Bacteria Pt 2 Flashcards

Question

What are characteristics of Vibrio, Campylobacter, and Helicobacter species? How do they differ?

Answer 1

curved, microaerophilic, gram negative associated with human disease differ in their environmental niches and disease manifestations

Answer 2

1. environmental organisms 2. toxin mediated diarrheal disease 3. wound infections 4. systemic infections- compromised host

Answer 3

1. Zoonotic infections 2. Diarrheal disease 3. Systemic infections- compromised host

Answer 4

1. Pathogen/commensal of human stomach 2. chronic gastritis 3. Peptic ulcer disease 4. Gastric cancer

Answer 5

Encounter: Asymptomatic vaginal carriers (60%), sexual contact Pathogenesis: Mycoplasma hominus, Ureaplasma urealyticum - gliding motility to spread - resistant to exfoliation of urinary tract epithelium Associations: - Endometritis - Male non-gonoccal urethritis (20%) - PID (

Answer 6

Growth: 6 hr doubling, Fried egg appearance after 5-20 days, No murein cell wall, Osmotically fragile, small genome Lab isolation: cell free media, Nutrient requirements: cholesterol, AA, nucleic acid precursors Encounter: Respiratory Droplets (moderately contagious) and colonized on respiratory epithelium

Answer 7

4-8 year cycles, HERD IMMUNITY Mini epidemics in closed populations - attachment to epithelium via terminal attachment structure with an adhesive protein (P1) that binds to sialylated glycoprotein on the hose cell - slow growing with incubation period of 2-3 weeks vs 1-3 days for most viruses - some infections localized as URI --- R epithelium only, no alveolar involvement, elicits mononuclear infiltrate surrounding bronchi or bronchioles (not a lobar process) - spread to other hosts by blocking ciliary clearance, mucosal irritation, cough

Answer 8

5-10% of cases progress to tracheobronchitis or pneumonia Walking (Atypical) Pnemonia - headache and cough - no cervical adenopathy - CXR- non lobar patchy interstitial pattern - Non-responsive to sulfonamides or penicillins - No causal agent by gram stain or routine culture Diagnosis: usually not specifically diagnosed because it is self limiting and difficult to culture (slow growing) Not effected by cell wall antibiotics Use Tetracycline, Erythromycin, Azithromycin

Answer 9

Classification: no gram stain, aerobe, slow growing rod, waxy coat, acid fast stain Encounter: brief encounters pose little risk, need close contact with infected individuals for infection Transmission: Inhalation (droplets) and fairly contagious Colonization: alveolar macrophages

Answer 10

Initial Spread: from initial point, spreads elsewhere in macrophages via blood and lymph, no symptoms within first few weeks Containment of Infection: - cell mediated immunity (CD4) - granuloma contains infection - if unstable containment, get active Tb diseases with caseous necrosis (normal host) and hematogeous spread (extra-pulmonary disease and miliary Tb) Primary vs Secondary Tb - 90%: primary infection contained, scar forms indiciating old disease - 10%: reactivation of disease given following conditions: - - illness, malnutrition, stress, immunocompromise (AIDS)

Answer 11

- Organism may remain dormant for years - Tb pneumonia-primary - Rare- patients with lacking immunity get miliary Tb (millet seeds in lung) - If caseous lesions liquefy and dishcharge, Tb spreads to other sites (caviation) - - growth of bacterial load (O2 access now), contagion (free in lung--> cough), spread to other sites in patient Diganosis: - PPD- Tests T cell immunity, not disease - -- False positive- BCG vaccination within 5 years, atypical mycobacterium, BCG treatment for bladder cancer - -- False negative- immunocompromised patients who cant respond - IFN gamma release assays test for immune response using T cells from blood Treatment: - multiple drug regimen to avoid resistant Tb, usually for 6-9 months - -- Spontaneous resistance in 10^-6-10^-7 - --- Heterogeneity in bacterial population - -- Multidrug resistant variants likely when more than 10^7 bacteria present, which is common in a granuloma - Isoniazid, rifampin, PZA, ethambutol- first line agents Chemoprophylaxis (treatment for latent Tb) - isoniazid and rifampin

