Nervous System Pathogens Flashcards

Question 1

Q

Types of meningitis

Answer

A

Neurotropism-_{^{Pathogens show inclination to diff CNS tissues}}
Bacterial (purulent)-_{^{Acute onset (hrs-days):}}
- ^{_{CSF turbid (cloudy)}}
- ^{_{polymorphonuclear dominate (60,000 neutrophils)}}
- ^{_{Glucose decrease w/HIgh protein increase}}
- ^{_{presence of bacteria}}
VIral (aseptic)-Acute onset:
- _{^{CSF clear}}
- _{^{Lymphocyte dominate (500)}}
- _{^{Normal glucose w/slight protein increase}}
Chronic-_{^{gradual onset (weeks-months):}}
- _{^{Lymphocyte dominate}}
- _{^{Increased protein w/possible low glucose}}
Encephalitis & Meningoencephalitis:
- _{^{Change in CSF (cell count, protein, & glucose)}}
- _{^{Similar to viral but MORE elevated}}

Question 2

Q

Bacterial Meningitis

Answer

A

0-3 months:_{^{E.coli, Strep (group B), Listeria mono}}
3 months-6 years: _{^{Strep pneumo (#1) & Haemophilus Influenzae (#2)}}
Over 6 years: _{^{Strep Pneumonia (common)}}
Proliferation if bacteria behind blood-brain barrier in subarachnoid space
_{^{Protection from phagocytosis, Ab, & comp}}
_{^{PMNs & proteins enter CSF=Increased pressure in subarachnoid space compress brain/SC}}
Symptoms: Fever, Headache, Stiff neck _{^{(may not be in children)}}
_{^{Bulging Fontanelle=Infants}}
_{^{Skin rash (50% widespread pataecciae)=}}Neisseria
_{^{Brudzinski’s sign (lifting neck observe LL)}}
_{^{Kernigs’s sign (Flex/extend leg observe pain in back exudate in lumbar)}}
CSF- _{^{HIGH increase in protein w/decrease in glucose=Hypoglycorrhachia}}

Question 3

Q

Bacterial Meningitis (clinical)

Answer

A

Diagnose:
Specimen-CSF _{^{(chemistry, cell count, gram stain)}}
- _{^{Chemistry-Cloudy w/HIGH increase in protein & Hypoglycorrhachia}}
- _{^{Cell count-Increased WBC & neutrophils}}
- _{^{Gram stain CSF-Any bacteria is significant}}
Treat: Empiric Treatment _{^{(treat even w/o firm diagnosis)}} w/in 30 mins of assessment
_{^{Ampicillin + Cefotaxime OR Ampicillin + Gentamycin Given IV for BBB}}
_{^{Dexamethazone (corticosteroid)-Anti-inflammatory used in children to minimize rxn to free LPS (Give 10-20 before antibio)}}

Question 4

Q

Strep Pneumoniae-General

Answer

A

Gram (+) encapsulated, Lancet-shaped _^(elongated) paired w/cocci _{^{(short chains)}}
Alpha hemolytic _{^{(stains green)}}
Optochin & Bile sensitive
Autolysis-Releases virulence factors
NO lancefield type due to lack of carb in cellwall
Reservoir: Humans nasopharyngeal more common children
Transmission: resp droplets & aspiration of normal flora
High risk: Children & elderly
_{^{Pts w/history of previous viral RT infection}}
- _{^{Ex. Post-influenza, asthma}}
_{^{Alcoholics & smokers}}
_{^{Chronic pulm disease pts}}
_{^{Congestive heart failure}}
_{^{Asplenic/Splenectomy pts}}
_{^{Trauma/Meningitis=CSF leakage to nose}}

Question 5

Q

Strep Pneumoniae-Pathogenesis

Answer

A

Polysaccharide capsule=_{^{Anti-phagocytic (90 serotypes)-Vaccines target}}
Teichoic acid & peptidoglycan: Activate alternative complement ^{(inflammation)}
Phosphrylcholine: Unique to SP=Cell wall component
Binds to receptors of platelets activating factor ^{(found on many cells)}
Bacteria “hide” phagocytes=Spread infection

