Microbes Lecture 21 Nervous System

What protects the CNS?

Meninges

Meninges

Layers of tissue that seperates bones from the brain/spinal cord

3 layers of meninges

Dura matter- under bone

arachnoid matter - middle layer. has subarachnoid space (between arachnoid and pia amtter) where CSF flows

Pia matter- cloest to brain/spinal cord. contains blood vessels to suplly nutrients to brain/spinal cord.

Blood brain barier

tighly joined cells that serve as a barrier to prevent entry of microbes and large molecules into spinal fluid

Spinal fluid should be…

sterile

neuroglila

provide support, protection, and nutrients for CNS

How can some bacteria pass blood brain barrier

certain virulence factors. viruses have easier time passing BBB because they are smaller.

NS infections are usually aquired when…

there is a problem or injury with the immune system

meninigitis

inflammation of meninges

encephalitis

inflammation of brain

meningioencephalitis

inflammation of meninges and brain

is bacteria or viruses more likely to cause CNS infections?

viruses

CSF function

shock absorber, provides nutrients, electoryles, and oxegyn to nervous tissues and removes waste products

CSF normal appearance

clear and colorless

CSF normal pressure

70-180 mm H2O

CSF normal total protein

15-60 mg/100 mL

CSF normal glucose

50-80 mg/100mL

CSF normal cells

0-5 WBCs; no RBCs

how is CSF collected?

Lumbar puncture (aka spinal tap)

how to microbes get in the CNS?

• Trauma, medical procedures,

• axonal transport in peripheral neurons (movement of mitochobdria, lipids, and proteins to and from a neurons cell body),

• microbes in blood or lymph penetrate BBB and infect cells of meninges

signs and symptoms of bacterial meningitis

• headache

• nausea vomitting

• irritability

• drowsniess, confusion, lethargy

• photosenstivity, seizures

• stiff neck

• sudden high fever

• abnormal CSF values

• can leasd to encephalitis and cause deafness, blindness, coma, or death

• rapid progression

bacterial meningitis can lead to

encephalitis (inflammation of the brain; can cause deafness, blindness, coma, or death)

major causitive agents of bacterial meningitis

• N. meningitidis

• H. influenzae

• S. pneumoniae

• S. agalacticae

• L. monocytogenes

Neisseria meningitidis infection age range

Infants and adolescents

is there a vaccine for Neisseria meningitidis

yes

route of infection for Neisseria meningitidis

Enters through nasopharynx (fimbriae) → capsule protects from phagocytosis
→ “blebbing” causes release of lipooligosaccharides (lipid A) → inflammation,
fever and vasodilation

Haemophilus influenzae infection age range

Children and elderly

Neisseria meningitidis transmsiion

inhilation of respirtory droplet

Myelitis

inflammation of the spinal cord. disrupt nerve transmisson

Neisseria meningitidis virulence factors

• fibrae (attatch to nasopharyngeal mucosa)

• capsule (avoid phagocytosis)

• LOS (released during blebbing; contains lipid A an dtriggers inflammation, fever, and vasodilation)

Neisseria meningitidis clinical manifestations

• headache, stiff neckphototphobia

• cognitive impairment, hearing loss, epilespsy

• can cause menigoccemia

  • purpura and petechial rash

  • septic shcok

  • DIC (dissemenentied intravascular coagulation)

Lab testing for bacterial meningitis findings

Cloudy CSF, low glucose, high protein, oincreased pressure, WBC in CSF

is there a vaccine for Haemophilus influenzae

yes

Haemophilus influenzae virulence factors

Capsule, IgA proteases, fimbriae, LPS

Haemophilus influenzae can cause hich infections

meningitis,septicema, pneumonia, pericarditis

Streptococcus pneumoniae infectionb age range

children and elderly

does Streptococcus pneumoniae have a vaccine

yes

Streptococcus pneumoniae virulence factors

toxins, capsule, and phosphorylcholine (mediates cell adehsion)

Streptococcus pneumoniae infection spread through

inhalation of respirtory droplets

Streptococcus agalactiae infection age range

infants

Streptococcus agalactiae infection route

vertical transmission from mothert to baby during birth

Streptococcus agalactiae causes

neonatal meningitis

is there a vaccine for Streptococcus agalactiae

no

Listeria monocytogenes infection age range

neonates, pregnant women, elsderly and immunocompromised

important factor to note of Listeria monocytogenes

grows at 4 degree C (refrigeration temp)

