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Flashcards in Gram Negative Bugs Deck (91):

Basics of Gram - bacteria:
what color do they stain, wall structure, habitat?

Don't retain crystal violet stain used in the gram staining method -> red
- have thin peptidoglycan layer of the cell wall (Gram + has a much thicker one) is sandwiched between an inner cytoplasmic cell membrane and the bacterial outer wall membrane
-All have a lipopolysaccharide outer membrane of cell wall - endotoxin
-Most, with few exceptions, don't form spores
- live in a wide range of habitats -> large intestines (enteric), zoonotic, respiratory, soil, water
-some are true pathogens and some are opportunists.


Medically relevant gram - cocci include 3 species responsible for?



Medically relevant gram - bacilli include species responsible for?

-respiratory illness
-urinary infections
-GI problems
-and many other ailments


Importance of the lipopolysaccharide (LPS)?

outer leaflet of outer membrane -> acts as an endotoxin
- if gm - bacteria enter blood stream, LPS can cause a toxic reaction which results in fever, increased RR, low BP
-this may lead to life threatening endotoxic sepsis and shock
-the presence of LPS also triggers an innate immune response and prod. of cytokines, which in turn, leads to inflammation, which can also produce host toxicity.


2 genera of gram - cocci

- Neisseria
-Moraxella cararrhalis: resides in the resp. tract and causes tracheobronchitis and pneumonia


Neisseria meningitidis & N. gonorrheae features

non-motile, gm -
usually diplococci


Neisseria gonorrheae

Gonorrhea may be most prevalent bacterial STI
- 2nd most commonly reported notifiable STI in US
- may be over 1 million infected


Where does gonorrhea present?

infection of cervix
-infection of urethra (men, inflammatory response -> purulent discharge)


How does gonorrhea present and how can it progress?

-urethral infections
-dysuria and fever
-male infection may extend to prostate and epididymis, causing sterility, infection of urethra -> discharge

-It can progress to systemic disease: arthritis, endocarditis, meningitis
- Gonorrhea neonatorum (ophthalmia neonatorum) is an eye infection during passage through birth canal, can lead to blindness.


Neisseria meningitidis

- causes meningitis, septicemia
- only natural reservoir is the human nasopharyngeal mucosa
- 10% nasal carrier rate
-transferred: direct contact or droplets


subclinical/minimal disease of N. meningitides

transient meningococcemia, short febrile flu-like episode, cleared spontaneously


overt disease of fulminant meningeal sepsis

-massive and rapid proliferation in the bloodstream
-blood culture: +, usually also involves meninges
- rapid clinical deterioration
- fever, severe HA, vomiting, neck/back pain, stiffness, petechial rash, altered mental status, shock, organ failure.


Overt disease of meningitis

fever, HA, vomiting, neck/back pain, irritability, skin rash, AMS


Why does shock and DIC occur in FMS/meningitis?

shock: endotoxin causes capillary leakage, poor vascular tone, intravascular micro thrombi, myocardial dysfunction
- C3a, C5a, inflam. mediators cause vasodilation, capillary leakage
-hypoperfusion -> shock

DIC: endothelial damage -> hemorrhages, micro thrombi (See in hands)
- endotoxin and cytokines create more of an inflammatory response -> deadly cycle


Dx of FMS or meningitis?

early dx is difficult but crucial!
- later stages: FMS- skin lesions appear 6-12 hours after, easier to recognize disease
-meningitis: skin lesions 12-18 h after onset, no lesions in 20% of pts

bacteriologic dx: FMS - gm stain of skin lesion biopsy specimen
- meningitis: only CSF +


Therapy for FMS/meningitis

survival little improved during last few decades
Most impt principles:
- therapy should never be delayed by dx procedures
-abx are most imp part of tx
- Cefotaxime or ceftriaxone + vanco
-pts in contact: prophylatic abx rochephin


Outcome of meningitis:
mortality and sequelae


Moraxella catarrhalis

gm - cocci that causes infections of:
-upper and lower resp (part imp cause of bronchopulm. infection in elderly, pts with chronic lung disease)
-middle ear
- joints

Resistant to PCNs, SMX/TMP, tetracyclines
- SO tx with fluoroquinolones, most 2nd and 3rd cep, macrolides, and augmentin