Answer 12

No gram stain, aerobe, slow growing rods, slow growth (days to weeks), acid fast stain Encounter: Ubiquitous in water M marinum- fish M fortuitum- complex nail infections Transmission: no human to human transmission Colonization: sputum, fish tanks, water containing items, surgical wounds Pathogenesis: found in sputum and may invade areas of abnormal lung, infects tissues and spreads to lymph nodes, may cause skin and soft tissue infection Clinical Presentation: pulmonary infections in elderly women and immunocompromised hosts - disseminated infections in advanced HIV/AIDS Prevention/Treatment: Direct probe to culture for some (MAC), grow repetedely on bronchoscopy or from tissue to prove infection Treatment is often worse than disease, and need multiple drug regimen to avoid selecting resistance for 12-24 months

Answer 13

No gram stain, not culturable in vitro, grows in 9 banded armadillo, acid fast stain Encounter: found in endemic areas Transmission: human to human, not easily transmitted Pathogenesis: infects cool areas of the body, anesthetic hypopigmented macules, pathology depends on host Clinical Presentation: Hansen's disease - - Lepromatous- multibacilliary, bad, poor T cell response, good humoral response - - Tuburculoid- not as many bacteria, good T cell response, poor humoral response Diagnosis: biopsy, clinical presentation in endemic area Treatment: multi drug regimen 2-5 years

Answer 14

- Gram + rod, aerobe, capsule forming (antiphagocytic) - invasive, non-motile, spore former Encounter: spores in soil deposited by dead/dying animals Transmission: damaged skin, inhalation, ingestion Colonization: skin, pulmonary system, GI tract

Answer 15

Toxins: AB- share a B Moiety (protective antigen) which is encoded by plasmid Edema Factor: AB- adenylate cyclase Lethal Factor: AB- produces IL-1 and TNF production by Mphage, induces Mphage apoptosis Capsule: Antiphagocytic PEPTIDE capsule (not polysaccharide)

Answer 16

Cutaneous anthrax (95%) - initial red papule--> ulcer - dark scab (Escher) forms surrounded by Edema - Minimal systemic symptoms - 5-20% mortality untreated Pulmonary Anthrax: - Mild fever and malaise, non productive cough (1-4 d), respiratory distress (2-4 d), poor local inflammation response - edema of neck and chest (EF mediated) - hematogenous spread - septic shock - high mortality after acute phase Gastrointestinal Anthrax - high mortality due to toxemia and sepsis Diagnosis: early diagnosis critical, readily cultured and identified for confirmation Cutaneous Anthrax: Antibiotics Pulmonary Anthrax: Antibiotics effective if given early Control: Vaccine (animals and at-risk workers)

Answer 17

Gram + rod, Facultative aerobe, non-spore former, intracellular invasion Cell-mediated immune response necessary to clear infection! Encounter: water, soil, birds, mammals, fish, 1-5% are fecal carriers Transmission: Foodborn (cheese, milk, under-cooked meat), transplacental at birth NOT in utero Colonization: Intestinal epithelium, intestinal macrophages

Answer 18

Lysteriolysin lyses the phagosome, replicates in the cytoplasm, and utilizes host cell actin for motility -- membrane collision results in projections towards a 2nd cell, projections pinch off to yield a vacuole with 2 membranes, vacuole lysed (PLC) in the new cell Damage: Septicemia or meningitis, rare focal infections (3%) - host-antibacterial response causes most pathogenesis (SEPSIS SYNDROME), NO SYSTEMIC TOXINS

Answer 19

High Risk Groups- Pregnancy -- Mother: febrile bacteremia causing labor induction, meningitis -- Baby: granulomatosis, disseminated infection with abscesses, fatal Neonates (3d), Immunosuppressed individuals -- Sepsis of unknown origin (fever, chills, hypotension), bactermemia, meningitis -- Meningitis and cerebritis is most common cause, patients have neoplastic disease, no neutropenia, occurs in previously healthy adults - Low mortality Diagnosis: Hx, Sx, Setting, Blood/CSF Culture, Direct Gram stain Treatment: ampicillin, penicillin, TMP/sulfamethoxazole