Question 6

Q

Haemophilus Influenza-General

Answer

A

Type B most VIRULENT type causes:
Localized infections in URT & LRT
Bacteremia_{^{(bacteria in blood)}}
**Meningitis **
Flora=Otitis media, Sinusnitis, pneumonia
Gram (-) pleomorphic Rod w/pink stain
Grow on chocalate agar or on Blood agar w/Strep aureus that lysis RBCs=Satellite Growth
Coccobacilli encapsulated w/diff types
Requires growth factors - **Ten(hemin) & five(NAD) **
Reservoir: Humans ONLY nasopharynx capsular type B & non-typable strains COMMON (Flora)
High Risk: Anyone-Unvaccinated children 2-4 or children w/severe infections

Question 7

Q

Haemophilus Influenza-Clinical

Answer

A

Polysaccharide capsule: Type B capsule made of polyribose-ribitol phosphatase (PRP)
IgA protease-Stops IgA
Endotoxin: Lipo-oligosacc (LOS) similar to Neisseria=Adherence, toxic to ciliated cells, Induce inflammation
Prevention: Hib vaccine-for type B capsular polysaccharide-_{^{(conj diphtheria or tetanus used to make it)}}
- _{^{Vaccine reduces carrier rate}}
Chemoprophylaxis_{^{(admin of meds to help minimize spread)}}: **Rifampin **eliminates carriers in HIGH risk groups by type B

Question 8

Q

Neisseria Meningitidis

Answer

A

Gram (-) Diplococcus _{^{(coffee bean shape)}} Capsulated
- _{^{Anti-phagocytic cap}}
Faculative intracellular & Oxidase (+)
Ferments glucose/maltose
Found in nasopharynx _{^{(asymptomatic carriers)}}
High Risk: Crowded areas _{^{(college, military, day cares)}}
Inherited def of Comp, Properdin _{^{(activator of comp)}}, Mannose-binding lectin _{^{(Innate immunity comp activator)}}
Virulence factors: Several serotypes A,B,C,Y, & **W135 **
_{^{Type A developing countries & B,C,Y in USA}}
_{^{Type B cap NOT immunogenic (no immune response)}}
_{^{LOS (lipooligosaccharide) No O but has A (endotoxin)}}
_{^{Surface proteins-Bind to factor H=prevention of comp activation}}

Question 9

Q

Neisseria Meningitidis (Clinical)

Answer

A

Meningitis: Abrupt onset fever, INTENSE headache, chills, Nuchal/Neck rigid-_{^{(Kernig’s/Brudinski’s)}}
Meningococcemia: Diffuse infection
_{^{Hemorrhagic rash (petechial)rapid progression petechiae coalesce (ecchymosis)=DIC & shock}}
_{^{Acute Meningococcemia gangrene}}
Waterhouse-Friderichsen syndrome: Adrenal destruction due to DIC
Treat: Penicillin G
- _{^{For allergies Cholramphenicol, Cefotaxime}}
Diagnose: Chocolate agar (+5% Co2) or Gram stain=Gram (-) inside PMN

Question 10

Q

Neisseria Meningitidis (Prevention)

Answer

A

Prophylactic antibios for pts exposed:
Rifampin _{^{(also used w/haemophilus)}} or Cipro-treat mucus membranes
Vaccine:
Serotype A, C, Y, W135
- Conj to diphtheria toxin
- Routine vaccination age 11-18 or Traverlers
Serotype B-NOT used due to cap made of sialic acid identical to human sialic acid
- NEW vaccine for B=Recomb proteins

Question 11

Q

Strep Agalactiae (general)

Answer

A

Gram + cocci, catalase (-) Capsulated
Beta Hemo=Bacitracin resistant (lance B)
CAMP (+) & Hippurate Hydrolysis (Blue-Glycine)
Normal flora of URT, GI, & Vagina _{^{(higher in African Americans)}}
High Risk: Neonates (due to delivery)
Virulence factor:
Capsule-Polysac rich in sialic acid
Anti-phagocytic & adhesion to meninges

Question 12

Q

Strep Agalactiae (Clinical)

Answer

A

Universal pre-natal screening @ 35-37 weeks
Early onset disease: 1st week of life
_{^{Infection acquired in utero or during delivery}}
High risk: _{^{Pre-term, maternal intrapartum fever, previous deliveries w/GBS}}
Sepsis, pneumonia, meningitis
Late onset disease: 1 week-3 months
_{^{Infection acquired from outside source (other infants)}}
**Sepsis & meningitis **
Adults: Postpartum endometritis, wound infection, UTI in pregers

Question 13

Q

Strep Agalactiae (Diagnose)