Aerobic gm - nonenteric bacilli

-pseudomonas & burkholderia: opportunistic pathogen
- Brucella & Francisella: zoonotic pathogens
-Bordetella & Legionella: mainly human pathogens
- Alcaligenes: opportunistic pathogen



small gm - rods w/ single polar flagellum
- free living: mainly in soil, sea water, fresh water, also colonize plants and animals
-impt decomposers and bioremediators
- freq contaminants in homes and clinical settings
- use aerobic respiration, don't ferment carbohydrates
-produce oxidase and catalase
-many produce water soluble pigments


Pseudomonas aeruginosa

-common inhabitant of soil and water
- intestinal resident in 10% people
-resistant to soaps, dyes, quaternary ammonium disinfectants, drugs, drying
-Freq. contaminant of ventilators, IV solns, anesthesia equipment
-opp. pathogen


Pseudomonas aeruginosa common cause of what infections, complications, presentation, tx

-common cause of nosocomial infections in hosts w/ burns, neoplastic disease, cystic fibrosis
- complications: pneumonia, UTI, abscesses, otitis(see blue green gunk in ear), and corneal disease
- endocarditis, meningitis, bronchopneumonia
-grape like odor
-greenish-blue pigment (pyocyanin)
-multidrug resistant
- tx w/ cephaloporins, aminoglycosides, polymixin, quinolones (oflaxacin: good for otitis), & monobactams


Brucella -> Brucellosis

- tiny gm - coccobacilli
- 2 species: brucella abortus (cattle), brucella suis (pigs)
- aka: brucellosis, malta fever, undulant fever, band disease -> zoonosis transmitted to humans from infected animals
-fluctuating pattern of fever (weeks to a year)
-tx w/ combo of tetracycline and rifampin or streptomycin
-animal vaccine available
-potential bioweapon
**the bacteria can spread to humans w/ contact of infected meat or placenta of infected animals, or unpasteurized milk and cheese


Brucellosis infection

- brucellosis: in humans usually assoc. w/ consumption of unpasteurized milk and soft cheeses made from milk of infected animals
- affects all age groups and both sexes
- can be insidious & may present in many atypical forms
-sxs are mild but may present as acute febrile illness which may persist & progress to a chronically incapacitating disease w/ severe complications
- carefully monitored in Mt but is present, still persists in elk and bison in greater yellowstone region


Francisella tularensis & Tularemia

-facultative intracellular coccobacillus
- causes tularemia: zoonotic disease of mammals, endemic to northern hemisphere, particularly rabbits (rabbit fever)
-transmitted by contact w/ infected animals, water and dust or bites by vectors
-HA, backache, fever, chills, malaise, and weakness
-10% death rate in systemic and pulmonic forms
-intracellular persistence can lead to relapse
-tx: gentamicin or tetracycline
-attenuated vaccine
-potential bioterrorism agent


Bordetella pertussis

- minute, encapsulated coccobacillus
- causes pertussis or whooping cough
- acute respiratory syndrome
-100 day cough
-often severe, life-threatening complications in babies
-reservoir: healthy carriers
-transmission by direct contact or inhalation of aerosols


Virulence factors of Bordetella pertussis

-receptors that recognize and bind to ciliated resp. epithelial cells
- toxins that destroy and dislodge ciliated cells: loss of ciliary mechanism leads to buildup of mucus and blockage of the airways.


Vaccine and tx for Bordetella pertussis

Tdap: acellular vaccine contains tetanus toxoid and protection against diphtheria and pertussis.
tx: macrolides -> azithromycin


Legionella pneumophila and Legionellosis

-widely distributed in water
- organisms inhaled in aerosolized mist
- live in close assoc. w/ amoebas
- 1976 epidemic of pneumonia afflicted 200 American Legion members in Philly and killed 29 hence the name legionellosis
AKA: legionnaires dises and pontiac fever


Presentation of legionellosis and treatment

Most prevalent in males over 50, nosocomial disease in elderly.
- fever, cough, diarrhea, abdominal pain, pneumonia fatality rate: 3-30%

Tx: azithro


The most common aerobic and non-fastidious bacterium in the gut?