Answer 20

Encounter: Gram negative bacilli, anaerobic, part of normal flora in GI tract, female genital tract Virulence: Produces beta lactamase Pathogenesis: Abscess formation due to capsular polysaccharide with repeating units of +/- charged sugars, capsule induces protective cell-mediated immune response If infection below the diaphragm, treat for bacteroides and clostridium

Answer 21

Above- gram positive cocci, Fusobacterium | Below- Bacteroides fragilis and Clostridum species

Answer 22

Oral Cavity: Gram + (Peptococcus species, Peptostreptococcus species) Gram - (Fusobacterium species) GI Tract: Bacteroides fragilis (gram -) Female Genital Tract: Clostridium (spore formers)

Answer 23

Gram negative Cat scratch fever (axillary lymph nodes, immunocompetent people) Bacillary angiomatosis- immunocompromised individuals Treatment: doxycycline, macrolides

Answer 24

Pleomorphic gram negative rod Produces Urease Facultative Intracellular Pathogens of cattle, pigs, sheep--> veterinary medicine Produce Brucellosis- a granulomatous disease/undulent fever with fever, headache, anorexia Can be followed by persistant infection, with potential for systemic symptoms Encounter: unpastuerized dairy products or penetration of mucous membranes with exposure to infected animals Spread: Acute phase: bateria move from site of infection to lymph nodes, predilection for RES, lives in macrophage, escapes phagolysosome fusion by generating a replicative vacuole Chronic: months to years--> undulant fever with manifestations of arthritis, epididymitis and orchitis, host attempts to control infection by forminga granuloma Diagnosis/Treatment: slow growing, involves multi-drug antibiotic treatment with one which can act in macrophage acidic environment (similar to Tb treatment) Tetracycline and rifampin

Answer 25

Commensal of GI or animals (cattle, sheep, goats etc.) - bile salt resistant, microaerophilic, motile, non-spore former, slow growth, prolonged incubation for lab growth needing selective media

Answer 26

Curved, gram negative rod Encounter: animal exposure, contaminated food, grows at 42, oxidase positive Virulence: cytotoxins, Enterotoxins, Flagellae GI Disease: Local infection with 12-24 fever, myalgia, malaise, abdominal cramps, diarrhea Can be invasive causing bacteremia, reactive arthritis Post Infectious Sequelae: Guillain-Barre syndrome (peripheral polyneuropathies- ascending paralysis Treatment: antbiotics

Answer 27

Gram - rod, facultative anaerobe, encapsulated, lactose fermenter, catalase positive Serotyping- H Ag (flagellar protein), O Ag (LPS polysaccharide- sepsis), K Ag (capsular polysaccharide) Encounter: colonized on intestinal epithelium Pathogenesis: Gene exchange (plasmids) causing frequent Ab resistance Virulence: plasmids, pathogenicity islands Clinical Presentation- Colitis/diarrhea Neonatal meningitis- 1st month --via maternal transmission, associated with K1 capsule (identical to Group B meningococci), bacteremia Opportunistic Infection -- pneumonia and bacteremia -- complement resistant siderophore, with increased risk if impaired immunity, intestinal trauma, or foreign body Most common cauase of G negative sepsis UTI- E. Coli is most frequent cause! - urethritis, cystitis, pyelonephritis, sepsis - pili formation (P type) - associated with hemosylin production, siderophore production, complement resistance

Answer 28

Entero-hemorrhagic Most common serotype:O157-H7 Encounter: person-person, contaminated meat, water Transmission: fecal-oral route with very low infectious dose (like Shigella) Colonizes: intestinal epithelium Damage: Thinning of enterocytes, loss of microvilli, pedestal formation (intimin), Shiga-like toxin (tagets 60s subunit of ribosomes) Clinical: Mild diarrhea, bloody Hemorrhagic Colitis (afebrile, abdominal pain, blood diarrhea) Hemolytic Uremic Syndrome -- hemolytic anemia, renal failure, thrombocytopenia, caused by Shiga Like Toxin

Answer 29

Enteroinvasive Rare in US Like less-virulent Shigella, self limiting, No Shiga Like Toxin Clinical Presentation is Diarrhea, Fever, Dysentary (inflammation of intestine)

