Microbiology: Gram Negative Bacteria Flashcards
(31 cards)
Types of E-coli
1) enteroinvasive E. coli (EIEC)
- invades intestinal mucosa and causes necrosis I and inflammation (can be bloody of watery diarrhea)
2) enterohemorrhagic E. coli (shiga-like toxin form) (STEC)
- most common serotype and is O157:H7
- produces shiga-like toxins which destroy GI tract tissues
- can cause hemolytic uremic syndrome (infection of kidneys after GI infection which causes apoptosis of glomerular and endothelial cells. also produces schistocyte red blood cells).
- symptoms: low grade-fever, bloody diarrhea, confusion, jaundice, ab pain
3) enterotoxigenic E. Coli (ETEC)
- uses heat liabile and heat stable enterotoxin s in the GI system (causes intestinal inflammation and watery diarrhea (NO BLOOD))
4) Enteropathogenic E. Coli (EPEC)
- similar to #1, but only seems to target yrs <2
- causes destruction of cell cytoskeleton which causes flattened cells that cant absorb water properly (watery diarrhea, NO BLOOD)
5) Uropathogenic E. Coli (UPEC)
- causes 90% of community UTIs and 50% hospital acquired UTIs
- cystitis is almost always shown
- ONLY ONE to not cause diarrhea
Treatment:
- doxycycline/cotrimoxazole (severe only)
- supportive care
- plasmapheresis/ corticosteroids (only in STEC with HUS present)
What are some diagnostic special agars and the respective pathogen they help diagnosis?
Eosin methylene blue: E. Coli
Cystine- telluride: diphtheria
Triple sugar iron agar: Salmonella species, yersinia enterocolitica
MacConkey agar: E. Coli, enterobacters, klebsiella (any (+) lactose fermenters)
Buffered Charcoal yeast extract (BYCE) agar: legionella, tularemia
Cefsulodin-irgasan- novobiocin (CIN) agar: yersinia enterocolitica
Thayer-Martin agar: Neisseria species
Chocolate agar: Haemophilus influenza and ducreyi, tularemia
Hemolytic uremic syndrome (HUS)
Caused by STEC E.coli O157:H7.
Causes the following the triad of symptoms:
- anemia
- thrombocytopenia
- acute kidney damage (proteinuria/hemouria/uremia)
What subtypes of E. Coli can cause bloody diarrhea?
EIEC
STEC
Salmonella typhi (typhoid fever)
Gram (-) bacilli
- is transmitted only by humans*
Characteristics:
- (-)oxidase*
- (-) lactose fermentation
- facultative intracellular
- facultative anaerobes
- (+) glucose fermentation
- (+) suffer producer (H2S)*
- (+) triple sugar iron agar (black precipitate)*
- motile
Virulence:
- capsule (polysaccharide capsule that prevent phagocytosis)
- VI capsular antigen (protect from leukocytes in Peyer patches, when invading M cells in distal ileum)
- *type 3 secretion system (a needle like protein that allows the pathogen to exocytosis effector proteins into the cytoplasm to prevent lysosome fusion)
- very dangerous in patients with asplenia or sickle cell disease and can hematogenous spread*
- requires large doses of bacterium since they are acid-liable*
Complications:
1) typhoid/enteric fever
- rose/salmon colored macula on the chest/abdomen
- abdominal pain
- diarrhea
- hepatosplenomegaly
- weakness
- headaches
- AMS
2) bacteremia/sepsis
Treatment:
- symptomatic management
- fluroquinolone and ceftriaxone*
- vaccine is possible (oral live or IM attenuated with the Vi capsule)*
- gall bladder surgery (carriers only)*
Salmonella (NOT s. Typhi)
Gram (-) bacilli
Characteristics:
- encapsulated
- motile
- facultative intracellular
- facultative anaerobes
- (-) oxidase*
- (-) lactose fermentation*
- (+) sulfate fermentation*
- (+) triple sugar iron agar* (turns black)
Complications:
- ulcerative colitis
- bacteremia/sepsis
- zoonotic infection very common type of food poisoning, especially among eggs and poultry and infected animals such as reptiles and dogs*
- requires a large amount of bacterium to infect due to acid-liable*
Treatment:
- symptomatic treatment
- antibiotics are only given if bacteremia/sepsis and/or patient is immunocompromised
Where specifically in the body does all salmonella and shigella species infect humans?
