else can you test in suspected encephalitis | you can get a brain specimen for biopsy for culture, histology and detection of viral antigen or nucleic acid |
| What are you looking for in CSF cytology and chemistry test | trying to culture and viruses or bacteria present or running assays such as PCR or serologic tests looking for presence of pathogens |
| HOw will you manage a CSF infection of bacterial origin | administer antimicrobial therapy, correct metabolic defects, hypoxia, saline depletion, monitor and control intracranial pressure with steroids or shunts, |
| What can you do if the CSF infection is of viral origin | supportive treatment except HSV which responds to antiviral drugs |
| What is the most common cause of bacterial meningitis of newborns | Group B Strep |
| What is the most common cause of bacterial meningitis in 2-18yr old children | Neisseria Meningitidis |
| What is the most common cause of bacterial meningitis in adults | Strept Pneumoniae |
| What is the most common cause of bacterial meningitis overall | strept pneumoniae |
| What causes meningococcal meningitis | Neisseria Meningitidis (kidney bean shaped diplococci) |
| Where are meningococci carried | nasopharyngeal flora carrier rate is 10% |
| Do meningococci infections generally present as epidemics or as isolated infections | epidemics they spread rapidly in corwded stressed environments |
| What are the most common sero groupd of meningococci that cause meningitis | B, C, and Y are most common A is associated with epidemic outbreaks |
| What is the pathogenesis of meningitis of menigococcal origin | meningococcus enters blood cuaseing bacteremia and endotoxemia and then gets into brain causing meningitis happens quickly |
| Why do you get petechiae on the trunk with meningococcal infection | The endotoxin release causes endotoxemia and causes damage to blood vessels causing vascualr collapse. |
| How does N. Meningitidis avoid immune system | the polysaccharide capsule is anti-phagocytic |
| What does the polysaccharide capsule of N. Meningitidis structurally similar too | Strucutrualy similar to brain shpingolipids aids in it avoiding immune system |
| What is the most frequent manifestation of Meningitis | Acute purulent meningitis starts with mild cold then fever headache pain and stiffness of neck and back nausea and vomiting petechiae and ecchymoses |
| How does meningococcemia without meningitis manifest | progressing to fluminant DIC and Shock destruction of Adrenal Glands (waterhouse-Frederichson syndrome |
| What is Waterhouse-Frederichson syndrome and what can cause it | destruction fo the adrenal glands caused by meningococcemia without meningitis |
| How do you diagnose meningococcemia meningitis | Direct Gram smears of CSF definitive diagnosis by culture of CSF, Blood and Skin lesions on blood agar or choclate agar |
| How do you get immunity to meningococcemia meningitis | Group-Specific anticapsular antibody is protective, natural immunite floowing infection or colonization, |
| What are some of the problems with the vaccine for menigococcemia | not effective for children under 2 yrs of age and is not long lasting |
| What is the Tx for meningococcemia | Penicillin because it gets good CSF penetration if resistant to penicillin use cephalosporins |
| What causes listerosis | Listeria Monocytogen a gram positive bacteria |
| What type of colony does listeria monocytogen produce on blood agar | Beta Hemolytic |
| What do listeria monocytogen produce that streptococci don't | they produce catalase |
| How do listeria monocytogen appear in fluid media | have a tumbling motility |
| Are listeria monocytogen resistant or susceptible to heat, cold, salt and extreme low Ph | resistant |
| Where do listeria monocytogen bacteria grow | inside of the host cells |
| What is the pathogenesis of listeria | after entering body listeria is taken up by professional and non professional phagocytes it then uses a surface protein internalin to get inside cell and listerolysin to get into cytosol it can then spread to other cells |
| Why do you get encephalitis and or meningitis with listeria | they gravitate to CNS |
| What problems do listeria present in pregnancy | they cross the placenta and can cause abscess in the fetus |
| How is the movement of listeria discribed and what do they use to move | like a comet through the evening sky using tail attained from host hytoskeletal actin filaments |
