bug parade week 2

Question 1

Bordetella pertussis: shape, gram stain, disease caused, motility, culture

Answer 1

small, non-motile gram-negative coccobacillus

hard to culture: requries Bordet-Gengou medium

Question 2

what disease is caused by bordetella pertussis? How is it spread? What is the incubation period?

Answer 2

whooping cough.

spread via contact with an infected aerosol (3-12 day incubation period)

Question 3

What happens during pertussis infection?

Answer 3

attachment to ciliated epithelial cells using bacterial proteins.
then, the bacteria produces toxins that disrupt ciliary activyt and cause epithelial cell death.
leads to mucus production: clogged airways and uncontrollable coughing.

Question 4

what are the three stages of pertussis infection?

Answer 4

1. catarrhal stage: runny nose, low-grade fever, cough. very contagious
   paroxysmal stage: 1-10 wks. lots of bad coughing. vomiting and exhaustion following coughing fits.
   convalescent stage: 2-3 wks.

Question 5

what are the three pertussis virulence factors that are found in the pertussis vaccine? What do these factors do?

Answer 5

pertussis toxin (helps with adhesion and interferes with ciliated epithelial cell metabolism), filamentous hemagglutinin (forms filamentous structures on the bacterial cell surface) and pertactin (attachment)

Question 6

How is pertussis diagnosed and treated?

Answer 6

diagnosis: symptoms and history. may be cultured on bordet gengou medium
treatment: supportive. may use antibiotics to stop spread, though antibiotics don’t always help speed up the recovery

Question 7

How is pertussis prevented?

Answer 7

whole cell pertussis part of the DPT vaccine or acellular vaccine containing pertussis toxin, pertactin, and filamentous hemagglutinin. this vaccine has fewer side effects. lasts 10 yrs. adults who work with kids should get the vaccine every 10 years as well.

Question 8

N. meningitidis: characteristics, cultivation

Answer 8

neisseria meniningitidis
gram negative diplococcus with a kidney bean shape.
use chocolate agar and make sure everything is warm.

Question 9

what makes N. meningitidis unique among human pathogens?

Answer 9

1. propensity to invate meninges

2. ability to proliferate in the blood, leading to endotoxemia-mediated shock and multiple organ failure.

Question 10

what happens during n. meningitidis infection?

Answer 10

aspiration of infective bacteria, attachment to epithelial cells of the nasopharynx and oropharynx, crossing of the mucosal barrier, bloodstream entry, and crossign of the blood/brain barrier

Question 11

what are the symptoms of meningitis?

Answer 11

headache, nausea, vomiting and photosensitivity. petechiae or purpura
fulminant meningococcemia: sudden high fever, chills, weakness, nausea, vomiting, hedache, restlessness, delirium. widespread purpuric and ecchymotic skin lesions.

Question 12

how does N. meningitidis attach and spread?

Answer 12

attacht to the non-ciliated columna epithelial cells of the nasopharynx via fimbriae. bacteria enter via parasite-directed endocytosis. membrane of the mucosal cell retracts and pinches off a vacuole that contains the bacteria.
vacule transported to the base of the cell and is relezed in to the subpithelial tissue.
“breach of the the endothelial barrier, and induction f strong inflammatory responses, appear key to pahtogenesis of meningococcal meningitis.”

Question 13

what are two critical virulence factors of N. meningitidis?

Answer 13

1. capsule: antiphagocytic and carry the polysccharides that allow us to serotype the bug (important serotypes are ABCY and W135)
   endotoxin: lipooligosaccharide: oligosaccharide attached to alipid A core (like LPS but shorter)

Question 14

what is the diagnosis, treatment, and prevention of N. meningitidis?

Answer 14

diagnosis: symptoms/history, esp. with a petechial rash.
treatment: antibiotics might work (OR NOT).
prevention: vaccine for groups A, C, AC, and ACYW135 available.

Question 15

Haemophilus influenzae: characteristics, motility, culture conditions. where does it normally live?