Answer

A

Treat: Penicillin G
Prevention: Intrapartum Antibios
Diagnosis:
Culture of Blood agar (Beta Hemo) LARGE area
Bacitracin resistant
CAMP test (best) positive
Hippurate hydrolysis (Blue-glycine)

Question 14

Q

E.Coli-Neonatal purulent Meningitis

Answer

A

Gram (-) rod, lactose fermenter (pink)-MacConkey
Found in colon/urogenital tract
Transmission: Mother to infant @ time of delivery
Virulence: Strains that cause meningitis=Capsular Ag K1 cross reacts w/group B strep capsule
Disease: Ecoli & group B strep #1 cause of meningitis in NEW BORNS

Question 15

Q

Listeria Monocytogenes (general)

Answer

A

Faculative Intracellular / Gram + rod or short chains
Motile _{^{(tumbling movement)}} & growth @ broad temp
Resistant to pasteurization temp & CAMP+
Ubiquitous (everywhere) and in GI of animals
Transmission:
_{^{Ingestion of contaminated food (meat or dairy products)}}
_{^{Vertical transmission (across placenta or delivery)}}
High risk: fetus, neonates or immunocompromised pts
Virulence: Infects various cells
_{^{Faculative intracellular-invade mononuclear phagocytic cells (moves like shigella)}}

Question 16

Q

Listeria Monocytogenes (Clinical)

Answer

A

Pathogenesis:
_{^{Cell adhesion & internalization-Adhesins & Internalins}}
Evasion of phagocytosis-
- _{^{Listeriolysin (hemolytic/cytotoxic)}}
- _{^{Phospholipase C helps bacteria get OUT of phagosome}}
_{^{Replication in cytoplasm}}
_{^{Release/entry into cell-ActA protein polymerase actin to push itself to next host cell (shigella)}}
Neonatal disease _{^{(abortion or premature):}}
Early onset (10 days) infection in utero
Granulomatosis infantiseptica-_{^{Sepsis w/pus lesions & granulomas made of L.mono in multiple organs}}
Late onset (2-3 weeks) infection during delivery
_{^{Meningitis or Meningoencephalitis w/septicemia}}
Adults: _{^{Immunocomp=Flu like or Pregers/Immunocompromised (disseminated bacterimia)}}

Question 17

Q

Listeria Monocytogenes (Diagnose)

Answer

A

Microscopy: CSF no organism few bacteria for detection
Culture: Small zone of hemolysis on Blood agar & POSITIVE CAMP test
Culture isolation improved w/cold isolation
Treat: Penicillin or ampicillin alone or combo
Prevention: _{^{Pregers & immunocompromised}}
Avoid soft cheeses
Throughly cook left overs
Wash raw veges

Question 18

Q

Crytococcus Neoformans (general)

Answer

A

Monomorphic yeast spherical-oval surrounded by wide polysac cap (Urease +)
Ubiquitous BUT most linked to pigeon droppings
Transmission: Aerosolized spores-Lungs then to CNS
High risk: Immunocompromised (HIV)
Virulence: Polysac cap
Disease: Cryptococcosis_^(chronic)
Cutaneous lesions seen in disseminated infection
Initial pneumonia-> meningocephalitis
- _{^{Headache (progressive & more severe)}}
- _{^{Mental aberrations (irribality to psychosis)}}
- _{^{Motor abnormalities (paralysis)}}
- _{^{CN dysfunctions (aphasia)}}
- _{^{Cerebellar dysfunctions}}

Question 19

Q

Crytococcus Neoformans (Clinical)

Answer

A

Microscopic: CSF+ w/Indian ink stains thick cap surrounding budding yeast
Culture: Blood agar = Urease +
Cap Ag detection in serum or CSF latex agglutination
Treatment: Ampotericin B or Fluconazole

Question 20

Q

Picornaviridae enterovirus (General)

Answer

A

ssRNA (+) Icosahedral-NAKED
Resistant to harsh enviroment & Stomach acid
Entry-URT & GI
Fecal-oral transmission
Entry mediated by viral receptors that bind to host cell:
ICAM-1=Intracellular adhesion mol _{^{(Coxsackie/Echo)}}
CD-55=decay accelerating factor_{^{(Coxsackie/Echo)}}
CD-155=Polio virus adhesion
- _{^{Found on macrophages, monocytes, CNS neurons}}

