Intro to Bacteria Part 2 Flashcards
Three major species of Staphylococci
S. aureus, S. epidermidis, S. saprophyticus
S. aureus on blood agar
gold pigment, B-hemolytic
Staph catalase test
all positive
Which type of staph is coagulase positive?
S. aureus, elaborates coagulase (activates prothrombin)
S. aureus virulence proteins
Protein A (protects from opsonization), coagulase (fibrin forms around bacteria), hemolysins, leukocidins, penicillinase (B-lactamase), penicillin binding protein
S. aureus proteins that degrade tissues
hyaluronidase (proteoglycans), staphylokinase (lyses fibrin), lipase, protease
S. aureus exotoxins
exfoliation - scalded skin syndrome
enterotoxins - vomiting and diarrhea
TSST-1 - super antigens that bind to MHCII causing massive T cell response
Diseases caused by release of S. aureus exotoxins
Gastroenteritis, TSS, scalded skin syndrome
Diseases caused by direct organ invasion by S. aureus
pneumonia, meningitis, osteomyelitis, acute bacterial endocarditis, septic arthritis, skin infections, sepsis, UTI
Presentation of gastroenteritis
nausea, vomiting, diarrhea, abd pain, fever lasting 12-24 hours
Pathology of TSS
penetrates vaginal mucosa and stimulates TNF and IL1
Presentation of TSS
high fever, N/V/D, diffuse erythematous rash, desquamation of palms and soles
Presentation of staphylococcal scalded skin syndrome
exfoliative toxin A and B, neonates typically affected, cleavage of middle epidermis
S. aureus pneumonia presentation
CA-pneumonia; follows viral influenza with onset of fever, chills, lobar consolidation, destruction of lung parenchyma
Meningitis, cerebritis, Brain abscess presentation
high fever, stiff neck, HA, coma, obtundation, focal neurologic signs
Osteomyelitis presentation
boys < 12 yo, warm, swollen tissue over bone with system fever and shakes
Acute endocarditis presentation
destruction of heart valves with high fever, chills, myalgias; may lead to vegetations on valves and embolization to lungs or brain
Septic arthritis presentation
acutely painful red swollen joint with decreased ROM, often occurs in peds and elderly
Impetigo
small vesicles lead to pustules; honey-colored crust, wet, flaky
Cellulitis
tissue becomes hot, red, shiny, and swollen
Local abscesses
collection of pus
furuncle
infection of follicle that penetrates into subcutaneous tissues
Carbuncles
furuncles bore through to produce multiple contiguous painful lesions communicating under the skin
Blood and Cath infections
S. aureus can migrate from the skin and colonize catheters resulting in bacteremia, sepsis, septic shock
MRSA
multi-drug resistant bug, mecA encodes penicillin binding protein 2A that avoids penicillin damage
CA-MRSA
often occurs among sports teams; skin and soft tissue infections in close contact settings, spreads much more quickly than HA-MRSA, still tends to be susceptible to some oral abx
S. epidermidis metabolism
catalase-positive, coagulase-negative, facultative anaerobe
Common source of S. epidermidis infection
foley catheter, IV line
S. epidermidis virulence
polysaccharide capsule that adheres to variety of prosthetic devices, highly resistant to abx
Common S. epidermidis infections
prosthetic joints, prosthetic heart valves, sepsis from IV lines, UTI, skin contaminant in blood culture
S. saprophyticus
leading cause of UTI second to E. coli among females, coagulase negative
Bacillus characteristics
G+, aerobic, spore forming rods
Bacillus anthracis capsule
only bacterium with capsule composed of protein
How is Bacillus anthracis acquired?
direct contact with infected animals or soil
How are Bacillus anthracis spores activated?
phagocytosed by macrophages, germinate and then become active
Cutaneous anthrax
exotoxin causes localized tissue necrosis, painless round black lesion with rim of edema (malignant pustule)
Pulmonary anthrax
spores taken up macrophages in lungs and transported to hilar and mediastinal LN where they germinate, mediastinal hemorrhage occurs and results in mediastinal widening and pleural effusions
GI anthrax
often results in death, exotoxin causes necrotic lesion with intestine, pt presents with vomiting, abd pain and bloody diarrhea
Three proteins of exotoxin of B. anthracis
Edema factor, protective antigen, lethal factor
Edema factor
active A subunit of exotoxin, increases cAMP which impairs neutrophil function and causes edema
Protective antigen
promotes entry of EF into phagocytic cells
Lethal factor
zinc metalloprotease that inactivates protein kinase, stimulates release of TNF and IL1
Bacillus cereus vs. B. anthracis
B. cereus is motile, non-encapsulated, resistant to penicillin
Major infection associated with B. cereus
food poisoning
Enterotoxins secreted by B. cereus
heat-labile toxin, heat-stable toxin
Heat-labile toxin causes what sxs
nausea, abd pain, diarrhea lasting 12-24 hours
Heat-stable toxin causes what sxs
nausea, vomiting, limited diarrhea
Clostridium characteristics
G+ spore-forming rods, anaerobic
Clostridium is responsible for what diseases?
