Immune Response Against Bacteria

Front 1

What is the nonspecific response to bacteria?

Back 1

complement
inflammation:
extracellular-phagocytes
intracellular-NK cells

Front 2

Specific response to bacteria?

Back 2

TH1: intracellular- DTH, CTLs, ADCC

TH2: extracellular- Ig to opsonize, activate complement, ADCC

Front 3

what happens when the innate system fails for extracellular bacteria and/or their products?

Back 3

APCs present Ag to TH0 and B cells
MC and APCs rel early cytokines for T cell differentiation, activation (TH2, IL4)
Humoral response- Ig

Front 4

What are the antibacterial roles of Ig?

Back 4

1. Block attachment/neutralize: bind fimbriae, lipotechoic acid, capsules
2. Block proliferation: Trigger complement mediated damage of G- (MAC) and activate Classical Complement Path (Ig-Ag complex); Inhibit transport mxns and receptors
3.Allow phagocytosis: Ig to M protein and capsules for opsonization via FcR (also ADCC) and C3R; Ig neutralize immunorepellents
4. neutralize toxins
5. Prevent dissemination: neutralize spreading factors, enzymes

Front 5

Streptoccocus pneumoniae: general characteristics

Back 5

Extracellular (doesnt invade)
G+ with thick CAPSULE (antiphagocytic)
diplococci

Front 6

Strep pneumoniae: virulence factors (enzymes)

Back 6

elastase- cleaves Ig (IgA) and complement
pneumolysin- pore forming toxin; destroys host tissue
mucinase- decr viscosity of mucus; allows dissemination
neuraminidase- invasion of alveolar tissue (not cells)

Front 7

Strep pneumoniae: how acquired and spread (epidemiology)

Back 7

spread person to person via resp. droplets
colonize in nasal pharynx
spread AFTER colonization with weakened immune system
EX: smoking, alocoholism, previous resp infection, COPD

Front 8

Strep pneumoniae: clinical disease

Back 8

Sinusitis
Otitis Media
Bronchitis
Pneumonia- if aspirated down bronchi into lung tissue of pt with weak immune system, can't clear infection

Front 9

Describe pneumonia assoc with Strep pneumoniae

Back 9

typical pneumonia:
SOB (exudate), pain with inhalation, productive cough
Lobar pneumonia
Infection in alveolar spaces
Pneumolysin- leak RBCs, PMNs, MPh into alveoli---> prod cough; thin (mucinase), blood-tinged
Severe shaking chills, fever 39-41C (IL-1,6, TNF a)
consolidation of BOTH lungs

Front 10

Strep penumoniae: prevention and resolution

Back 10

Prevention:
innate-inflammation
adaptive-adherence blocking Ig (vaccination or exposure)
(mult capsular serotypes)
Resolution:
Ig-opsonize to brk capsule
Ig-neutralize enzymes

Front 11

Clostridium Botulinum: general charac

Back 11

extracellular
G+ bacilli
Anaerobic
Spore former

Front 12

Clostridium Botulinum: virulence factors

Back 12

Spores
hydrolytic enzymes
NEUROTOXIN:
AB toxin-R mediated endocytosis
Cholinergic nn.; block rel of ACh
Flaccid paralysis

Front 13

Clostridium Botulinum: epidemiology

Back 13

neutral, alkaline soil: spores
foodborne:
food intoxication, infection due to consumption of toxin
common in very young children

Front 14

Clostridium Botulinum: clinical disease

Back 14

Weak, dizzy, dry mouth, blurred vision, diplopia, dysphagia, constipation
bilateral descending paralysis
NO FEVER

Front 15

Clostridium Botulinum: Tx

Back 15

recovery months to yrs
supportive Tx for resp distress
antitoxin-req typing from pt

Front 16

Clostridium botulinum: prevention and resolution

Back 16

prevention:
no vaccine b/c many strains
innate- pinocytosis to remove toxin
inflamm to remove spores/active cells
adaptive- Ig to neutralize toxin (from previous exposure); Ig to block adherence of vegetative cells

Resolution: Ig to neutralize toxin

Front 17

general charac mycobacterium tuberculosis

Back 17

facultative intracellular (can be extracellular to move; contributes to ability to evade intracellular destruction by phagocytes)
acid fast
strict aerobe

Front 18

virulence factors for mycobacterium tuberculosis

Back 18

intracellular growth
no enzymes, toxins

Front 19

epidemiology m. tuberculosis

Back 19

reservior: mainly humans; other animals also sources
aerosol transmission (resp droplets)

Front 20

what are some populations that are at high risk for ACTIVE m. tuberculosis?

Back 20

immunocompromised (TH1)
alcoholics
intravenous drug users
homeless
incarcerated

Front 21

clinical disease: primary Tb

Back 21

in immunologically naive ppl
mid-low lungs
tubercle-infected MPh, surr by langerhans, epitheliod cells, lymphocytes (TH1, DTH rel IFN to upreg MPh intracell killing)
active replication 3-6 weeks, then dormant
disease may stop here (dep on infectious dose and host immune competence)
insig clinical findings if stopped
pos PPD and Xray w/ granuloma

Front 22

clinical disease: secondary Tb

Back 22

in previously exposed ppl with weak immune system
microbe brks out of granuloma
moves to upper lungs (high O2)and is reactivated
initiates 2ndary immune response->cavitating lesions (bystander damage)

Front 23

what are sx of 2ndary Tb?

Back 23

blood in sputum
cough( highly contagious)
anorexia
night sweats
fever

Front 24

prevention and resolution of M. Tb

Back 24

prevention:
innate-inflammation (wall off)
adaptive-BCG vaccine for areas with high prevalence; adherence-blocking Ig
resolution:
adaptive-DTH for intracellular phase; opsonizing Ig for extracellular phase