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24 Cards in this Set

  • Front
  • Back
What is the nonspecific response to bacteria?
intracellular-NK cells
Specific response to bacteria?
TH1: intracellular- DTH, CTLs, ADCC

TH2: extracellular- Ig to opsonize, activate complement, ADCC
what happens when the innate system fails for extracellular bacteria and/or their products?
APCs present Ag to TH0 and B cells
MC and APCs rel early cytokines for T cell differentiation, activation (TH2, IL4)
Humoral response- Ig
What are the antibacterial roles of Ig?
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
Streptoccocus pneumoniae: general characteristics
Extracellular (doesnt invade)
G+ with thick CAPSULE (antiphagocytic)
Strep pneumoniae: virulence factors (enzymes)
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)
Strep pneumoniae: how acquired and spread (epidemiology)
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
Strep pneumoniae: clinical disease
Otitis Media
Pneumonia- if aspirated down bronchi into lung tissue of pt with weak immune system, can't clear infection
Describe pneumonia assoc with Strep pneumoniae
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
Strep penumoniae: prevention and resolution
adaptive-adherence blocking Ig (vaccination or exposure)
(mult capsular serotypes)
Ig-opsonize to brk capsule
Ig-neutralize enzymes
Clostridium Botulinum: general charac
G+ bacilli
Spore former
Clostridium Botulinum: virulence factors
hydrolytic enzymes
AB toxin-R mediated endocytosis
Cholinergic nn.; block rel of ACh
Flaccid paralysis
Clostridium Botulinum: epidemiology
neutral, alkaline soil: spores
food intoxication, infection due to consumption of toxin
common in very young children
Clostridium Botulinum: clinical disease
Weak, dizzy, dry mouth, blurred vision, diplopia, dysphagia, constipation
bilateral descending paralysis
Clostridium Botulinum: Tx
recovery months to yrs
supportive Tx for resp distress
antitoxin-req typing from pt
Clostridium botulinum: prevention and resolution
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
general charac mycobacterium tuberculosis
facultative intracellular (can be extracellular to move; contributes to ability to evade intracellular destruction by phagocytes)
acid fast
strict aerobe
virulence factors for mycobacterium tuberculosis
intracellular growth
no enzymes, toxins
epidemiology m. tuberculosis
reservior: mainly humans; other animals also sources
aerosol transmission (resp droplets)
what are some populations that are at high risk for ACTIVE m. tuberculosis?
immunocompromised (TH1)
intravenous drug users
clinical disease: primary Tb
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
clinical disease: secondary Tb
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)
what are sx of 2ndary Tb?
blood in sputum
cough( highly contagious)
night sweats
prevention and resolution of M. Tb
innate-inflammation (wall off)
adaptive-BCG vaccine for areas with high prevalence; adherence-blocking Ig
adaptive-DTH for intracellular phase; opsonizing Ig for extracellular phase