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25 Cards in this Set

  • Front
  • Back

Four enterobacteriaceae species

E. coli


Shigella


Salmonella


Yersinia

Escherichia coli description, modes of pathogenicity, clinical, diagnosis

Gram negative facultative rods. Normal flora of colon.



Have 4 P's for pathogenicity: alpha hemolysin (pore forming toxin), aerobactin siderophore, polysaccharide capsule (reduces phagocytosis, K1 capsule causes meningitis), and pili



Enterotoxigenic e. coli (ETEC) causes Travelers Diarrhea. Heat labile AB toxin is adenylate cyclase similar to cholera which produces diarrhea.



Enteropathogenic e. coli (EPEC) has bundle forming pili (BFP) that attaches to intestinal epithelium. Causes attachment and effacement lesions while making pedestal. Type III secretory pathway. Makes toxin, translocates it by forcing Tir receptor into cell membrane, adhering to it with Intimin, and shoving toxin inside.



Enterohemorrhagic e. coli (EHEC) (O157H7) has type 3 pathway also, but can cause hemolytic-uremia syndrome with its shiga-like toxin. Results in anemia, renal failure, decreased platelets, CNS dysfunction. O157H7 fails to ferment sorbitol.



Causes nosocomial pneumonia, UTI (uropathogenic e. coli UPEC via type I/P pili bladder/pyelonephritis), bacteremia, and intra-abdominal infection. Meningitis in neonates, diarrhea.



Diagnose with MacConkey agar.

Salmonella characteristics, clinical, diagnosis

Gram negative facultative rod.



Has TWO type III secretion systems. SPI-1 for ruffling enterocytes so it can get into phagosomes and multiply. SPI-2 for dissemination. Salmonella is all about secretion.



Large #'s needed to inoculate bc most killed by stomach acid. Huge cause of diarrhea, nausea, vomiting. Can lead to Typhoid fever (Rose spots, bacteremia, prolonged fever).



Can lead to carrier state, shedding for years.



Diagnose with culture.

Yersinia pestis characteristics, clinical, diagnosis

Ysera is a bloody cause of The Black Death that results in a lot of puking (of dreams). Gram negative rods.



Colonizes the flea foregut, blocks blood meal passages, forces regurgitation of blood meal to inoculate. Travels to lymph nodes, multiplies to form bubos. Goes to bloodstream where its LPS is cleaved, leading to septic shock. Ends up infecting macrophages in lungs, leading to spread by aerosol.



Has type III secretion system for its YOPs (Yersinia outer prots), Fra1 (anti-phagocytic capsule) and Pla (plasminogen activator).



Bubonic Plague: transmission by rat/flea. Fever, chills, myalgia, arthralgia. Enlarging bubo which leads to sepsis and death.



Pneumonic Plague: same as above, but add bloody cough and dyspnea



Septicemic Plague: nausea, vomiting, diarrhea from direct inoculation into bloodstream.



Grows on blood agar, look like closed safety pins.

Pseudonomas aeruginosa characteristics, clinical, diagnosis, treatment

Pseudonomas aeruginosa is a cautious, air-loving opportunistic gram negative strictly aerobic rod that is a nightmare of nosocomial infections. Loves moist environments in hospitals.



Cautiously pathogenic: it does quorum sensing, has exotoxin A (like diphtheria), elastases, type III secretion system, and alginate exopolysaccharide responsible for mucoidy phenotype in CF patients.



Colonizes CF patients lungs, causes necrotizing nosocomial pneumonia, sepsis, UTI/wound infections, hot tub folliculitis, and ecthyma gangrenosum.



Diagnose grape odor, oxidase positive, blue/green fluorescence.



Has high intrinsic and acquired resistance. Treat with aminoglycosides + another drug. Penicillin/cephalosporin not effective.

