410 exam 3 not old

Mycobacterium TB quick facts

Acid fast

Niehl-Neelsen stain bright red

non motile

obligate aerobe

creates granuloma

takes away muscle and fat

TB transmission: inhalation of an infected droplet, only needs 2-4 bacilli to start an infection

inhalation of an infected droplet, only needs 2-4 bacilli to start an infection

TB macrophage ingestion

Organism multiplies which leads to Th cells to activate IFN, activate macrophages that then activate TNFalpha and the growth of the organism is inhibited or destroyed

What does TNFalpha do?

Trigger inflammy

TB Granulomas

Localized collection of activated macrophages. Could heal, could calcify. Could even be present for life in a healthy person and in an unhealthy one, could liquify or rupture (milliary TB)

TB Infection process

Step 1- Inhalation into the trachea and alveolar air sack

Macrophages uptake (extravaste stage) then activate

Step 2- 2-21 day incubation hang out time

Step 3- T cells and TNFalpha present

Granuloma formation of active TB can either A. night sweats, weight loss, coughing, fever or heal spontaneously or go latent then reactivate causing a constant release of TNFalpha

TB stages of infection

Start

extravasale: early tubercle, pass through vessel walls

tubercle

Rupture: Milliary or ghon complex

TB clinical symptoms

Weight loss

night sweats

bloody sputum

chronic cough

TB How is it diagnosed?

Specimens collected from sputum or other infected sites

TB How is it cultured for diagnosis

Egg based lowenstein jensen media

PPD test: purified protein derivative of lepromin

TB 2 phases

Sensitization phase: First exposure

Effector phase: Delayed hypersensitivity reaction

TB treatment

Chemo

Directly Observed treatment

Vaccination of BCG

M TB still aka GA Hansens

Describes the granuloma

Outler layer or epithelial cells

T cells

macrophages

giant cells

M TB and Caseum in inner most layer

TB Where does it attack?

Attacks all senses

Goes after Motor, sensory, and autonomic nerve cells and replicates in histocytes and schwann cells

TB leprosy General information

Paucibacilliary: Has few localized bacteria,

Positive lepromin test

Negative SSS test

Makes granulomas

Lepromataus leprosy general information

Highly contagious

visible lesions

Attacks ulnar nerve in elbow and knee

No or bad T cell response

epiphora: tears running down face

negative lepromin test

M TB treatment

2 drugs for 6 months, up to 2 year treatment

Lepromatous TB treatment

3 drugs for 30 months, up to 2 year treatment

S. pneumonia general facts

Encapsulated: Mucoid, virulent

Nonencapsulated: Flatter, rough, dry

Attacks both alternative and classical pathways

S. Pneumoniae virulence factors

Capsular polysac

Pneumolysin: Form pores

Adhesions: CbpA

S. pneumoniae pathogeniss

Colonization: adhesins and pneumolysin

Tissue destruction: Activation of alt and classical pathways

Evades immune system: Capsule, pneumolysin

S. Pneumoniae targets

Middle ear: Otitis

SInutis

Lungs

bacterenmia

Mengitis

S. pneumoniae 2 types

Lobar: Localized in the lung

Bronchial: all over the lung

S. pneumonia pathogenesis of meningitis

Nose throat colonization: Impaired defenses, aspiration

Lung

Bloodstream

CbpA adhesions

Receptors: Polymeric immunoglobulin receptor

Causes inflammation: From bacterial lysing, triggers IL 2 to attract macrophages

S. pneumoniae meningitis diagnoses

Blood test

CSF test

Clinical eval

Quelleng reaction

S. Pneumoniae prevention/vaccines

PPSV23 poly: 23 different polysaccharides, contains T independent Ag to stimulate B cells without T cells. Not for kids cause their immune system is weak

Prevnar14: 13 different polysaccs, conjugated to non toxic inactivate diphtheria toxin T cell dependent immune response with antibody production

S. Pneumoniae treatment

Anti-inflammy for meningitis in combo with

Antibiotics: pencilly

Listeria- silent killer of fetuses

Too toasty at 37 c

Actin based spread to spread through the zipper/exclusive entry

Listeria virulence factors

Internalins: InlA binds to E-cadherins

LLO: Forms pores

Catalase: Allows to hang in macrophages

Actin rockets

Listeria, how does it spread?

