Neuro Micro – Flashcards

1. Bacterial Meningitis=Strep pneumoniae, H. influenzae type b, Neisseria meningitidis

2. Neonatal meningitis=Strep agalactiae, E. coli, Listeria monocytogenes

3. Tetanus=Colstridium tetani

4. Botulism=Clostridium botulinum

5. Tuberculoid Leprosy=Mycobacterium leprae

6. Lepromatous Leprosy=

sudden fever

severe headache

stiff neck

nausea, vomiting, confusion, SEIZURES, photophobia, flu-like symptoms

rashes--meningococcal meningitis (Neisseria)

constant crying

poor feeding 

sleeping constantly

irritability

MOPS

Meningitis

Otitis Media

Pneumonia

Sinusitis

also Conjunctivitis

Gram +

alpha hemolytic

OPTOCHIN SENSITIVE

extremely unstable in the environment

Normal flora of URT

spread by respiratory droplets

polysaccharide capsule(antiphagocytic and antigenic)

enzymes (autolysin/pneunmolysin and IgA protease)

Disease mechanism: lungs-->blood-->meninges

-in meninges, they replicate-->mac response (IL-1, TNF-alpha)

Distinguishing features

-prolonged fever (IL-1 is fever inducing)

-hearing loss; hydrocephalus

Diagnosis

-gram stain CSF

-isolate bacteria from CSF (confirmation)

-rapid tests for S. pneumoniae antigens

Prevention

Vaccine conjugate-Prevnar

gram -

non-motile

oxidase +

cat +

aerobic

ferments glucose AND maltose

polysaccharide capsule

Serovars

A=africa

B/C=developing countries and U.S.

W-135

Y

;

lives in respiratory tract

Polysac capsule (can survive in blood)

pili=adherence, antigenic variation, phase variation

LPS=Sialic acid addition (mimic RBCs)

IgA protease

outer memb proteins

winter

close contacts=military, schools, etc.

spread by droplet transmission (15% of healthy ppl carry it in their URT)

;

adhere to non-ciliated columnar ep (1-4 days)-->blood-->meningococcemia/LOS-->septicemia-->meningitis

it survives bc of its capsule!

gram stain of CSF

culture of CSF, blood, or skin lesions

rapid agglutination tests-polysaccharide capsule (for partially treated patients)

Natural immunity-group specific opsonizing ab

quadrivalent meningococcal conjugate vaccine

-protects against A, C, W-135, Y (not B)

pleomorphic gram -

facultative anaerobe

grows on Chocolate agar supplemented with NAD and Factor X

found in URT

polysac capsule

IgA protease

non-immunized kids btw 1 month and 3 yrs

INVASIVE! enters blood then invades meninges

gram stain CSF

culture confirmation (choc agar)

immunological tests to demonstrate abs to capsular antigen

1. Strep agalactiae

2. E. coli

3. Listeria monocytogenes

gram +

beta hemolytic

cell wall antigen=B (GBS) 

CAMP test positive

bacitracin resistant

polysac capsule with sialic acid

C5a peptidase

pre-term delivery

early rupture of membranes

prolonged labor

fever

CAMP test positive

-express a phospholipase-->can synergize with the alpha toxin of S. aureus-->produces an ARROW HEAD hemolysis when put together on a plate

transmission occurs DURING BIRTH

early onset=less than 7 days after birth=pneumonia/bacteremia

late onset=more than 7 days after birth=meningitis

post partum or post-surgical fever and endometritis-->bacteremia-->meningitis

mothers dont usually get this

screening is done 35-37 weeks gestation

gram -

facultative anaerobe

oxidase negative

ferments lactose-MacConkey agar (turns pink)

motile

K antigen=allows organism to adhere to meninges

others: O antigen (LPS), H antigen (flagellum)

Intestinal disease

UTI

neonatal meningitis

nosocomial infections

transmitted DURING BIRTH-->K1 capsular antigen associated with the disease (may promote adherence to brain endothelial cells)

NO intrauterine transfer, unlike Strep agalactiae

short, non-spore forming

gram +

facultative anaerobe

ubiquitous in the environment

CONTAMINATES PREPARED MEATS, COLD CUTS, DIARY PRODUCTS (SOFT CHEESE)

intracellular parasite

grows at 4 degrees-food borne infections

small zone of beta hemolysis

TUMBLING MOTILITY only at 22-25 degrees

1. mother to child

2. food born infection

enters through GI tract-->macs + internalin (host protein) engulf Listeria-->Once inside it is encased in a phagosome-->fuses with lysosome-->should cause death of lysteria, but it doesnt bc of LYSTERIOLYSIN O. This allows it to escape into the cytoplasm of the host cell