| What are the CNS manifestations of listeria infection | Fever, Headache, stiff neck, vomiting, impaired consciousness, convulsions |
| What are the manifestastions of a listeria infection of the GI tract | nausea, abdominal pain, diarrhea, fever |
| How do we get immunity to Listeria | cell mediated immune response of both CD4+ and CD8+ T cell subsets. |
| how do you Dx listerosis | gram staining of CSF reveal gram positive rods that when cultured form Beta hemolytic colon on blood agar |
| how can you prevent listerosis | no vaccine, Cook meat and poultry, wash raw vegetables and fruits, Pregnant women should be careful eating cheese and other dairy products especially refrigerated leftovers |
| What is the Tx for listerosis | penicillin, ampicillin and TSX fulminant cases use gentamicin and ampicillin |
| What is hansen's disease | leprosy |
| What causes hansen's disease | mycobacterium leprae aerobic acid fast rod shaped bacterium |
| Do mycobactrium leprae grow in culture | no only in livin cells, foot pad of mice or armadillos |
| Where does M. leprae grow once a person is infected | they grow in macrophages and Schwann Cells |
| What are the virulent factors of M. Leprae | Phenolic Glycolip PGL-1 and Lipoarabinomannan LAM |
| What are the two manifestations of hansens disease | tuberculoid leprosy and Lepromatous leprosy |
| how is tuberculoid leprosy marked | large flattened plaques on face, trunk and limbs edges are raised and erythamatous centera are dry, pale and hairless |
| How does lepromatous hansen's disease manifest | bacterial growth is uncontrolled, extensive skin lesions, symmetric and diffuse more on skin. Take on leonine appearance. Severe cases result in loss of fingers or toes, nasal bone or septum may also be lost |
| what provides protection form leprae infections | cell mediated immune response. Extent of disease depends of DTH response |
| If you have a postive lepromin test what type of leprosy do you have | tuberculoid- minimal diseas |
| if your lepromin test is negative what type of leprosy do you have | progressive and sever form of disease- Lepromatous |
| How do you Dx M. Leprae infection | acid fast stained specimen found in scrapings of nasal mucosa or ear lobe |
| How do you tx hansen's disease | tuberculoid- treat with sulfones with rifampin lepromatous- sulfone, rifampin and clofazimine for 2 years minimum |
| What cause botulism | clostridium botulinum gram positive spore forming anearobic rod |
| What strains of clostridium botulinum are of human importance | A, B, E and F are responsible for human cases |
| Where do you find C. Botulinum | found in soils and aquatic sediments. |
| What two types of botulism are msot common and which one has taken over prevelance now | Food Borne botulism was common but no Intestinal botulism is more common |
| What is the pathogenesis of Botulism poisoning | Endospores find anaerobic environment to grow in and secrete neurotoxin that causes paralysis |
| How can you get intestinal botulism | eat honey or dust that is contaminated with C. Botulinum |
| What are the causes for viral meningitis and which is most common | Enteroviruses most common such as picornaviruses Coxsackie virus mumps virus Echovirus |
| How do you get enterovirus | fecal oral route of transmission |
| how do you get mumps virus | trasmission via respiratory tract peak incidence in fall and winter |
| Where are the primary sites of initial infection by enterovirus and mumps virus | throat and intestinal epithelium then spreas into bloodstream cuasing viremia and then cause meningitis and rashes and chest pain |
| What do you see in CSF Glucose levels if the infection is do to a virus rather than a bacteria | Glucose levels witll remain normal |
| What are the symptoms of viral meningitis | fever, headache stiffness of neck nausea vomiting and sensitivity to light |
| What is the tx for viral meningitis | no treatment only supportive care |
| How do you prevent viral meningitis | hand washing and avoid swimming pools if meningitis infections are present in community |
| What are the virus that can cause sporadic viral encephalitis | HSV, Mumps, Measles and EB-virus |
| What is the most common cause of epidemic viral encephalitis in the USA | LaCrosse encephalitis Virus a bunyavirus |
| How are the 4 leading causes of viral encephalitis transmitted | by mosquito |
| What are the 4 leading causes of viral encephalitis | LaCrosse encephalitis Virus St. Louis Encephalitis Virus West Nile Encephalitis Virus Easter and Western equine encephalitis virus |