Escherichia coli -> most prevalent enteric bacillus
- 150 strains
- some have developed virulence through plasma transfer, others are opportunists


Pathogenic strains of E. coli -> Enterotoxigenic E. coli

enterotoxigenic E. coli: causes severe diarrhea due to heat-labile toxin and heat-stable toxin - stimulate secretion and fluid lost alsi has fimbriae (spikes -> attachment pili)


Pathogenic strains of E. coli -> Enteroinvasive

causes inflammatory disease of the large intestine


Pathogenic strains of E. coli -> enteropathogenic

linked to wasting form infantile diarrhea


Pathogenic strains of E. coli -> enterohemorrhagic

O157:H7 strain, causes hemorrhagic syndrome and kidney damage


How does E. coli present?

pathogenic strains frequent agents of infantile diarrhea of many forms is the greatest cause of mortality among babies
- causes 70% of traveler's diarrhea
- causes 50-80% UTI in women
- colifrom count: ind. of fecal contamination in water


Tx of E. coli

Most will respond to SMX/TMP, nitrofurantoin, fluroquinolones (cipro)


Other Coliforms: Klebsiella pneumoniae

normal inhabitant of respiratory tract, has large capsule, cause of nosocomial pneumonia, meningitis, bacteremia, wound infections and UTIs


Other coliforms: Enterobacter sp.

UTIs, surgical wounds


other coliforms: Serratia marcescens

produces a red pigment; causes pneumonia, burn and wound infections, septicemia and meningitis, UTIs


Other coliforms: Citrobacter sp

opportunistic UTIs and bacteremia


Yersenia Pestis (Plague) background and history

Black death killed 75-200 million people, peaked in Europe in 1346-53
-world pop. didn't recover to pre-plague levels until the 17th century.
- the black death isn't a thing of the past. In the last 20 years, there have been as many as 5,000 cases of the plague resulting in 100-200 reported deaths a year.


How is the plague spread?

spread by fleas
- is on CDC's list of reemerging diseases
- percolating in rodent communities -> campgrounds, Eastern African nations are hardest hit


Description of Yersinia pestis and virulence factors

- tiny, gram - rod, unusual bipolar staining and capsules
- virulence factors: capsular and envelope proteins protect against phagocytosis and foster intracellular growth: coagulase, endotoxin, murine toxin


How do humans develop the plague?

through contact with wild animals (sylvatic plague) or domestic or semi domestic animals (urban plague) or infected humans
- found in 200 species of mammals -> rodents, w/o causing disease
- flea vectors: bacteria replicates in the gut, coagulase causes blood clotting that blocks the esophagus, flea becomes ravenous


Pathology of the plague

ID 3-50 bacilli
Bubonic: bacillus mult. in flea bites, enters lymph, causes necrosis and swelling called a bubo in groin or axilla

Septicemic: progression to massive bact. growth, virulence factors cause intravascular coag. subcutaneous hemorrhage and purport - black plague

Pneumonic: infection localized to lungs, highly contagious; fatal w/o tx


Dx and Tx of the plague

dx depends on hx, symptoms, and lab finding from aspiration of buboes.
-tx: streptomycin, tetracycline, or chloramphenicol
- killed or attenuated vaccine available
- prevention: by quarantine and control of rodent population in human habitats


Yersinia enterocolitica (Enteric Yersinia pathogen)

found in domestic and wild animals, fish, fruits, veggies, and water
- bacteria enter small intestinal mucosa, some enter lymphatics and survive in phagocytes; inflammation of ileum can mimic appendicitis
- more lymph node inflammation seen in this compared to Y. pseudotuberculosis


Y. pseudotuberculosis (enteric Yersinia pathogen)

TB like sxs, localized tissue necrosis and granulomas in the spleen, liver and lymph nodes. Plague probably evolved from this organism 1500-20,000 years ago.


Pasteruella multocida

zoonotic genus: normal flora in animals, causes wide range of diseases in wild and domesticated animals -> significant disease in poultry flocks world wide -> avian cholera follows bird migration routes (esp. snow geese)
- result in opportunistic infections in humans
- animal bites or scratches cause local abscesses that can spread to joints, bones, and lymph nodes
- immunocompromised are at risk for septicemia and complications


Tx of Pasteruella multocida

penicillin and tetracycline


Haemophilus basics

genus of tiny gm - pleomorphic rods
- fastidious (complex nutritional requirements), sensitive to drying, temperature extremes, and disinfectants
- none can grow on blood agar w/o special techniques -> chocolate agar
- require hemin, NAD, or NADP
- some species are normal colonists of upper respiratory tract or vagina (H. aegyptius, H. parainfluenza, H ducreyi)
- others are virulent species responsible for conjunctivitis, childhood meningitis, and chancroid


H. influenzae

acute bacterial meningitis, epiglottitis, otitis media, sinusitis, pneumonia, and bronchitis