Legionella characteristics, clinical, diagnosis

Legionella is a really cute gram negative aerobic rod that normally loves water and loves infecting amoebas. It thinks macrophages in lung are amoebas and gets into them by coiling phagocytosis. Once inside phagosome, it recruits ribosomes to help make the phagosome a good home for it while using its dot locus (Defect in organelle trafficking) to express prots to help prevent phagolysosome fusion. Encodes type 4 secretion system. Also has phospholipase C to help it burst out. Get from aspirating water, cooling towers, air conditioning, mists.



Causes SEVERE fever above 40oC along with other respiratory symptoms (nausea, vomiting, diarrhea)



Poor gram stain. Use silver test, buffered-charcoal yeast agar, antibody tests.

Vibrio spp characteristics

Gram negative rod, comma shaped, causes cholera/gastroenteritis (vulnificus) after exposure of wound to seawater, especially in liver compromised.

Helicobacter pylori

Gram negative, rod, slender curved shape bacteria that are microaerophilic. Grows in mucous overlying gastric mucosa.



Has urease to cleave urea into ammonia so it can alkalinize the local environment. Slender curve shape helps it move around in mucous. VacA cytotoxin that kills epithelial cells. Type 4 secretion system that causes inflammation. All this leads to peptic ulcers.



Risk factor for adenocarcinoma/MALT lymphomas of the stomach, but can be treated with antibiotics.



Silver stain, urea breath test, serological.



Treat with PPI + multiple drugs.

Haemophilus influenzae description, clinical

Gram negative, facultative coccoballi that causes inflammation of anything remotely connected to respiratory tract: otitis, sinusitis, meningitis, bronchitis, epiglotitis, and pneumonia.

Bordetella pertussis description, clinical, prevention

gram negative strict aerobe coccobacilli. Cause of Whooping Cough.



Needs to grab onto the airway on the way down. Adheres via filamentous hemagluttinin (FHA) on galactose residues on epithelial cells in airway. Gets into phagosomes in neutrophils by binding CR3 residues.



Hexameric Pertussis AB toxin S1-S5: ADP-ribosylates a G protein, leading to increase in cAMP, interfering with leukocyte function, upregulates CR3 receptors, and survives in phagocytes while blocking neutrophil recruitment



3 stages: incubation, catarrhal (like a cold, very infectious), paroxysmal (explosive, uncontrollable coughing followed by whooping gasping for air. Leads to exhaustion, cyanosis, vomiting, convulsion)



Acellular vaccine given with TDAP, but runs out over time without boosters



Brucella and tularemia description and clinical

Brucella: Gram negative aerobic coccobacillus from cattle, goats, hogs. Veterinarians and meat inspectors. Causes fever, malaise, chills, drenching sweats like Cruella de Ville. Lasts for a LONG ass time due to its ability to survive in macrophages.



Francisella tularensis: gram negative facultative coccobacillus. Rabbits, squirrels, muskrats, beavers, deer. The rabbits multiply in macrophages in a very localized corner, then disseminate. Causes localized lymphadenopathy, local ulcer, fever + chills, pneumonia and dissemination.

Pasteurella description

Gram negative coccobacillus, normal flora of mouth of cats and dogs. Infection from bite.

Neisseria description, clinical

Gram negative diplococci



Neisseria mengitidis: meningitis + sepsis


Neisseria gonorrhea: STD

Rickettsiaceae description, clinical

Gram negative coccobacilli, obligate intracellular. Often transmitted by insect vector. Rickettsia rickettsii causes Rocky Mountain Spotted Fever.

Coxiella burnetii description, clinical

Qoxiella burnetii goes BAA



Gram negative obligate intracellular coccobacilli. Cause of Q fever: fever, pulmonary infiltrates, NO rash.



Harbored by sheep, spread during birth of lambs/animals due to abundance in placental membranes.

Ehrlichia chafeensis and Anaplasma phagocytophylum

Both gram negative obligate intracellular, transmitted by tickets.