The M cells located in the distal ileum Peyers patches
Pseudomonas aeruginosa
- VERY challenging bacteria to fight and is common among immunocompromised individuals*
- commonly found in humid/wet areas (similar to legionella)*
Gram (-) rod
Characteristics:
- obligate aerobic
- motile
- non spore forming
- (+) catalase*
- (+) citrate*
- (+) oxidase*
- (-) lactose fermentation
- HAS A GRAPE LIKE ODOR
Virulence:
- *multi-drug efflux pumps: allows for safe exocytosis of numerous antibiotic drugs
- B-lactamase: inhibits beta lactam drugs
- biofilms and exopolysaccharide capsule
- *type 3 secretion system (uses a needle like protein to secrete other virulence factors out in cytoplasmic environment and into endothelial tissues)
- *Phospholipase C: (degrades host cellular membranes)
- *exotoxins A: (inactivates EF-2 and prevents intracellular protein synthesis)
- endotoxins: causes inflammation and produces fevers
- *pyoverdine and pyocyanin pigments (iron chelator that enables increased iron digestion for growth and generates ROS respectively)
- these are what causes the grape like odor*
Complications:
- *“Hot tub colliculitis” (infection of hair follicles that produces a widespread rash)
- *ecthyma gangrenosium (blister like lesions that quickly turn to necrotic lesions)
- pneumonia (common in CF patients)
- sepsis/bacteremia
- *osteomyelitis (usually only if you have diabetes)
- *otitis externa
- nosocomial secondary infections (UTIs via catheter is the most common)
- *tricuspid value specific endocarditis
Treatment: “CAMPFIRE”
- Carbipenames
- Aminoglycosides
- monobactams
- polymyxins
- fluroquinolones
- ceftriaxone/cefepime (third gen cephalosporins)
- pipicillin/ticarcillin (extended spectrum penicllins)
- note folliculitis only requires symptomatic treatment*
Enterobacters (cloacae and aerogenes)
Is an opportunistic infection and is only a problem in immunocompromised individuals or patients that OVERUSE ANTIBOTICS
Gram (-) bacilli
Characteristics:
- Motile
- facultative anaerobic
- non- spore forming
- (-) oxidase
- (+) urease
- (+) lactose fermentation
Virulence:
- fimbriae ( allow for easier attachment)
- hemolysin ( destroys RBCs if it enters blood system)
Complications: (pretty much only affects immunocompromised)
- tracheobronchitis
- pneumonia
- pleural empyema
- UTIs
- bacteremia/sepsis
- endocarditis (tricuspid value)
- cellulitis/fasciitis
- myositis
- peritonitis
Treatment:
- carbapenems
- fluroquinolones
- Aminoglycosides
- polymyxins
Klebsiella pneumoniae
Gram (-) bacilli
common lobar pneumonia producer in alcoholics and diabetics and 3rd most common cause of UTIs
Characteristics:
- non motile
- facultative anaerobic
- non- spore forming
- (+) urease*
- DARK RED JELLY SPUTUM*
- PINK COLONIES*
- (+) lactose fermenter*
- (+) capsule
Virulence:
- VERY HIGH LPS*: disables compliment activation
- sideophores*: iron chelating compounds to aid in growth
- B-lactamase
Complications:
- lobar pneumonia* (common in alcoholics and diabetics)
- lung abscesses
- UTIs* (cystitis, prostatits, pyelonephritis)
- meningitis
- bacteremia
- spontaneous bacterial peritonitis* ( only in cirrhosis or ascites patients)
Treatment:
- third gen cephalosporins (ceftriaxone)
- Aminoglycosides
- fluroquinolones
- carbapenems* (only for extended spectrum B-lactamase klebsiella)
- colistin/fosfomycin* (only for carbapenamase resident klebsiella)
Legionella pneumophillia
- VERY COMMON IN WARM HUMID AREAS SUCH AS: AC units, hot tubs, smoke stacks, irrigation systems*
- most common route of transmission is inhalation of infected water droplets*
Gram (-) bacilli
Characteristics:
- *requires silver staining to best visualize
- (+) charcoal yeast agar (grows silver “cut-glass” colonies)
- obligate aerobe
- (+) oxidase
- (+) catalase
- facultative intracellular
- non spore forming
Virulence:
- *factor B system: (allows legionella to invade phagosomes and inhibit phagolysosome fusion)
Complications:
- legionnaires disease: ( high fever >40C, headache, and severe pneumonia)