Answer 30

``` Enteropathogenic Colonizes intestinal epithelium Similar to EHEC, No Shiga Like Toxin Diarrhea with mucous but little or no blood Malaise, vomitting, fever Childhood Diarrhea ```

Answer 31

Enterotoxigenic Rare in US Colonizes intestinal epithelium via pili via CFA Produces Toxins-- Causing Diarrhea -- Heat Labile Toxin, and Heat Stabile Toxin Clinical Presentation: Afebrile watery diarrhea, infant diarrhea, travelers diarrhea

Answer 32

Enteroaggregative Colonizes intestinal epithelium Pathogenesis: Aggregative adherance fimbraie (AAF) encoded on pAA plasmid, stack brick pattern of adherance Many stains encoded on plasmids and chromosomes, Shiga like toxin in some strains Clinical Presentation: Travelers diarrhea and diarrhea in HIV pts, inflammatory watery diarrhea, vomiting, nausea, fever, growth impairment in children

Answer 33

Gram negative, coccobaccili, facultative intracellular pathogen, highly infectious, causative agent of tularemia (rabbit fever), very low infectious dose (chemical warfare) Encounter: natural pathogen of animals, contact with mucous membranes is enough for infection Transmission: aerosol, man with infected animal (skinning a rabbit), bite of infected tick/fly, can survive and growth within macrophages Clinical Presentation: Acute onset of fever/chills, ulcer at cutaneous infection site and lymph nodes inflamed/painful, sepsis can develop if severe Treatment: Streptomycin (aminoglycosides)

Answer 34

Gram -, curved, microaerophilic, slow growth, tightly coiled, motile with flagellae, urease positive, oxidase positive Encounter: oral-oral contact, vomit Transmission: fecal-oral, Gastric-oral Colonization: gastric mucosa Pathogenesis: Infection with multiple strains, infected for long time (at least decades) and exhibit low grade gastric inflammation with neutrophil invastion Virulence: Adhesins (RBC agglutination) CagA Virulence Island LPS Urease- local CO2 production allows survival in acidic environment Clinical Presentation: Chronic Gastritis (antral) Gastric Cancer (aenocarcinoma- CagA+ H pylori) Primary gastric non-hodgkins lymphoma low grade MALT lymphoma GERD- CagA+ stains protect from GERD Non-ulcer dyspepsia Peptic Ulcer Disease- 2 hit hypothesis of acid production and gastric inflammation, duodenal ulcer Diagnosis: Upper GI endoscopy, serology, breath test, stool antigen Treatment: Triple Therapy- PPI, Amoxicillin, Clarithromycin

Answer 35

Gram -, needs silver stain to visualize, aerobe, fastidious growth, intracellular pathogen, charcoal-containing media, among 3 most common causes of community acquired pneumonia, oxidase positive Encounter: aerosol from contaminated water system Transmission: NOT PERSON TO PERSON Colonization: Alveolar macrophage

Answer 36

2-10 d incubation period, and then establishes infectious niche - bacterium killed by PMN, no macrophages - macrophages phagosome infected, and L pneuomphila modifies the phagosome - -- smooth vesicles bud from phagosome, removing macrophage proteins which would allow for proper phagosome function - -- pores formed in cells to transfer effector molecules - -- DOT- defect in organelle trafficking - -- phagosome associates with RER, and bacteria replicate in this phagosome Bacterial Differentiation - Exponential phase- non-virulent - Post-exponential phase- virulent - switch from replicating, avirulent phenotype to post-exponential, virulent phenotype induced by amino acid starvation Damage - vigorous immune response - cytokines signal monocytes, neutrophils - Microabscesses: PMN, macrophage, fibrin, RBC, debris - LPS and hydrolytic enzymes contribute to inflammation

Answer 37

Pneumonia - fever, malaise, non-productive cough, pleuritic chest pain, rales early in course, mortality as high as 50%, Pneumonia with headaches and diarrhea Control of Infection - cell-mediated immunity, IFN gamma activation of macrophage - down-regulation of transferrin receptor, suppressing growth by limiting iron - antibodies may serve auxillary role promoting uptake b neutrophils Risk Factors - age, chronic lung disease, immunosupression, smoking Diagnosis: CXR, Sputum, culture (days), serology (4-12 weeks), urine antigen test Treatment: treat upon suspicion with tetracycline, ezytrhomycin, azithromycin, fluroquinolones