- vaccine: Hib


H. aegyptius

conjunctivitis, pink eye


H. ducreyi

chancroid STD


H. parainfluenzae and H. aphrophilus

normal oral and nasopharyngeal flora,infective endocarditis


How do you tx Haemophilus infections

amoxicillin, azithro, cephalosporins, fluorquinolones, and clarithro


Characteristics of anaerobic infections

most pathogenic anaerobes are usually commensals -> originate from our own flora


Predisposing conditions (RFs) of anaerobic infections

- breeches in mucocutaneous barrier (displace normal flora)
- compromised vascular supply
- trauma w/ tissue destruction
- antecedent infection


Complex flora of anaerobic infections

multiple species -> abdominal infection: avg of 5 species -> 3 anaerobic and 2 aerobic
- less complex then normal flora
- fecal flora: 400 diff species
- those predominant in stool are not infecting species: veillonella, bifidoabacterium -> rarely pathogenic
- species uniquely suited to cause infection predominate


synergistic mix of aerobes and anaerobes

e.coli -> consume O2 so this allows growth of anaerobes
anaerobes -> promotes growth of other bacteria by being antiphagocytic and producing B-lactamases


What are the clues to an anaerobic infections?

1. infections in continuity to mucosal surfaces
2. infections w/ tissue necrosis and abscess formation
3. putrid odor
4. gas in tissues
5. polymicrobial flora
6. Failure to grow in the lab
in the lab: use analytical profile index, and gas chromatography


Bacteroides fragilis

Major disease causing strict anaerobic after abdominal surgery, none-spore former
- prominent capsule: anti-phagocytic, abscess formation
- endotoxin: low toxicity, structure different than other lipopolysaccharide


Campylobacter jejuni
- leading cause of what?

leading cause of bacterial diarrheal illness
- transmission is oral/ fecal route, ingestion of cont. food & water, uncooked meat
- assoc. w/ feed lots, chicken houses, raw milk
- most raw chicken is probably contaminated (don't wash!!)


How is campylobacter jejune tx?

azithro, b/c increasing resistance to fluroquinolones


Lyme disease (Borrellia burgdorferi)

- Most common tick borne disease in the northern hemisphere
- early sxs may include fever, HA, and fatigue
- Rash occurs in 70-80% of infected persons but may or may not appear as the bull's eye
- left untreated later sxs involve joints, heart, and CNS (mimic other diseases)
- In most cases: disease is eliminated by abx especially if tx early


Dx of lyme disease

- unique bull's eye raise
- Elisa: measures levels of abs against lyme bacteria
- Western blot: ID's abs directed against a panel of proteins found on lyme bacteria. This test is ordered when the ELISA result is either positive or uncertain


Tx of lyme disease

sooner treated -> more complete recovery
- doxy or amoxicillin taken orally for 2-4 weeks


Prevention of lyme disease

-avoidance of deer ticks
-wear long sleeves and tightly woven clothing light in color
- wear shirt tucked into pants
- pants tucked into socks or boots
- walk in center of trails
- Apply tick repellents with DEET or permethrin to clothing
- check yourself, family and pets for ticks after trips outdoors


Chlamydia trachomatis

-obligate intracellular human pathogen
- clinical signs and sxs often indistinguishable from gonorrhea
- female pts may not have sxs
- common STI in US, 1 million cases, 2nd to HPV
- possible to have chlamydia and one or more other STIs at same time
- at one time was single most important infectious agent assoc with blindness, spread from eye to finger to eye, shared towels, coughing, eye-seeking flies or during childbirth


Tx of chlamydia trachomatis

- tx both partners with azithro, doxy, or ofloxocin


Lymphogranuloma venereum (LGV)

- uncommon STI caused by 3 invasive servers of Chlamydia trachoma's
- chronic long term infection of lymphatic system
- Most common in men in central and south america
- Rare in developed nations before 2003, recent outbreak among gay men in the Netherlands has led to increase of LGV in Europe and U.S. -> majority HIV co-infected


symptoms of LGV

- swollen inguinal nodes
- drainage through the skin from buboes or abscesses in inguinal nodes
- painful BMs (tenesmus)
- small painless sore on genitals
- swelling of the labia
- blood or pus from rectum


Dx and Tx of LGV
- what happens if left untreated?

dx usually made serologically and by exclusion of other causes of inguinal adenopathy or genital ulcers

TX: abx -> doxy, erythro, azithro
- buboes may require I&D
- prognosis more favorable w/ early tx
- untreated chronic condition may cause fistulas of penis, urethra, vagina, uterus, rectum



Parrot fever
- zoonotic disease caused by chlamydia pssitaci, contracted from parrots, pigeons, ducks, chickens, gulls
- sxs in humans range from unapparent to systemic illness with severe pneumonia
- may mimic typhoid in early stages: high fever, arthralgia, diarrhea, conjunctivitis, epistaxis, and neutropenia, splenomegaly
- severe HA can mimic meningitis
- mimics bacterial pneumonia as it progresses: dyspnea, high fever, cough, patchy infiltrates or whiteout on CXR
- DD for these sxs lengthy!!