| How doe HSV-1 and HSV-2 cause sporadic viral encephalitis | Probably is a reactivation of latent virus or newly acquired virus via olfactory route |
| What are you likely to suffer from even after recovery from sporadic encephalitis caused by HSV | Paralysis, Epilepsy, deafness and Cognitive impairment |
| What type of HSV causes sporadic encephalitis in newborns and where do they likely acquire it | HSV-2 causes more cases in newborns likely acquired in birth canal during delivery |
| What are the primary hosts of arboviruses that cause viral encephaltiis | insects, birds and rodents. |
| What are the manifestations of arbovirus caused encephalitis | fever, headache, vomiting, NS involvement with disorietnation, paralysis, deafness, seizures or coma |
| What is the best practice in regards to arbovirus caused encephalitis | prevention, avoid high mosquito time and use screens on windows and porches. |
| What is the tx for arbovirus encephalitis | no treatment only supportive care no antivirals avaialable |
| What virus group do polioviruses belong to | enterovirus which is subgroup of picorna virus |
| How is polio virus transmitted | fecal oral route |
| What is post polio syndrome | rcovered patients may develop muscle pain, increased weakness, and muscle degeneration 15-50yrs after recovery |
| What is the pathogenesis of poliovirus | virus enters orally, infects the intestinal epithelial cells and then invades blood stream gets to CNS by crossing blood brain barrier and has afinity for motor neurons |
| What are the three types of manifestation of polio virus infection | abortive poliomyelitis aseptic meningitis paralytic poliomyelitis |
| What percent of polio infections go unnoticed | 90% |
| What type of polio virus infection is marked by nonspecific febrile illness for 2-3 days without CNS involvement | Abortive Poliomyelitis |
| What type of polio virus infection manifestation is marked by signs of meningeal irritation stiff neck, pain and stiffness of back in addition to signs of abortive poliomyelitis. Has rapid and complete recover in a few days no paralysis | aseptic meningitis |
| Polio Manifestation that starts as a minor illness followed by signs of meningeal irritation, asymetric flaccid paralysis, and no significan sensory loss, severe cases all four limbs may be paralyzed and can become life threatening with respiratory | Paralytic Poliomyelitis |
| What is the tx for polio infections | first prevention with vaccine If infected supportive tx artificial ventilation and physical therapy after recovery |
| How many serotypes of polio virus will OPV (sabin's) and IPV (salkes) vaccines protect against | all three serotypes of polio |
| What are the chief reservoirs of rabies in the united states | bats, skunks, and raccoons |
| What type of virus is rabies virus | rhabdovirus |
| How long can the incubation period of rabies virus be | as long as 6 years |
| Can giving vaccination at time of exposure help prevent spread or is it to late for the person | immunization at time of exposure can help stop the spread of the infection |
| what is the characteristic lesion of rabies | negri body an eosinophilic cytoplasmic inclusion body within the nerve cells widespread in brain |
| What does the negri body represent | site of virus replication |
| What are the early manifestations of rabies infection | fever, head and muscles aches, sore throat, fatigue, twitching sensation at site of viral entry |
| What are the manifestations indicating that Rabies has entered the CNS | agitation, confusion, hallucination, seizures, increased sensitivity to light, sound and touch, hydrophobia, increased salivation and foaming at mouth. ending in Coma and death within 4 days |
| HOw do you dx rabies | PCR of CSF and saliva, main mode those is detection of viral antigen by immnofluoresecent stain. Negri body in biopsy of brain tissue |
| What is the Tx for rabies | no effective tx after symptoms begin so avoid suspected animals and wash site of bite wound if biten by random animal and get rabies vacine and antiserum pronto |
| if you get a wound and don't wash it out or treat it properly apart from gangrene what can you get | C. Botulinum infection that diffuses into blood stream |
| What is the tx for botulisum infection | administer antitoxin, wash and enema to remove unabsorbed toxin, cleaining and surgical debridement of wound and supportive care |