- Pontiac fever: (high fever > 40C, but NO PNEUMONIA. Flu-like symptoms)
Treatment: (only required for legionnaires disease. Symptomatic treatment ONLY for Pontiac fever)
- macrolides
- fluroquinolones
Yersinia enterocolitica
gram (-) cocobacilli
common blood diarrheal disease that is most commonly transmitted via dog feces or contaminated animal products
Characteristics:
- facultative anaerobe
- non spore former
- facultative intracellular
- (-) lactase*
- (-) lactose fermentation*
- (-) oxidase*
- (-) hydrogen sulfate producer (CANT grow on Triple sugar iron agar)*
- motile at 25C*
- non-motile at 37C*
Virulence:
- adhesions (YadA): attaches to gut epithelial cells specifically
- type 3 secretion system* (T3SS): proteins that block pro inflammatory cytokines (TNF-a/IL-8) and macrophages, preventing immune response*
- siderophores: chelating agents for iron that promote growth
- enterotoxin YST*: promotes diarrheal disease states
Complications:
- terminal ileitis
- enterocolitis
- psudeoappendicitis
- sepsis/bacteremia (only immunocompromised)
- reactive arthritis* (if having the HLA-B27 antigens on host leukocytes)
- erythema Nodosa* (if having the HLA-B27 antigens on host leukocytes)
- high amounts of bloody diarrhea
Treatment:
- ceftriaxone
- TMP-SMX
- Aminoglycosides
- fluroquinolones
- tetracyclines
Serratus marcescens
Gram (-) bacilli
common water and soil and hospital-acquired infections
Characteristics:
- facultative anaerobic
- motile
- (+) urease
- (+) catalase
- (+) DNase, Lipase and gelatinase*
- (+) lactose fermentation (macconkey)*
- (+) PRODIGIOSIN (makes the bacteria look RED)
Complications: (very high in immunocompromised people)
Pneumonia
UTIs
Infective endocarditis (tricuspid)
- sepsis/bacteremia
- meningitis
- cellulitis/fasciitis (only in burns or deep surgical wounds)
Treatment: (B-lactams (+))
- Aminoglycosides
- piperactillin-tazobactam
- fluroquinolones (only if the above doesn’t fix it)
Neisseria Gonorrhoeae
Gram (-) dipolococci
Characteristics:
- obligative aerobe
- non-motile
- non sporeforming
- (+) catalase
- (+) oxidase
- (-) maltose fermentation*
- (+) Thayer Martin agar growth
- (-) capsule*
- most commonly spread via sexually or perinatal*
Virulence
- IgA proteases: destroys IgA in mucosal tissues
- pilli: helps swap genetic information between bacterium
- antigenic protein variation*: phase variation occurs with self-antigens at each infection (cant build a vaccine against it)
- lipooligosaccharides* (LOS): cell wall antigens that trigger widespread sepsis in blood stream
- Sialylation*: wraps LOS cell wall w/ sialic acid which mimics host cells and helps evade immune system
Complications:
- sepsis/ bacteremia (gonococcemia)
Septic/gonococcal arthritis*: more common sexually active teenagers
- gonorrhea*
(males = urethritis/prostatitis/ epididymitis)
(females = urethritis/vaginitis/cervicitis) - neonatal conjunctivitis*: 2-5 days after birth from infected mother
- fitz-Hugh-Curtis syndrome*: inflammation of the peritoneum as a complication of pelvic inflammatory disease (PID)
(causes violin string adhesions which attach liver to peritoneum) - diagnosed with NAT (nucleic acid amplification testing)*
Treatment:
- ceftriaxone*
- azithromycin/doxycycline in conjunction (if coinfection with chlamydia)*
- use condoms to lower infection rates
- erythromycin (for neonatal conjunctivitis ONLY)
Neisseria meningococcal (meningitidis)
Gram (-) dipplococci
Characteristics:
- obligate aerobes
- non spore forming
- non-motile
- (+) capsule*
- (+) catalase
- (+) oxidase
- (+) maltose fermentation* (turns yellow)
- (+) Thayer Martin agar growth
- most commonly transfers via oral and respiratory droplets*
Virulence:
- Pilli w/ OPA/OPC proteins*: help bind to host cells
- NO CAPSULE*
- NO ANTIGENIC VARIATION*
- IgA proteases: destroys mucosal IgA
- lipooligosacchardies (LOS): cell wall antigens that trigger widespread sepsis/bacteremia and widening of endothelial cells.