Question 21

Q

Picoviridae-Coxsackie & Echo

Answer

A

ssRNA + icosahedral NAKED
- Coxsackie A/B
- Achovirus MANY serotypes
_Transmission: _
Coxsackie-Oral fecal + aerosol
Echovirus-Oral fecal _{^{(Common in summer-early fall)}}
Bornholm (pleurodvnia): Cox B Infection of intercostal muscles=_{^{Trouble breathing w/NO minor lung involvement}}
Presents as aseptic meningitis, upper resp infections
90% of all VIRAL meningitis
COX A=Herpangina (Hand-foot-mouth)
COX B= Myocardial, pericardial infections
- _{^{Both can cause polio-like paralytic disease}}

Question 22

Q

Picornaviridae enterovirus (Pathogenesis)

Answer

A

Replication of oropharynx w/primary infection in local lymphoid tissue _^(GALT)
Transient viremia_{^{ (blood)}} can infect CNS
Viruses show Dual tropism
Ex Polio-CD 155 affinity for epi/lymph of gut & CNS
- _{^{Replication in CNS “grey matter” motor neurons ant. horn of SC & brain stem}}
- _{^{Plaques form due to lytic replication w/inflammation by immune response}}
- _{^{Death of these neurons=paralysis of muscles}}

Question 23

Q

Picoviridae-Polio (general)

Answer

A

ssRNA (+) - Naked icosahedral ^{_{(3 serotypes-most infectious is TYPE 1)}}
Transmission: Fecal-oral
High risk: Unvaccinated in early childhood (mild) & adolescent (severe)
Asymptomatic (90-95%) _{^{w/viral shedding}}
Abortive poliomyelitis (5%) 3-4 days mild illness, headache, sore throat, nausea (spont recovery)
Non-paralytic (2%) _{^{Aseptic meningitis-fever, headache, stiff neck}}
Paralytic (1%) _{^{attacks ant horn = flaccid paralysis & Brain cells=life-threatening resp paralysis}}
Post-polio syndrome: _{^{deterioration of neurons affecting muscles (years later)}}

Question 24

Q

Picoviridae-Polio (Clinical)

Answer

A

Diagnose: Cell culture from stool, throat, CSF
Treatment is supportive
Prevention=Vaccine (live & inactive)
Salk vaccine (IPV 1955): Inactivated vaccine safe w/NO mucosal immunity & requires 1+ dose
Sabin vaccine (OPV): Live attenated oral only 1 dose, gives mucosal immunity w/Life long immunity
- SE: Reversion to virulent strain

Question 25

Q

Rhabodoviridae-Rabies (general)

Answer

A

ssRNA (-) Enveloped helical “Bullet shaped”
Transmission: _{^{Bite or body fluids}}
- _{^{Respiratory exposure to bat droppings}}
High risk: Animal handlers & vets
_{^{Neurotropic (cross BBB-infect nerve) due to G-protein spikes}}
- _{^{Glycoprotein surface protein (N-terminal sequence)}}
Diagnosis: Sample saliva, CSF, skin
- _{^{Detect Ag with Immunofluor}}
- _{^{Brain biopsy = Negri bodies (inclusion bodies)}}
Treatment: Passive & active immunization
- _{^{Clean wound w/soap & apply anti-rabies Ab @ site}}
- _{^{Apply human (equine) rabies immunoglobulin (HRIG)}}
^{_{Active Immuno-Inactivated virus (HDCV) made in human diploid cells (Day 1, 3, 7, 14, 28, 60)}}
Animal vaccination=_{^{Live recombo expressing G protein}}

Question 26

Q

Rhabodoviridae-Rabies (Pathogenesis)

Answer

A

Bite/wound multiplication in muscle cells
Passive ascent via sensory & replicates @ dorsal ganglion
Protein G binds to Acetylcholine receptor
Travels retrograde to ganglion neurons to punkinji & other CNS cells
Once brain infected descending infection to other organs

IP _{^{(60days-1year)}}-virus in muscle
Prodrome _{^{(2-10 days)}}-_{^{Virus in CNS/Brain=Fever, pain @ bite}}
Neurologic _{^{(2-7 days)}}-Diffusion of virus w/Ab in serum
- _{^{Hydrophobia, spasms, psychoactive}}
Coma-death HIGH titer in brain/CNS

Question 27

Q

Clostridium Tetani-Tetanus (general)

