catalase negative, B hemolytic, bacitracin resistant, coccus
mostly A hemolytic and optochin resistant in oral cavity and URT
What is S. pneumonia not resistant to?
What is the number 1 cause of dental caries?
changes food to acid, causing tooth decay, making it acid tolerant
gram positive coccus in pairs, fastidious, capsulated, growth enhanced by CO2, A hemolysis on blood agar
colonizes nasopharynx, mostly in children,
removed from airways by ciliated epithelial cells, capsule is primary virulence factor, non encapsulated are harmless
S. Pneumoniae, often preceded with viral illness, high fever, cough, lung pain, rusty sputum as blood leaks from capillaries
Otitis Media (OM)
S. Pneumoniae, 75% of children have one episode by 3rd birthday, severe earache with fever
3 most common with infection of middle ear:
s. pneumoniae (+)
Moraxella catarrhalis(- coccus)
haemophilus influenzae (- rod)
S. Pneumoniae, leading cause of meningitis, higher fatality, never neurological defects
sub acute endocarditis, common in those with damaged heart valves
ID S. Pneumoniae
rusty sputum, produces green color, sensitive to optochin
E. faecalis and E. faecium, gram +, cocci pairs and short chains, high salt, bile, temp, and antibiotic resistant
endogenous infections, nosocomal infections
UTIs in hospitalized patients
What is the bacitracin resistant coccus?
Optochin sensitive streptococci?
A 29 yr old female has dysuria, urgency. urine yields gram +, catalase negative coccus
UTI, catalase positive coccus,
large, gram + rods, non motile/fastidious/hemolytic, form spores= very resistant
What is the capsule of B. Anthracis made of?
greatest bio warfare threat
can't be transmitted human to human, disease of grazing herbivores
What accounts for all the virulence in B. Anthracis?
2 large plasmids; lethal toxin and edema toxin
Action of Anthrax toxin
binds to receptor and forms ring, makes binding sites for toxins, endocytosis, toxins released in human cytosol, adenylate cyclase raises cAMP, brings water in cell, lysis
B. Anthracis, spores in skin, necrosis, edema, move to lymph nodes, very black necrosis tissue with edema
Inhalational Anthrax (woolsorther's disease)
B. Anthracis spores reach alveoli, multiply in mediastinum, blocks lymphatic drainage, respiratory complications, septic shock, blood in sputum, widening on mediastinum on x-ray
oropharyngealor abdominal, muscosal ulcers, sever GI problems: bloody vomiting/diarrhea, almost 100% lethal
ID B. Anthracis
capsule, comma shaped projections, strongly adherent to each other, non hemolytic, non motile, string of pearls
large, facultative, gram +, rods, non-fastidious, B hemolytic on sheep blood agar, spores everywhere in environment, from contaminated food or injuries, produces 2 toxins:diarrheal (slow) and emetic (rapid)
represents all gram + anaerobic spore formers
gram +, spore forming, anaerobic rod, rapid growth, produce 12 toxins: soft tissue infections or gastroenteritis
C. Perfringens, in tissues after surgery, damage to arteries, to reduce O2 supply, not involving muscles, lass aggressive than gas gangrene
C. perfringens, muschle planes without necrosis or systemic symptoms
Clostridial Myonecrosis (Gas Gangrene)
C. perfringens, more common in ag regions, knife and gun wounds, aggressive infections, sudden onset of pain and gas bubbles, foul smell, hemolysis, shock, renal failure, death with in 2 days
C. perfringens, spores germinate in partially cooked food, diarrhea
Necrotizing enteritis and enteritis necroticans (pig-bel)
common in New Guinea in 60s, after pig feast, necrotic destruction of jejunum and ileum, ab pain, bloody diarrhea, shock
round terminal spores with tennis racquet appearance, gram + rod, strictly anaerobes, common in fertile soil, rare in US, most cases in newborns, tetanus toxin
What does the tetanus toxin (neurotoxin) do?