Dx and Tx of Psittacosis

dx: exposure hx!!!!
microbiological cultures from respiratory secretions or serology from blood cultures
tx: doxy and chloramphenicol


Relapsing fever: 2 types
and cause

tick borne (TBRF)
louse borne (LBRF)
cause: Borellia spirochetes


Where does TBRF occur

in Western US, linked to sleeping in rustic, rodent infested cabins in mountainous areas


Where does LBRF occur

transmitted by human body louse and is generally restricted to refugee settings in 3rd world. Occurs in epidemics, more severe in TBRF


Sxs of relapsing fever

flu-like sxs: sudden fever, chills, HAs, arthralgias, nausea, may develop a rash


Dx and Tx of relapsing fever

dx: blood smear -> spirochetes
tx: doxy, may cause Jarisch-Herxheimer run in over 1/2 tx
b/c acts like endotoxin when spirochetes die off -> produces rash and fatigue


Salmonella sp

motile, flagellated gram neg.
- 1800 known servers
- responsible for common salmonella gastroenteritis (diarrhea, abdominal cramps, fever) to enteric fevers (including typhoid fever) which can be life threatening
- asymptomatic carrier state can occur (typhoid mary)
- most common form of "food poisoning" presents with uncomplicated gastroenteritis, usually self limited disease
- Non-typhoid fever salmonellosis is worldwide disease of humans and animals -> animals being the main reservoir, usually food borne illness can spread from person to person


What kind of sxs will salmonella cause?

- enteric typhoid fever- severe systemic disease, any species of salmonella may cause, but S. type most studied:
- N/V/D
- fever, anorexia, HA, myalgias


Dx and Tx of enteric typhoid fever-severe systemic disease (salmonella)

Dx: stool and/or blood cultures, serology for abx
- often fatal if not tx
- replace fluids by oral or IV
- pain control and tx nausea and vomiting
- Abx: cipro
most patients will recover w/ approp. tx



intestinal disease
- bloody diarrhea, may have abdominal pain or cramps, fever
- usually seen in children 2-4
- passed through direct contact w/ stool: child care setting, staff not washing hands after changing diapers, or while toilet training toddlers, drinking or swimming in contaminated water


Dx and tx of shigella

- dx: stool studies
tx: replace lost fluids,water or pedialyte, may need IV fluids
- usually self limiting w/in a week
- increasing resistance to abx: cipro or cefixime (3rd gen) should be used if abx indicated


Vibrio species: 2 groups

cholera infections


Non-cholera vibrio infections

associated with improperly cooked contaminated food or eating raw shellfish
- combo of increased water temp and salinity where shellfish are harvested may contribute to increased contamination rates of shellfish.


Non-cholera vibrio gastroenterits tx

Usually self-limited w/ fluid replacement, abx usually not indicated
- non-cholera wound infection or septicemia will need doxy or a quinolone, aggressive fluid replacement, vasopressors for hypotension, fasciotomy, debridement of infected wound
- several deaths in florida every year (septicemia: have cut, swimming -> get infected)


Vibrio cholerae

secretes cholera toxin that causes profuse watery diarrhea, in endemic areas 75% of cases are asymptomatic, 20% mild to moderate and 5% are severe
- sxs: watery diarrhea, occasional vomiting, cramps
- rapid dehydration ensues.. death due to dehydration can occur in a few hours to days in untx children
- 60% mortality in untx cases,


Acinetobacter baumanni

-commonly isolated from the hospital enviro and hospitalized pts
- often cultured from sputum, respiratory secretions, wounds, urine
- may colonize irrigating solns and IV solns
- low virulence but is capable of causing infection in organ transplants and febrile neutropenia
- infections conc. in ICU
- may cause respiratory and UTIs -> ventilator assoc nosocomial pneumonia
- mortality and morbidity more likely as a result of underlying severe illness rather than superimposed acineobacter
- mult- drug resistance: including carbapenems