botulism, tetanus, gangrene, pseudomembranous colitis
C. botulinum produces…
lethal neurotoxin that blocks the release of Ach and causes flaccid paralysis
Adult Botulism is acquired from
smoked fish or home-canned vegetables
Presentation of adult botulism
afebrile, bilateral cranial nerve palsies, diplopia, dysphagia, general muscle weakness, respiratory paralysis and death
Infant botulism is acquired from
food contaminated with C. botulinum spores
Presentation of infant botulism
constipation 2-3 days, difficulty swallowing and muscle weakness; “floppy baby”
Presentation of wound botulism
fever, high white count, cranial nerve palsies, respiratory paralysis
Clostridium tetani
causes tetanus, releases tetanospasmin
tetany
sustained contraction of skeletal muscles
Presentation of tetany
severe muscle spasms especially in jaw, risus sardonicus (grotesque grin)
C. perfringens infections
causes gas gangrene; cellulitis, clostridial myonecrosis, diarrheal illness
Cellulitis/wound infection by C. perfringens
grows and damages local tissue; moist, spongy, crackling consistency to skin (crepitus)
Clostridial myonecrosis (C. perfringens)
C. perfringens in muscle will secrete exotoxins that destroy adjacent muscle, seen on CT as pockets of gas in muscles and subcutaneous tissue
Diarrheal Illness (C. perfringens)
toxin production in gut and subsequent watery diarrhea, can lead to hemorrhagic necrosis of jejunum
Clostridium difficile
associated with abx-associated pseudo-membranous colitis following use of broad spectrum antibiotics
Toxin A C. diff
causes diarrhea
Toxin B C. diff
cytotoxic to colonic cells
Diagnostic tests for C. diff
PCR for toxin A and B, Enzyme immunoassay
Non-spore forming gram positive bacteria commonly present in what patients
pediatric patients
Corynebacterium diphtheriae
responsible for diphtheria; colonizes pharynx, releases toxins into blood stream that damages heart and neural cells
Clinical presentation of Corynebacterium diphtheriae
child with sore throat and fever, dark inflammatory exudate on child’s pharynx
Culture medium for C. diphtheriae
potassium tellurite agar (gray to black colonies), Loeffler’s coagulated blood serum
Diphtheria antiotoxin
inactivates circulating toxin that has not reached target tissue
DPT vaccine
formalin inactivated diphtheria toxin
Similarity between Grp A B-hemolytic strep and C. diphteriae
must be lysogenized by bacteriophage to produce toxin
Rhodococcus equi
G+, aerobic nonmotile, bacillary bacteria; typically infects animals; can form necrotizing pneumonia when inhaled
Characteristic presentation of Rhodococcus equi
upper lobe lung nodules that form air-fluid levels, may stain partially acid-fast
Listeria monocytogenes characteristics
facultative anaerobe, non-spore forming G+ rod
How is L. monocytogenes grown?
low temperatures
L. monocytogenes virulence factor
listeriolysin O, allows bacteria to escape phagolysosomes and avoid intracellular killing
Who is most at risk for L. monocytogenes?
Pregnant women, neonates, elderly, immunocompromised
L. monocytogenes in pregnant women
infection occurs in third trimester, fetus will be infected and may die or be born prematurely with active infection
How may L. monocytogenes be acquired?
contaminated foods such as soft cheeses and cold cuts, through vaginal colonization
L. monocytogenes in neonates
neonatal meningitis presenting 2 weeks post-partum
L. monocytogenes in elderly and immunocompromised
second most common cause of meningitis
L. monocytogenes as a facultative intracellular organism
bacteria able to survive inside or outside of cells, in immunocompetent pts it will be killed via cell-mediated immunity
Major pathogenic G- cocci
N. meningitidis, N. gonorrhoeae
N. meningitidis major disease association
meningitis
N. meningitidis capsule
antiphagocytic polysaccharide capsule
N. meningitidis endotoxin
blebs of endotoxin cause blood vessel destruction and sepsis (petechiae)
N. meningitidis IgA1 protease
cleaves IgA in half
N. meningitidis and iron
bacteria can extract iron from transferrin
N. meningitidis pili
allow attachment to human NP cells and undergo antigenic variation to avoid attach by immune system
N. meningitidis carriers
bacteria is a part of their normal flora of the nasopharynx, develop anti-meningococcal antibodies
N. meningitidis high risk groups
infants 6mo to 2 yo, army recruits, college freshmen
How does N. meningitidis spread?