Answer 38

Gram negative diplococci, non-maltose fermenter, and lacks a capsule. This bacteria lives in humans and is transmitted sexually (more frequenty male to female), or perinatally during delivery In women, it moves its way up the fallopian tubes and uses Pili and Opa proteins to form tight adhesions to mucosal cells (can make micro-colonies) These bugs survive in host due to its ability to acquire iron (has receptors for human transferrin), resisting phagocytosis, and bind Human factor H, which inhibits complement N. gonorrhoeae attaches to human cells and use Opa to facilitate their endocytosis and invasion. Also uses a LPS-like molecule, Lipooligosaccharide (LOS) that is cytotoxic to ciliated Fallopian tube epithelial cells. Will also take advantage of antigenic/phase variation In women, causes Cervicitis, pelvic inflammatory disease, infertility, ectopic pregancy. In men, causes purulent urethral discharge and epididymitis. Disseminated Gonococal Infection leads to arthritis, rarely causing endocarditis and meningitis Treat with ceftriaxone and azithromycin or doxycycline to treat possible chlamydial coinfection

Answer 39

Gram negative diplococci possessing a capsule and is a maltose fermenter. Transmitted by respiratory and oral secretions. Generally asymptomatic respiratory carriers but colonization can be caused by smoking or by an earlier virl infection. Found on the non-ciliated columnar epithelium of the nasopharynx. Spreads locally first and then to bloodstream, but minimal local inflammation. Will spread to the CNS (crosses BBB) and causes meningitis 50% of the time. Its damage is mediated by release of high doses of lipooligosaccharide (LOS) which leads to endotoxic shock and vascular shock Virulence is dictated similarly to N. gonorrhoaea with Pili/Opa aiding adherence and entrance into host cells, iron acquisition, will avoid phagocytosis because of the capsule, has LOS, and has antigenic and phase variation. Is preventable with vaccine (type B vaccine not widely available), and treated with ceftriaxone or penicillin G

Answer 40

Gram negative rod, motile, non-lactose fermenting, oxidase positive strict aerobe. Has many means of avoiding treatment (efflux pumps, effective porins), so are sometimes difficult to treat. Most effective treatment is synergistic (piperacillin/tazobactam, cephalosporins, carbapenems) Transmission is through "moist" sources as they are frequently found in water. Uses pili and polar flagella to colonize Nasty bug because it has membrane degrading toxins (leukocidin which forms pores in cells and PLC which causes cell lysis). Has exotoxin A which inactivates EF-2, pyocyanin (generates reactive oxygen species), and delivers Exotoxins S, T, and U via Type III Sec system. Proteases to spread through infected tissue, LPS as well Has capsule to avoid phagocytosis Causes: pneumonia, sepsis, ecthyma gangrenosum (rapidly progressive necrotic cutaneous lesion typically seen in IC patients), UTIs, osteomyaelities, otitis externa, and general skin infections

Answer 41

Gram negative rods that can disseminate hematogenously and have flagella Typhi: Colonizes human macrophages and remain in phagosomes (prevent lysosomal fusion) and add bacterial proteins into the vacuole membrane that permits the acquisition of nutrients. Can also colonize gall bladder with a long-live asymptomatic carrier state. Is the cause of enteric fever (Typoid) which is a systemic infection with fever, abdominal symptoms, rose spots. Can cause intestinal hemorrage and perforation as well as focal infections (pericarditis, liver abscess, spleen abscess) Typhimurium: Transmitted person to person but first encountered in contaminated food, colonizes the intestinal epithelium. Once in host, will deliver proteins via type III secretion. Will cause gastroenteritis, nausea, vomiting, fever, chills, headache, loose stools lacking blood/mucous, and an inflammatory cell response (dealt with by PMNs)

Bacteria Pt 2 Flashcards

(65 cards)