ActA=causes formation of actin filaments. Gets a tail, which propels the organism to the cytoplasm of the host cell-->forces a protrusion into an adjacent cell-->produces a phospholipase

Risk factors: impaired cell-mediated immunity (bc it is an intracellular pathogen)

Presentations:

1. Gastroenteritis=48 hrs following ingestion, diarrhea, fever, self limiting, no antibiotics

2. Bacteremia=fever, chills, myalgias

3. Meningitis=in ppl with risk factors

bacteremia

flu-like illness, no CNS involvement

early onset: infection IN UTERO, disseminated disease (sepsis), granulomas, meningitis, DEATH

late onset: acquired AT BIRTH, meningitis in 3rd-4th week, lower mortality

culture from blood, CSF

resistant to cephalosporins!

Immunity=cell mediated!

gram +

anaerobe bacilli-SPORE FORMER

DAMAGED BY OXYGEN (so difficult to send to lab for colonization bc it will be dead)

found in soil and human intestine

C. botulinum=botulism

C. tetani=tetanus

C. perfingens

C. difficile

they are not very aggressive, but elaborate very POTENT NEUROTOXINS

Botulinism=flaccid paralysis

Tetanus=Tetanospasmin... contractile paralysis, opisthotonos (arching of back), Lock Jaw

Eventually people will die bc of inability to BREATH

large, blunt-ended rods

spores look like "TENNIS RAQUET"

anaerobe and motile

causes disease in old ppl--waning immunity

-metalloproteinase blocks the synaptic vesicle release of INHIBITORY NTs

-the toxin has a heavy and light chain-->light chain cleaves synaptobrevin-->prevents inhibitory release

-the spore is inoculated into a wound (where there is little oxygen)-->7-21 day incubation period

-->multiply locally-->releases tetanospasmin

-->taken up by neurons-->retrograde (axonal) transport to CNS

muscle spasm, lock jaw, back spasm, paralysis of back muscles, trouble breathing

childhood immunization

IgG response to neutralize the toxin

7 serotypes (A-G)

spores in soil and fresh water, fruits, veggies, honey, roasted peppers

germinate in anaerobic

BOTulinsm=BOTtles

The toxin is resistant to gastric enzymes

Metalloproteinase acts on presynaptic membranes at NMJs-->blocks the release of ACh

targets peripheral nerves

1. classic=12-36 hrs after ingestion, GI symptoms, blurry vision, dysphagia, PROGRESSIVE DESCENDING SYMMETRIC FLACCIDPARALYSIS

2. infant=2 weeks-8 months, ingest toxin or spore-->germinates in the gut, constipation, lethargy, paralysis, Floppy baby syndrome

3. wound=rare, inoculation of spores, IV drug users

clinical observation

reportable disease

isolating/culturing of organism

acid fast bacilli (pink, Ziehl-Neelson method)

mycolic acid=waxy in nature. They repel gram stain.

slow growth (4-12 weeks)

Aerobes

non-motile

non-spore former

Mycobacterium tuberculosis

Mycobacterium avium-intracellulare

MYCOBACTERIUM LEPRAE

causative agent of Leprosy 

low infectivity; requires prolonged contact!

has not been grown in culture, BUT has been grown on armadillios

rare in U.S. 

majore cause of disease worldwide (tropical and subtropical areas, Asia, Africa)

transmitted by nasal secretions, through nasal mucosa, or through skin lesion

LONG INCUBATION

chronic granulomatous disease, effects peripheral nerves, skin and nasal mucosa

mycobacterium is taken up by MACS and Schwann cells-->replicate-->release PGL-1, which prevents the fusion of a lysosome with a phagosome

-->survival of organism-->body responds by bringing in additional macs and immune cells

-->formation of granulomas

1. Tuberculoid=if individual has a strong immune response

2. Lepromatous=if poor cell-mediated response

granulomatous lesion has extensive epithelium giant cell and lymphocyte infiltration; FEW bacilli

symptoms: large, flattened plaques on the face, trunks and limbs (raised erythmatous edges and dry, pale, hairless centers). Patchy anesthesia

diagnosis=clinically and histologically. Lepromin skin test (type 4 hypersensitivity)