via respiratory secretions
Classic clue to invasive meningococcal infection
petechial rash, due to release of endotoxin
Meningococcemia
abrupt onset of fevers, chills, arthralgia, muscle pains, petechial rash
Fulminant meningococcemia
Waterhouse-Friderichsen syndrome; bilateral adrenal gland hemorrhage, abrupt hypotension and tachycardia, DIC, coma, death
Meningitis
usually infants <1 yr; fever, vomiting, irritability, lethargy, bulging anterior fontanelle, possibly a stiff neck
Medium for N. meningitidis growth
Thayer-Martin VCN (chocolate agar with antibiotics); vancomycin, colistin, nystatin; increased CO2
Nisseria and maltose metabolism
meningitidis will produce acid, gonorrheae cannot
Second most common STI
gonorrhea
N. gonorrheae pili
have hypervariable aa sequences, protect bacteria from abx and our own immune system, prevent phagocytosis
N. gonorrheae outer membrane protein porins
promote invasion into epithelial cells
N. gonorrheae Opa proteins
promote adherence and invasion into epithelial cells
Presentation of gonorrhea in men
urethritis, painful urination and purulent discharge; epididymitis, prostatitis, urethral strictures
Rectal gonococcal infection presentation
MSM, anal pruritis, tenesmus, rectal bleeding and purulent discharge
Presentation of gonorrhea in women
most likely to be asymptomatic with minimal urethral discharge although they may develop urethritis; reddened and friable cervix, lower abd pain, dyspareunia, purulent vaginal discharge
Pelvic inflammatory disease
infection of uterus, fallopian tubes, or ovaries resulting from gonococcal infection of cervix; pt will present with ffever, lower abd pain, abn menstrual bleeding, cervical motion tenderness
PID and menses
menstruation allows bacteria to spread upward, most cases present within one week of menstruation, IUD will also increase risk
Complications of PID
sterility, ectopic pregnancy, abscesses, peritonitis, peri-hepatitis
Gonococcal bacteremia presentation
bacteria invades blood stream and manifests as fever, joint pains, skin lesions; further complications include pericarditis, endocarditis, meningitis
Septic arthritis due to gonococcal infection
acute fever with pain and swelling of 1-2 joints, increased WBC. G- diplococci
Gonococcal disease in infants
ophthalmia neonatorum, eye infection that may cause blindness
Moraxella catarrhalis is associated with what diseases
otitis media and URI in pts with COPD or in the elderly
G- bacteria known to cause endocarditis
Haemophilus Actinobacillus Cardiobacterium Eikenella Kingella
Enterics
G- bacteria part of normal GI flora or cause GI disease
Main groups of enterics
Enterobacteriaceae, vibrionaceae, pseudomonadaceae, bacteroidaceae
Classifying the enterics
ability to ferment lactose, production of H2S
EMB agar
Methylene blue inhibits G+ bacteria, lactose fermenters become deep purple to black
MacConkey agar
Bile salts inhibit G+ bacteria, lactose fermentors develop pink-purple color
Testing for coliforms
ability to ferment lactose, green colonies on EMB agar
O antigen on enterics
most external component of LPS
K antigen on enterics
capsule that covers O antigen
H antigen on enterics
makes up bacterial flagella subunits
Diarrhea without cell invasion
bacteria bind to intestinal epithelial cells resulting in electrolyte and fluid loss; watery diarrhea without systemic problems (E. coli, V. cholera)
Diarrhea due to invasion of intestinal epithelial cells
toxins destroy cells, WBC and RBC in stool, fever (Enteroinvasive E. coli, Shigella, Salmonella enteriditis)
Diarrhea due to invasion of LN and vlood stream
abd pain, diarrhea containing RBC and WBC, fever, HA, high white count, mesenteric LN enlargement, bactermia, sepsis (S. typhi, Y. enterocolitica, C. jejuni)
Common nosocomial G-‘s
E. coli, K. pneumoniae, P. mirabilis, Enterobacter, Serratis, P. aeruginosa
E. coli virulence factors
mucosal interaction (pili and epithelial cell invasion), exotoxin production (heat-labile, heat stable toxin; shiga-like toxin), Lipid A, Iron binding siderophore
Diseases caused by E. coli
diarrhea, UTI, meningitis, G- sepsis
Enterotoxigenic E. coli (ETEC)
traveler’s diarrhea, LT and ST prevent reabsorption of Na and Cl and stimulate secretion of bicarb and Cl, extreme water loss
Enterohemorrhagic E. coli (EHEC)
shiga-like toxin prevents protein production and leads to cell death; bloody diarrhea with severe abd cramps
Hemolytic uremic syndrome
anemia, thrombocytopenia, renal failure due to E. coli 0157:H7
Enteroinvasive E. coli (EIEC)