Answer

A

Gram + spore former-Slender bacillus “Tennis racket” due to terminal spores (local infection)
STRICT anaerobe-Found in soils
_High Risk: _
Trauma/Deep wound
Skin popping drug addicts
Neonatal-Unclean cutting of umbilical cord
Virulence factors:
_{^{Cell produce-Tetanospasmin (AB) carried retrograde to CNS}}
_{^{AB toxin diffuses to inhibitory neurons-Degrades synaptobrevin=NT inhibitor (glycine/GABA)}}
^{_{Result acetycholine secreted continuously=Unopposed contraction}}

Question 28

Q

Clostridium Tetani-Tetanus (Clinical)

Answer

A

Tetanus-Strong muscle contraction _{^{(from top to bottom)}}
_{^{Lockjaw (Trismus) masseter muscles-Spasms (Risus sardonicus)}}
_{^{Drooling, sweating, presistent back spasms (opisthothonos)}}
No loss of consciousness
Localized confined to primary site
Neonatal: infection of umbilical stump _{^{(mortality 90%)}}
Diagnose: Symptoms are best way
Treat: Metronidazole or passive immunization
- _{^{Penicillin inhibits the release of GABA (contraindicated)}}
Tetanus toxoid-_{^{Conj diphtheria toxoid/pertussis-DPT/DaPT}}
- Booster every 10 years

Question 29

Q

Papovaviridae-JC Virus (general)

Answer

A

Slow agent of CNS (gradual onset & fatal)
NAKED ds DNA
80% seropositive humans _{^{(Kidney/brain)}}
High risk: Immunocompromised & cell mediated immunity issues
Treat: Help support immunocompromised def
_{^{Primary replication in tonsils, GI & epi cells of kidney (sheds in urine)}}
Latent infection in kidney-Bcells
_{^{Viremia=Crossing BBB to CNS infect oligodendrocytes & astrocytes}}
- _{^{Loss of white matter-Myelin}}

Question 30

Q

Progressive multifocal leukoencephalopathy (JC)

Answer

A

Occurs in immunodef or immunosupression
Activation of latent infection:
Fatal demylenating disease-white matter _{^{(multiple areas of brain)}}
Progressive weakness (visual, speech & personality)
Diagnosis: Detect JC virus in urine
MRI show lesions non-enhancing white matter lesion

Question 31

Q

Subacute sclerosing Panencephalitis (SSPE)

Answer

A

Slow CNS agent
Serious late neurologic sequela found in measles pts
From defective form of measles virus _{^{(paramyxovirus)}}
High risk: Children younger than 2 _{^{(can appear 7 yrs later)}}
Symptoms:
personality & memory changes
Muscular jerks & blindness

Question 32

Q

Prions (General)

Answer

A

Transmissible spongioform _{^{(neurodegerative)}}
PrP _{^{(proteinacious infectious protein)}}
No nucleic acid-resistant to heat, proteases, formaldehyde, radiation
Normal PrPc found on cell surface _{^{(Alpha helical)}}
PrPsc-scrapie prion altered conformation of PrPc
- _{^{Found in cytoplasm, protease & heat resistant, Beta sheet}}
- Sporadic, acquired, germline mutation (alpha to beta)
Transmission-exposure to infected tissue or medical device, inherited, transplantations, or feeding
*

Question 33

Q

Prions (Pathogenesis)

Answer

A

Lack of antigenicity _{^{(no immune response)}}
Lack of infammation & Interferon production
- _{^{Generation & accumualtion of PrPsc = Neuronal dysfunction}}
Vacuolation of neurons _{^(spongiform)} & amyloid-like plaques/fibrils
Diagnose: EEG, CT, MRI
Prevention: Avoid exposure
Proper sterilization of neurosurgical tools/electrodes
Autoclave (121C for 1hr)
1 M of NaOH

Question 34

Q

Prions (Disease)

Answer

A

Kuru (Ingestion)-_{^{Tremors/Ataxia & later stages dementia}}
_{^{PrPsc plaques in biopsy}}-death 7-9 months after symptoms
High Risk: Cannibals & Autopsy
Creutzfeldt-Jacob (Inherited)- Dementia & tremors in pts 50-70 years old
Amyloid tangles & Spongiform encephalopathy
New variant Cruetzfeldt-Jacob (ingestion): Contaminated beef appeard MORE plaques then CJD
Animal Scrapie = Sheep/goats