acts at mho-neural junctions and blocks release of GABA to inhibit motor neurons and cause muscle spams
C. Tetani- virulence
spores enter body through wounds, germinate and produce toxins, which migrate along nerves in CNS- muscles are over stimulated (lock jaw), patient in conscious, causes death
C. tetani, in developing countries, crying, truisms, spasms, 90% fatal
spores, produce very potent neurotoxin, prevents Ach release, flaccid paralysis from NT inhibition
4 forms of botulism
mild to severe, blurred vision, constipation, ab pain, no fever, death from respiratory paralysis (10%)
common in infants from ingestion of spores, constipation, flaccid paralysis, honey most common contaminated source
after injury and contaminated soil
rapid onset, bioterrorism concern, flaccid paralysis, outbreak with no common soure, common geo source
gram +, spore forming, rod, anaerobe
diseases in association with antibiotic use, spores survive gastric pH, makes 2 toxins : A enterotoxin; B cytotoxin
Mild C. Dificile
diarrhea, ab cramp, fever, mild leukocytosis
severe c. dificile
peritonitis, marked leukocytosis, highly fatal
C. dificile overgrowth
small gram + coccobacillia in pairs, pathogen that can grow in the refrigeratorm, #1 food borne mortality in US, saprophyte, can infect fetus
L. monocytogenes intracellular life cycle
internalins help internalization, ActA helps build a tail, which propels it intracellularly. immunity is cell mediated- no antibodies
L. monocytogenes, after eating contaminated food, watery diarrhea, fever, nausea, headache
L. monocytogenes disease in pregnant women
bacteria can cross placental layer and infect fetus= stillbirth or premies
L. monocytogenes neonatal disease, abortion, still birth, premies, granulomas in liver, lung, kidney, etc.
gram +, short mycolic acids, non acid fast irregular rods,
gram + pleomorphic rod, non fastidious, colonize nasopharyn and skin through aerosol droplets in crowded areas
virulence due to toxin, tox gene dependent on iron (produced in absence)
What does the C. Diphtheriae toxin inhibit?
protein synthesis, inactivates ribosomes
Local cytotoxicity in C. Diphtheriae leads to...
What does C. Diphtheriae toxin cause?
fatal heart failure and polyneuritis
C. Diphtheriae sore throat and fever lead to difficulty in breathing. presence of pseudomembrane
toxin reaches distant organs, may cause paralysis and congestive heart failrure
gram+ anaerobic rod, non toxic, in pilosebaceous glands, causes acne
considered fungi, branching filamentous, true bacteria with no mitochondria or nucleus, resistant to antifungals
gram +, anaerobic, non acid fast rod in mouth, colon, vagina, low virulence
Actinomycosisdiseases are more common in who?
men, bad hygiene
what do infected Actinomycosis tissues contain?
in soft tissue, abscess, or mass lesion spread to cranium, spine or thorax
few cause human infections, but M. tuberculosis is most virulent
aerobic acid fast bacilli with a complex lipid coat liked to PG layer, grows very slowly, can survive in latent infections for decades
What is arabinogalactan important in?
host interaction and survival
contains long chains of my colic acid that makes acid fastness
1/3 of world infected, mostly africa, asia, E europe, multi drug resistance, spread by air droplets, cell immunity may fight off, but can reactivate when low resistance
during 1st yr after exposure, low transmissibility, lesions, grow in places with high O2 (lungs, kidney). Fever, cough, weight loss
tests for Tb (BCG vaccine gives false positive)
QuantiFERON Tb gold test
blood is mixed with MTB antigens- no false positive from Tb vaccine
slow growing, acid fast intracellular parasite, on skin or linings of nose and throat, children more susceptible
attacks dermis and spreads up nerve sheath to cause loss of sensation
limited, few bacteria, few lesions, pale or slightly red dry and numb to touch
absent CMI, widespread, many more lesions, thickening of peripheral nerves
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