bacteria invade epithelial cells and produce shiga-like toxin, systemic inflammatory disease with fever and diarrhea (RBC and WBC)
E. coli UTIs
pili allow E. coli to travel up urethra to bladder and possibly to kidneys, most common cause of UTIs; presents as dysuria, frequency, bladder fullness
E. coli meningitis
common cause of neonatal meningitis after Grp B Strep
E. coli sepsis
most common cause of G- sepsis, often occurs in debilitated hospitalized pts
E. coli pneumonia
fairly common cause of nosocomial pneumonia
Klebsiella pneumoniae
encapsulated, non-motile enteric (no H antigen), can cause sepsis and UTIs especially in hospitalized and debilitated patients (pneumonia)
Presentation of pneumonia due to K. pneumoniae
Hospitalized or alcoholic patient with bloody sputum, violent pneumonia that destroys lung tissue
Proteus mirabilis
very motile, splits urea, cross-reactive with Rickettsia; urine will be alkaline
Enterobacter
highly motile G- rod part of normal GI flora
Serratia
bright red pigment, causes UTI, wound infections, or pneumonia
Shigella species
dysenteriae, flexneri, boydii, sonnei
Shigella characteristics
non-motile, does not ferment lactose and will not produce H2S
Populations often affected by Shigella
preschool aged children, nursing homes
Where is Shigella normally found in the body?
NO WHERE! It is always a pathogen
Shigella action
invade intestinal epithelial cells and release Shiga toxin; often begins with a fever, abd pain, diarrhea (blood and pus)
Shiga toxin
B subunits bind to cell, A subunits inactivate ribosomes
Salmonella
Non-lactose fermenter, mobile, produces H2S
Vi antigen of Salmonella
polysaccharide capsule that surrounds O antigen and protects bacteria from antibody attack
How is salmonella most commonly acquired?
contaminated food or water with animal feces (chicken and eggs in US)
Disease states in human due to Salmonella
typhoid fever, carrier state, sepsis, gastroenteritis
Typhoid fever
invades intestinal epithelial, lymph nodes, and then seeds organ systems; facultative intracellular parasite
Presentation of typhoid fever
1-3 weeks after exposure, fever, HA, abd pain esp in RLQ, enlarged spleen, diarrhea, rose spots on abdomen
Salmonella carrier state
harbor S. typhi in gallbladders
What tissues does salmonella target in sepsis?
Lungs, bone, brain
Salmonella osteomyelitis
sickle-cell patients are most prone due to lack of effective spleen
Yersinia enterocolitica characteristics
G- motile rod that causes gastroenteritis
Which organism is Y. enterocolitica closely related to?
Y. pestis (causes bubonic plague), differs in that enterocolitica is transferred via fecal-oral route
Presentation of gastroenteritis due to Y. enterocolitica
fever, diarrhea, abd pain after ingestion of domestic milk or fecally contaminated water
Vibrio cholera
G- rod with single flagella, fecal-oral transmission
Cholera diarrhea
no epithelial cell attachment, release choleragen and causes rice water diarrhea
Vibrio parahaemolyticus
marine bacterium that causes gastroenteritis after ingestion of uncooked seafood
Campylobacter jejuni
One of the most common causes of diarrhea in the world, zoonotic disease, fecal-oral transmission
C. jejuni diarrhea presentation
fever and HA followed by abd cramps and bloody, loose diarrhea
H. pylori
most common cause of duodenal ulcers and chronic gastritis
Most of our intestinal flora is made up of what bacteria family?
bacteroidaceae, obligate anaerobic G- rod
B. fragilis
no endotoxin, often a common form of abscesses following intestinal laceration
B. melaningoenicus
produces a black pigment when grown on blood agar, involved in necrotizing anaerobic pneumonias due to GI aspiration, associated with periodontitis
Fusobacterium
periodontal disease and aspiration pneumonia, can cause abscesses and otitis media
Anaerobic G+ cocci
peptostreptococcus and peptococcus are apart of the normal flora but can be involved in abscesses and aspiration pneumonias
Pseudomonas aeruginosa
often colonizes very sick patients (wind, wires, wound, water) and is very resistant to antibiotics; G- obligate aerobe, green-blue color with a grape like scent
Common P. aeruginosa infections
pneumonia (CF and immunocompromised pts), osteomyelitis (diabetics, IV drug users, puncture wounds of foot) burn wound infections, sepsis, UTI, endocarditis, malignant external otitis, corneal infections
Burkholderia cepacia
oxidase positive, aerobic G- bacillus; common in CF patients
Actineobacter
aerobic G- found in soil and water; often causes nosocomial infections
