Cns Infections

Front 1

What are three infections associated with the CNS and what do they affect?

Back 1

Meningitis - inflammation of the meninges (tissues surrounding the brain)

Encephalitis - inflammation of the brain

Myelitis - inflammation of the spinal cord

Front 2

What is an abscess?

Back 2

a localized area of puss (leukocytes, bacteria, PMNS, serum)

Front 3

What is the causes menigitis?

Back 3

a breakdown of the blood - brain barrier that allows microorganisms to enter the bloodstream (normally a sterile zone).
This causes an inflammatory response (characterized by an increase in neutrophils) in the cerebral spinal fluid and subsequent damage to the brain.

Front 4

what are the two types of meningitis? What are the major characteristics of each?

Back 4

Septic and Aseptic meningitis.

Septic - caused by bacteria; high WBC count (over 1000); high proteins; low glucose level (b/c the immune cells use it for energy to fight off the infection); may be FATAL if untreated.

Aseptic - caused by mycobacterium, viruses, or fungi; normal WBC count (50 - 500); normal/slightly elevated protein; normal glucose levels

Front 5

How is viral meningitis treated?

Back 5

Viral men. is normally self - limiting (goes away on its own) and does not require treatment.

Front 6

What type of meningitis can be a secondary infection in HIV affected individuals?

Back 6

aseptic men.

Front 7

What is the leading cause of bacterial meningitis? What is the second?

Back 7

First: Neisseria meningitidis
Second: Strep. Pneumoniae

Front 8

What are some characteristics of the leading cause of Neisseria men.?

Back 8

respiratory spread (normally carried in the nasopharynx);

type A and C cause epidemic outbreaks;

highest incidence of outbreaks is found in young children;

vaccines are required for colleges/universities and the military

Front 9

What is the morphology of Neisseria meningitidis? Is it aerobic or anaerobic

Back 9

gram negative diplococci
aerobic

Front 10

Why are Lumbee Indians in NC more susceptible to meningitis than others?

Back 10

They are genetically more prone to complement deficiencies

[REMEMBER Immunology: ppl missing late complement components (6-9) can survive but are more susceptible to infections by Neisseria]

Front 11

What are the virulence factors of Neisseria men.?

Back 11

1) Antiphagocytic capsule;
2)LPS and sialic acid residues (make bac. serum resistant --> doesn't activate complement);
3)Hemolysis
4)Pili attach to epithelium

Front 12

What is the basis of Neisseria men. pathogenesis?

Back 12

it has the ability to colonize in the nasopharnyx;
effects of LPS (LOS --> Lipid Oligosaccharides);
it avoids septicemia by being unable to be phagocytosed or cleared by the spleen;
the presence of specific antibody/intact complement cascade

Front 13

What is fulminant meningococcemia?

Back 13

an often fatal septicemia characterized by a hemorragic rash

Front 14

What drug is normally used to treat Neisseria men.?

Back 14

penicillin

Front 15

What vaccines are used to prevent bacterial men.?

Back 15

Rifampin in children (resistance is high)
Ciprofloxacin in adults

Polysac. vaccine for groups A,C,Y, and W135; required for entry into college

Note: vaccine is ineffective in children under 2yrs old.

Front 16

What system does Group B Strep. (GBS) affect? What disease is caused in this system?

Back 16

CNS

meningitis

Front 17

If you were to make a gram stain of GBS meningitis, what would it look like (physical description; ie rod shaped/spherical purple, pink, etc.). What does this mean (technical terms; ie gram -/+,rod, cocci)?

Back 17

spherical and stained purple;

gram pos cocci in pairs and short chains

Front 18

What color would a growth of GBS on a streak plate be? Is this beta or alpha hemolytic?

Back 18

clear; beta hemolytic (weakly)

Front 19

If you were to add a drop of peroxidase to a colony of GBS what would happen? What is this called?

Back 19

no bubbles will form, GBS is catalase negative

Front 20

What are the epidemiological effects of GBS?

Back 20

cause early onset disease in approximately 1:2000 live births [rate of infec. has declined by 80% b/c of guidlines established by the CDC];

transferred by vertical transmission;

causes sever infection in diabetic or immunosuppressed adults

Front 21

What is the cause of virulence in GBS?

Back 21

polysaccharide capsule

Front 22

Does GBS grow aerobically or anaerobically?

Back 22

both, GBS is falcultative

Front 23

What are characteristics of Early Onset disease in GBS?

Back 23

occurs normally in low birth weight babies;

targets the lungs;

bacteremia may occur in the first 3 days of life; children normally have low APGAR scores b/c of poor inspiratory effort;

high mortality

Front 24

What are characteristics of Late Onset disease in GBS?

Back 24

occur in children with a normal birth weight;

occurs btwn 1wk and 2mos of age (most cases are btw 7 and 21 days after birth)

lower mortality rate than in early onset disease

Front 25

How is GBS prevented in newborns?

Back 25

Intraparum antimicrobials are given during pregnancy to women who screen pos for GBS (btwn 86 and 100%)

Front 26

What is the primary treatment for GBS?

Back 26

penicilin

macrolide and clindamycin used in penicillin allergic patients [~30% resistance to macrolide and ~20% resitance to clindamycin)

Front 27

What drug is still in development for prevention of GBS in infants? What should it do? Why hasn't it gone beyond clinical trials yet?

Back 27

Polysaccharide capsular vaccine;

vaccine would be given to the mother and would protect the baby by passive transfer of opsonic Abs against the GBS capsular polysaccaride;

no companies have committed to make the vaccine b/c it would be targeting a relatively small patient population (pregnant women)

Front 28

Which microorganism's eggs does cysticercosis come from?

Back 28

Taenia solium --> pork tapeworm

Front 29

what are some characteristics of the pork tapeworm

Back 29

size: 2 -7m
scolex (knoblike anterior end) --> 4 suckers and an armed rostellum (tubular mouthpart) with hooks
proglottids (segment of tapeworm containing male and female reproductive organs) --> uterus with 7-10 side branches

Front 30

What are two ways to acquire a pork tapeworm?

Back 30

eating undercooked pork

poor hygiene when handling raw pork

Front 31

Where would you be most likely to find cases of Cysticercosis? Why?

Back 31

Mexico and other latin American countries, Africa, India, and China.

Because of either high pork consumption or poor sanitation

Front 32

What problem does Cysticercosis normally cause in Mexico and Central and South America? Does it primarily affect children or adults?

Back 32

causes seizure disorders in adults

Front 33

Do humans get Cysticercosis from eating pork?

Back 33

No, they get it from ingesting T. solium eggs from human feces.

Front 34

What causes cyst formations in people with Cysticercosis?

Back 34

T. solium eggs can't complete their lifecycle in the human body and become encapsulated in the body, forming cysts.

Front 35

What is the life cycle of T. solium eggs in the body?

Back 35

Larval phase (oncosphere/cysticeri) --> larvae penetrate the gut wall and are carried into the bloodstream

Cyst --> Cysterceri encyst in the brain and cause seizures or hydrocephalus

Front 36

How can cystercercosis be confirmed in a lab?

Back 36

positive serilogic test from blood or CSF (combined tests ~85% sensitive)

Front 37

Petichal Rash

Back 37

Lots of tiny bruises. Presents with neisseria meningitis, due to it's hemolytic properties.