- Factor H binding protein*: disables alternative complement pathway
Complications: (is more dangerous In immunosupression patients)
- DIC* : due to widespread endothelial vessel cell damage via LOS and factor H binding protien (severe bleeding through out the body due to clots being formed to repair blood vessels)
- water-house frechreich syndrome*: pooling of blood in adrenal gland, causing ischemia/necrosis of adrenal gland.
- meningitis*: only known bacteria to cause outbreaks of meningitis
(LOS causes widening of the endothelial cells in the BBB, allowing pathogen to go into CSF and grow) - meningiococcemia (sepsis with meningococcal, marked by petechiae rash usually in trunk and lower extremities)
Treatment:
- ceftriaxone*
- penicillin G ( only once antibiogram determines its okay)
- rifampin (as a prophylaxis for people who were in contact with someone who had it)
- vaccine* (especially babies/children/teens/immunocompromised adults)
Helicobacter Pylori
Gram (-) curved bacilli
- common ulcer pathogen that likes to be in the GI system specifically the antrum of the stomach and duodenum (less acidic)*
Characteristics:
- motile
- microaerophile* (needs oxygen but less than normal atmospheric pressure)
- (+) urease* (allows it to produce an alkaline environment for living in GI system)
- (+) oxidase*
- (+) catalase
Virulence:
- cytotoxin-associated gene A (cagA)*: interferes w/ gap junctions of epithelial cells and induces chronic inflammation of GIU system
- increases chances of MALT lymphoma and adenocarcinomas*
- also chronic inflammation increases acidic environment, so increases chances of ulcer productions*
- exotoxins-vacuolating cytotoxin A (vacA)*: causes epithelial cell necrosis and leads to ulcer production
Complications:
- peptic ulcers*: very common pathogen associated with this
- MALT lymphoma and adenocarinoma
Treatment:
- triple therapy*
1) amoxicillin
2) clarithromycin
3) proton-pump inhibitor
Types of gastritis with respect to where an ulcer is likely to be seen
Antral gastritis: Duodenal ulcers
Corpus gastritis: Gastric ulcers
Campylobacter jejuni
Gram (-) curved-bacilli
most common cause of gastroenteritis worldwide and bloody diarrhea in children. Route of transmission in poultry/cows/and unpasteurized milk
Characteristics:
- motile
- (+) oxidase
- microareophile*
- thermophile* (is the only bacterium that commonly infects humans that grows best at 42C or higher)
Virulence:
- fimbriae-like filaments (help attach to GI epithelium
Complications:
- Gillian-barre**: IS THE MOST COMMON CAUSE OF SECONDARY GILLIAN- BARRE (done via host production of autoreactive anti-ganglioside antibodies)
- reactive arthritis*
- bloody diarrhea
- peptic ulcers
- toxic megacolon
Treatment:
- symptomatic treatment
- erythromycin*
Vibrio cholerae
gram (-) curved bacilli
- very contagious cause of gastroenteritis and “rice water” (usually not bloody) diarrhea. Due to poor water sanitation, iOS more endemic to 3rd world countries*
Characteristics:
- motile
- non spore Former
- facultative anaerobe
- (+) oxidase*
- (+) can only grow in alkaline media*
Virulence:
- cholera enterotoxin* (choleragen): stimulates G(a) subunit of g-protein connected to adenylate Cyclase. Induces chronically elevated cAMP levels, and chronically secrete chloride (and water as a side effect) into intestines
Complications:
* high risk for severe infections in patients with decreased gastric acidity and/or O-blood type*
No symptoms primarily, but after 4 hrs of chronic diarrhea, will shows signs of dehydration/low electrolytes:
- kussmaul breathing (metabolic acidosis)
- disorientation
- swollen tongue
- cold/clams skin
- dry mouth
- sunken eyes
- shriveled dry skin
- severe cramps
- headaches/seizures
- hypovolemic shock
Treatment:
- hydration and symptomatic/palatative care
- TMP-SMX/tetracycline (severe only)
Yersinia pestis
Gram (-) cocci-bacilli
causes plaque and is transmitted by fleas and rodents
Characteristics:
- non motile
- non spore former
- facultative anaerobe/intracellular
- (-) oxidase*
- (-) urease*
- (+) catalase
- (-) indole*
- (-) lactose fermentation*
- (-) hydrogen sulfate fermentation*