LLO forms pores with phospholipase

Attach to ActA for actin to boost for intracellular mobility, avoiding extracellular phase

Escapes to another cell

Listeria pathogenesis

Cells pinch off from Villus area

Listeria gets in

Peyers patch: Sample cell uptake pathogen

M cells do something

Listeria pathogensis

Invades intestinal mucosa

Enters circulation

Pathway 1: Spread to organs in immunocompromised person

causing a systemic infection, meingitis

Pathway 2: Cleared by macrophage in healthy people

Pathway 3 (focus): pass through placenta, infects fetus

still birth or birth defects

Listeria infection in fetus

InlA bingds to e-cadherins in syncytiutrophoblasts that contains tryptophan. W regulates T cells, low W enviornment prevents T cell response and causes immune tolerance

Listeria clinical symptoms

Tropism for CNS

Meningitis

Vommie

Fever

Listeria diagnoses and preventation

Gram stain, CSF or blood culture

Proper storage of cheese

Pregnant people avoid deli meat

Listeria treatment

Penicilly

B. Anthracis general info

soil is reservoir

B. anthracis virulence factors

Weird poly y thing

Edema toxin: Acts as adenylate cyclase EF to more cAMP to activation of PKA to activation of NFkappaB

Lethal toxin: Cleaves MAPK, lots of phosphorylation switches

Capsule

B. ANthracis toxin type

compound AB toxin

Furin cleaves PA to PA20 and PA63

B. anthracis toxin receptors

CMG2 located in the gut

B. Anthracis 3 types

Cutaneous: necrotic eschar (black scab), edema

Inhalation: Mediastinal swelling chest x ray for diagnoses

Gastrointestinal: Ulcer

B. Anthracis diagnoses

Gram stain, smear

B. anthracis prevention

Strict control of handling wool and hide

Food regulations concerning meat

B. Anthracis treatment

Combo meds for 60 days cause of spores

penicilly, cipro, doxycli

B. Anthracis vaccine

US version: Nonencapsulated, adjuvant, need repeat doses

fear of contamination from EF or LF

not really used

B. Pertussis Virulence factprs

Adhesions to ciliated cells (main target)

Pili

Pertractin

Pertussis toxin type

Complex AB

A: Adp ribosylation

B

Tratcheal cytotoxin: kills ciliated cells

Dermonecrotic toxin that causes lesions

Pertussis method of infection

ADP ribosylates Ginhibitory when bound to GDP

cAMP turns on PKA that phosphorylates to turn on Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) which causes Cl- to export which causes fluid build up

Pertussis virulence Gene regulation

2 component regulatory system

BvgA phosphorylated:

Low amounts yields adhesins

high amount yields: toxin

Pertussis pathogenisis

Exposure through aerosols

Attach to ciliated cells of bronchial

Immobilized cilia from toxin

Replication

Toxin production

Pertussis diagnosis and culture

Marked lymphocytes in paroxymal stage

Cultured on Bordet-gengou agar

Pertussis vaccine/prevention

DPT

DTaP

Pertussis Treatment

Antibiotics: Enthromycin depends on when caught

Diphtheriae toxin type

Simple AB

A: Adp ribosylation, steals adp ribose and attaches to EF2

B: Binds to HB EGF (common in heart and nerve cells)

Diphtheriae where go?

Kidneys

Heart

Nervous system

Diphtheriae targets

heart and nerve cells

Diphtheriae diagnosis

Clinical eval

Grown on cysteine tellurite

Elek test

Diphtheriae clinical symptoms

Shortness of breathe

irregular heartbeat

neurological symptoms

Pseudomembrane

Eschar- black scab

Diphtheriae Prevention/treatment

DPT shot: has inactivated Diphtheriae

Schick test: to test immune system response

Diphtheriae treatment

Antitoxin from horse, can trigger serum sickness

Tracheotomy: if pseudomembrane

Antibiotic

C. Botulinum toxin type

Simple AB

A- protease

B

C. botulinum target nervous system

PNS

C. botulinum target for A and B toxin

A: SNAP25 of snare complex

B: synaptobrevin of snare complex

Attacking the Na+ channel excitatory

C. botulinum prevents the release of what?

Acetylcholine

C. botulinum clinical presentation

Vommie

Disarrhea

Flaccid paralysis

C. botulinum prevention

No bad cans

For the love of God no honey for babies

C. botulinum treatment

Antitoxis

C. tetani toxin type

attacks umbilical stump

Simple AB

A- protease

B

C. tetani target nervous system

CNS

C. tetani attacks where

Synaptobrevin of the SNARE complex in neuro transimtters

(Cl- inhibitory channel)

C. tetani prevents the release of ?

GABA

Glycine

C. Tetani clinical symptomes

Back spasms

Lock jaw

Spastic paralysis

C. tetani prevention

DTaP vaccine

C. Tetani treatment

wound debridement to aerate the bacteria

tetanus antibody

Vaccine

antibiotics