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24 Cards in this Set

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What is the nonspecific response to bacteria?
complement
inflammation:
extracellular-phagocytes
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)
diplococci
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
Sinusitis
Otitis Media
Bronchitis
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
Prevention:
innate-inflammation
adaptive-adherence blocking Ig (vaccination or exposure)
(mult capsular serotypes)
Resolution:
Ig-opsonize to brk capsule
Ig-neutralize enzymes
Clostridium Botulinum: general charac
extracellular
G+ bacilli
Anaerobic
Spore former
Clostridium Botulinum: virulence factors
Spores
hydrolytic enzymes
NEUROTOXIN:
AB toxin-R mediated endocytosis
Cholinergic nn.; block rel of ACh
Flaccid paralysis
Clostridium Botulinum: epidemiology
neutral, alkaline soil: spores
foodborne:
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
NO FEVER
Clostridium Botulinum: Tx
recovery months to yrs
supportive Tx for resp distress
antitoxin-req typing from pt
Clostridium botulinum: prevention and resolution
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
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)
alcoholics
intravenous drug users
homeless
incarcerated
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)
anorexia
night sweats
fever
prevention and resolution of M. Tb
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