Listeria monocytogenes enters body through

contaminated food or drinks

Listeria monocytogenes pathogenesis

induces phagocytosis but escapes phagosomes → multiplies intracellularly → reaches bloodstream and CNS.

dangers of Listeria monocytogenes in pregnant women

can cause spontaneous abortion and stillborn

dangers of Listeria monocytogenes in newborns

can cause meningitis in newborn

why would a pregant woman be told not to eat certain meats?

want to avoid high risk foods for Listeria monocytogenes

Listeria monocytogenes associated with what foods

fresh cheeses, deli meats, leafy greens

Listeria monocytogenes can survive

refrigeration and high salt concentrations

botulsim caused by

toxins form clostridum botulinum

virulence factor of C.botulinum

endospores

botulism associated with

home canned goods

botulism disease is not the result of infection, but more so

result of intoxication that affects neurons of peripheral NS

botulism pathogensisis

irreversibly binds to neural cytoplasmic meemreabnes, thus preventing vesicle fusion between AcH secretion into synaptic cleft between neuron and muscle cell which presents muscle contraction causing flaccid paralysis

foodborne botulsim

• ingestion of botulism toxin in food

• blurred vision, constipation, abdombinal pain, nausea

• paralysis of skeletal muscles

• paralysis of diaphragm may occur, causing death

infant botulism

• ingestion of bacteria or endospores

• dont give baby honey because spores survive well in honey

• constipation, failure to thrive,muscle weakness, diffuculty breathing

• floppy baby syndrome

wound botulism

• traumatic inoculation (ex open wound)

• presentation similar to foodborne

botulism prevention

proper canning, cooking, prevent eating foods from swollen cans, avoid feeing honey to infants

tetanus caused by

clostridum tetani

tetanus infection route

through deep breaks in the skin with soil contaminated with endospores

tetanus pathogensis

tetanospasmin irreversibly blocks release of inhibitory neurotransmitters preventing muscle relaxtion causing spastic paraylsis

tetanus clinical presentation

• constant muscle contraction

• lock jaw (tight jaw and neck muscles)

• sweating, drooling, grouchiness

• back spasms

• arching of back and extremeties

• contraction of diaphragm prevents exhalation

is there a vaccine for tetanus

yes! DTaP

conjunctivitis

inflammation of conjunctiva. aka pinkeye

keratitis

inflammation of cornea

some pathognes thta cna cause diseases of eye

Chlamydia trachomatis,
Streptococcus pneumoniae,
Staphylococcus aureus

which causes more NS diseases? bacteria or viruses

viruses

poliomyelitis

virus. causes polio

poliomyelitis spread by

fecal-oral route

poliomyelitis pathogensis

is ingested, binds to intestinal cells, moves to skeletal muscle and replicates, progresses up motor neurons to CNS, lysis of infected neurons causes severe inflamation, attacks spine and brain

polio can lead to

paralysis

poliomyelitis virulence factors

non eveloped, protein coat protects form stomach acid

is there a polio vaccine

yes

signs of polio

• flu-like symptoms

• muslce weakness and paralysis

  • can be symmetric or asymmetric

• complete flaccid paralysis

rabies transmission

direct contact with saliva or brain/nervous system tissue. zoonotic disease spread between people and animals

rabies symptoms

• pruitic, painful, and hypersenstive lesion at site of infection

• vomiting, anxiety, agitation

• encephilitis, hydrophobia, aggressiveness, paralysis

rabies mechanism

shut down neuron functioning. over 2-12 months replicated in muscle cells, reaches PNS and travels to CNS, invades brain cells and goes back to PNS, replicates and shed from tissues that are well supplied with nerves (ex salivary glands)

Variant Creutzfeldt-Jakob Disease (vCJD) causitivr agent

a prion

Variant Creutzfeldt-Jakob Disease (vCJD) other names

mad cow disease or bovine spongiform encephalopathy

vCJD pathogeneiss

Abnormal CJD prion proteins serve as an enzyme that refolds normal prions into
abnormal prions, which continue the process, progressing causing brain damage

vCJD transission

Transmitted through the ingestion of infected meat, organ transplant, or transfusions.

vCJD causes

destruction of brain tissue, loss of motor control, memory failure, cognitive
impairment, muscle spasms, spongiform lesions in brain