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three general groups
endospore formers
non endospore formers
irregular shaped and staining properties
bacillus anthracis
anthrax
when spores enter the body
develop under all condistion
bacillus anthracis found where
soil, domestic and wild animals
types of bacillus anthracis
cutaneous: spores enter through skin
pulmonary: inhalation of spores
gastrointestinal: ingested spores
injection: in heroin users in north europe
clostridium perfringens found in
spores found in soil, human and animal intestine
common in raw meet and poultry
clostridium perfringens causes
food poisoning
gas gangrene
food poisoning
outbreaks linked from hospitals or foods where food is kept warm for a long time
enterotoxins: cause diarrhea
gas gangrene pathology
not invasive, needs damage tissues and anaerobic conditions
exotoxins: released caused much of damage gangrene
fermentation of carbs cause gas and tissue destruction
clostridium tetani location
soil and Gi tract of animals
common w/ geriatric patients, drug abusers and neonates
pathology of clostridium tetani
cause tetanus/ lock jaw
spores enter through puncture wounds, burns, frostbite, etc
need anaerobic environment
tetanospasmin
death by paralysis of respiratory muscles
tetanospasmin
neurotoxin block release of acetylcholine used in muscular contraction inhibition
treatment for clostridium tetani
antitoxin therapy
inactivate circulating toxin
muscle relaxants
penicillin or tetracycline
C. Diff location
normal resident of colon
C diff pathology
antibiotic killing other bacteria which makes C. Diff grow
dysbiosis
cause: antibiotic associated colitis
enterotoxins, diarrhea
clostridium botulinum
spore forming, anaerobe
found in soil and water, canned food
cause botulism
pathogenesis of botulism
spores present on food due to improper handling
anaerobic conditions
botulin is released
botulin toxin
blocks acetylcholine necessary for contractions
symptoms: flaccid paralysis
death: respiratory failure
infant botulism
ingested spores that germinate and release toxin
flaccid paralysis
listeria monocytogenes
non spore forming gram positive
1-4 flagella w/ no capsules
resist: cold, heat, salt, pH and bile
listeria monocytogenes virulence
indue phagocytosis and avoids humoral immune system
listeria monocytogenes pathology
reservoir is soil, water and animal intestine
contaminate food
listeriosis
listeriosis
dairy and poultry meat
epidemiology of listeria monocytogenes
patients, fetuses, neonates
corynebacterium diphtheriae epidemiology
reservoir of healthy carriers
cases occur in non immunized children
acquired from respiratory droplets
corynebacterium diphtheriae pathology
local infection
diptherotoxin and toxemia
local infection
upper respiratory tract inflammation
sore throat, vomit, swollen lymph nodes
cutaneous diphtheria as ulcers is possible
diptherotoxin production and toxemia
pseudomembrane formation from inflammation and excess fluid across pharynx can cause asphyxiation
toxin absorbed into blood targets heart and nerves
mycobacteria characteristics
gram + irregular bacilli
acid fast
strict aerobes
catalase
mycolic acids and unique peptodoglycan
mycobacterium tuberculosis
no exotoxins or enzymes
tubercle bacillus
virulence factors of mycobacterium tuberculosis
complex waxes
cord factor
prevent destruction by lysosomes or macrophages
tuberculosis epidemiology
improper health
15 mil carries in the US
very resistant
transmitted by airborne droplets
primary TB
ID: 10
multiple intracellularly
after 3-4 weeks form tubercles
tubercles
granulomas consist of central core containing bacilli surrounded by WBC
secondary TB
reactivation of bacilli
tubercles expand and drain into bronchial tubes and upper respiratory tract
60% mortality rate
extrapulmonary TB
bacilli disseminate to regional lymph nodes, kidneys, long bones, genital tract, brain and meninges
mantoux test
injection of PPD
look for induration: red wheal to form
size of wheal indicates result
interferon-gamma release assays
blood test for TB detection
used when there is a previous vaccine or lack of time
types of diagnosis for tuberculosis
in vivo
x rays
identification of acid fast bacilli
culture isolation and biochemical testing
mycobacterium leprae
strict parasite
multiples in host cells in large packets (gobi)
cause leprosy: beings in skin moves to nerves
epidemiology and transmission of leprosy
transmission not verified
not virulent its based on health and living conditions
course of infection for leprosy
weak macrophage or slow T cell response: wont kill bacillus
grow slow in schwann and macrophages
tuberculoid
shallow lesions damage nerves
loss of pain reception
lepromatous
deep nodular infection
face and extremities disfigurement