Virulence:
- type 3 secretion system: (needle like projection that spurts out proteins into the cytosol of cells and the environment to decrease immune response)
- Yersinia outer proteins (YOPs)*: prevents pro inflammatory cytokines to be secreted And inactivates macrophages
- siderophores: helps it get iron from the environment
Complications:
- *bubonic plaque: limited sepsis that is marked by extreme lymphadenopathy since it is only in lymph nodes
- cancer symptoms but can see Buboes in the inguinal or axilla region*
- *septicemic plaque: sepsis that is marked by increased presence of blood stream and DIC prominence
- hypotension, purpura skin lesions, tissue necrosis*
- *Pneumonic plaque: get plaque into the lungs via the bloodstream (secondary) or from respiratory droplets from infected individuals (primary)
- dyspnea, hemoptysis and cough*
Treatment: (lasts 14 days)
- Aminoglycosides (gentamicin/streptomycin)*
- doxycycline/tetracycline (only if Aminoglycosides dont work)
Haemophillus influenza
Gram (-) cocobacillius
Characteristics:
- can be in capsulated (A-F types) or uncapsulated (nontypeable)
- Type B and nontypeable are the most common infectious ones*
- non motile
- non spore former
- facultative anaerobic
- (+) catalase
- (+) oxidase
- (+) growth on chocolate agar*
Virulence:
- IgA proteases: destroys IgA found in mucosa
- capsule with HMW1/2*: helps adhere to host cells
- lipooligosaccharides (LOS): helps colonize respiratory tract and can trigger widespread sepsis if it gets into blood stream.
- antigenic phase variation*: cant build adaptive response against
Complications:
- epiglottis* (most common cause of this in children)
- cellulitis
- meningitis
- bacteremia/sepsis
- spetic arthritis
- otitis media
- sinusitis
- bronchitis
- pneumonia
- fatal bacterial superinfection*: (occurs when Haemophilus influenza co-infects someone with a influenza virus)
- common infections in people without a spleen, in children or people who have cancer*
Treatment:
- *amoxicillin (+/-) clavulanate acid (for active infection)
- ceftriaxone (meningitis only)
- rifampin (for people who have come in contact as a prophylaxis only)
- vaccine (type B only)
- DOES NOT CAUSE THE FLU*
Bordetella Pertussis (whooping cough)
Gram (-) coccobacillus
Characteristics:
- facultative aerobe
Virulence:
- filamentous hemaglutinin*: helps anchor the bacteria to mucosal epithelium
- tracheal cytotoxin*: paralysis of the cilia in the host (this is the cause of the actual coughing)
- pertussis toxin*: increases levels of T-cells in the mucosal blood without letting them into tissues and increases inflammatory reactions in the throat (this is the cause of the classic “whooping” sound)
- adenylate Cyclase toxin*: prevents extravasion of phagocytes as well as causes the to under go apoptosis.
Treatment:
- macrolides*
- TMP-SMX (if allergic to macrolides)
- DTaP vaccine*
Phases of a pertussis infection
1) incubation phase:
- lasts 1 week
- patient is asymptomatic
2) catarrhal phase (best to treat at this phase or earlier if possible)
- lasts 2 weeks
- low grade fever
- coryza (inflammation of nose mucosa causing congestion)
- coughing begins here*
- is now infectious at this stage*
3) paroxysmal
- lasts 1-6 weeks
- “ machine gun bursts” of coughing w/ whooping sound will come and go
- whooping noise is present still
- pertussis vomiting can occur
- petechiae in the face can occur here
- epiglottis forms here if it is going to*
- very dangerous for children in this phase
4) convalescent phase
- slow improvement and symptoms slowly go away
Brucella
Gram (-) cocobacilli
Characteristics:
- obligate aerobe
- non motile
- non spore formers
- facultative intracellular
- (+) urease
- (+) catalase
Virulence:
- type 4 secretion system (similar to type 3 where it lowers immune system and phagocytosis of macrophages
- Lipopolysaccharides: (prevents phagolysosome fusion)
Symptoms:
- undulating flu-like symptoms*
(fever, night sweating, headache, myalgia, weight loss, arthralgia)
- hepatosplenomegaly
- lymphadenopathy
- granulomas in the liver and spleen* (brucella abortus ONLY)
Treatment:
- doxycycline + rifampin/streptomycin*