Ehrlichia infects monocytes/macrophages, anaplasma infects neutrophils. Causes fever, headache, myalgia, thrombocytopenia (low platelet), leukopenia (low WBC)

Bartonella description, clinical

Clint Barton has a cat



Gram negative facultative intracellular. Causes cat scratch disease

Chlamydia trachomatis, pneumoniae, psittaci description, clinical

Gram negative coccobacilli, obligate intracellular.



Trachomatis causes the STD



Pneumoniae and psittaci cause pneumonia

Mycoplasma description, clinical

No cell wall. Smallest free living/self replicating organisms aside from viruses.



Common cause of CA-pneumonia

Borrelia spp, description, clinical

Aurora borreliasis are lyme colored and recur often at the poles.



Borrelia burgdorferi: Diderm spirochetes that cause lyme disease via tickets



Borrelia recurrentis: spirochete causing relapsing fever from ticks/lice

Treponema pallidum

Alex Levin trips a lot, but he's a pal.



Spirochete, causes syphillis

Leptospira description, clinical

Leptospira Lets Up after its primary phase, but comes back. Has two P's in it because its transferred by urine.



Aerobic spirochete. Transmitted by exposure to water with animal urine.



Primary phase: fever, chills, headache, muscle pain. Then goes away as bacteria are cleared.



Secondary phase: symptoms come back, some get meningitis

Mycobacterium tuberculosis description, general symptoms, three types of TB, mechanism of pathogenicity, diagnosis, treatment, prevention

Gram positive, acid fast, strict aerobe.



Exposure: in the room with coughing person


Infected: inhaled aerosol, replicating in macrophages


Disease: showing symptoms



Survives in phagosomes in macrophages by prevengin fusion with lysosome. Spreads to lymph nodes, disseminates. Usually controlled by immune response, but if that fails, you get Primary TB (symptoms). 10% see latent Reactivation TB, usually in first two years after infection.



Fever, night sweats, weight loss, upper pulmonary lobe lesions if in lungs. Infected macrophage recruits macrophages, monocytes, neutrophils. Macrophages differentiate into foamy macrophages (multinucleated), lymphocytes surround, fibrous layer forms around (now called granuloma), leads to dying macrophages necrosis in the center (caseating granuloma)



Mycolic acid cell envelope lipids for defense, along with slow growth



Pulmonary TB: chronic productive cough, blood tinged



Extrapulmonary TB: lymph nodes, lung pleura, spine (Pott's disease), common in HIV-infected, immunocompromised



Miliary TB: widely disseminated TB, not controlled by IS. Hepatomegaly, splenomegaly, lymphadenopathy, CXR reveals snowstorm pattern



Diagnose with PPD test (cross reacts with BCG vaccine), Interferon-Gamma Release Assays, culture with Lowenstein Jensen media, look for radiolabel O2, acid fast stain.



Treat with isoniazid, rifampin. Can be resistant or extensively resistant.



Prevent with BCG vaccine and respiratory isolation



Mycobacterium leprae description, mechanism of pathogenicity, three types of leprosy, treatment

Obligate intracellular. VERY slow division.



Dense, inert lipid capsule, no toxins-- directly kills Schwann cells.



TB Leprosy: intense cell-mediated immune response, low bacteria count, noncaseating granulomas, Th1 response. Hypopigmented skin lesions with raised edges, depressed center. Large peripheral nerves enlarged, neuronal damage leads to muscle atrophy and contractures.



Lepromatous leprosy: no cellular IS, many bacteria present, Th2 response. Any shape raised skin lesions usually on face, ears, wrist, elbows, buttocks, knees, scrotum (colder), then on face (leonine appearance), lead to 'saddle nose'



Borderline leprosy in between



Culture in armadillos. Treat with dapsone and rifampin.

M. avium-intracellulare complex (MAC)



M. kansasii



M. abscessus/M. fortuitum



M. marinum

gastrointestinal disease



pulmonary infection like TB



rapid growers, post-op wound infections and venous access line fections



soft tissue infection after contact with fish tanks, fish, saltwater