Answer 15

small non-motile gram negative rod or coccobacilli
requires chocolate agar beacuse of heme and NAD needs
lives in nasopharynx, esp. as a non-encapsulated strain and transmitted via resp. route. humans are the reservoir

Question 16

what diseases can be caused by H. influenzae?

Answer 16

meningitis in kids from 3 mo. to 3 yrs (kids of this age can't make antibodies agains the polysaccharide capsule) 
septic arthritis
cellulits
epiglottits (can be fatal)
otits media/sinusits

Question 17

what are the virulence factors of H. influenzae (3-4)

Answer 17

1. capsule: type b polysaccharide capsule very viulent. helps to penetrate nasopharynx epithelium and invade blood capillaries.
2. fimbriae: increase adherence to human mucosal cells
3. IgA protease and neuraminidase

Question 18

how is H. influenzae diagnosed, treated, and prevented?

Answer 18

diagnosis: age, vaccination status and s/s of disease. gram negative coccobacilli.
treatment: good, if caught early. antibiotics?
3. vaccination, esp. with a vaccine that conjugates the carbohydrate to a protein carrier

Question 19

What are the characteristics of mycoplasma pneumoniae: characteristics, growth

Answer 19

very small! no cell wall- sterols predominate in the membrane. grow on many media but take weeks

Question 20

what disease is caused by mycoplasma pneumoniae? how do they colonize/spread?

Answer 20

atypical pneumonia which is mild but long-lasting
colonize: attachment to epithelial cell surface and the cessation of ciliary movement. contamination of the resp. tract and a dry cough.

Question 21

what are the three virulence factors of mycoplasma pneumoniae?

Answer 21

1. adherence: P1 protein
2. toxicity: H2O2.
3. inflammation: toxin causes pulmonary and lymphatic inflammation

Question 22

how is mycolplasma pneumoniae diagnosed and treated?

Answer 22

diagnosis: clinical presentation/history
treatment: MACROLIDE antibitotics. not cell wall active antibiotics!!
resistance is a prob.

Question 23

chlamydioophila pneumoniae: characteristics

Answer 23

obligate intracellular bacteria (need host for ATP and nutrients)
gram-neg architeture
2 forms: one for replication (reticulate body) and one for spread (elemental body)

Question 24

what disease is caused by chlamydophila pneumoniae, and how is it spread?

Answer 24

person-to-person transmission of resp. secretions

causes atypical pneumonia, pharyngitis, bronchitis, sinusitis, and atherosclerosis (maybe)

Question 25

What is the pathogenesis of chlamydophila pneumoniae?

Answer 25

EB attaches to host cell and gians entry through endocytosis. endosome changes to RB form 2. RB form replicates via binary fission 3. RBs transform into EBs which spread to neighboring cells

Question 26

How is chlamydophila pneumoniae diagnosed, and treated?

Answer 26

diagnosis: clinical picture. many infections are asymptomatic/mild treatment: macrolide antibiotics

Question 27

neisseria gonorrheae: characteristics. growth features, reservoir, transmission

Answer 27

gram negative diplococcus often found within neutrophils from purulent cerivcal/urethral discharge. humans are the only known host transmission: sexual, including oral

Question 28

what is the pathogenesis of neisseria gonorrheae?

Answer 28

adherence and invasion of superficial mucosal surfaces likned with columna epithelium (male urethra, female cervix, nasopharynx, conjuctiva) uses pili, enters cells via endocytosis, gonorrheae pili undergoes Antigenic Variation (thus, you can calso get gonorrhea over and over again)

Question 29

how is gonorrhea diagnosed?

Answer 29

PCR, gram stain

Question 30

what are the clinical manifestations of gonorrhea?

Answer 30

Men: urethritis (yellow, malodorous, urulent urethral discharge with dysuria (pain on urination). may be asymmptomatic usually presents 2-3 days after sexual activity with infected partner women: half are asymptomatic. others present with cervicitis: yellow malodorous purulent cervical discharge. looks like a yeast infection. both: pharyngitis: young adults. present with severe sore throat, fever, and greenish exudate. oral sex is transmission method.

Question 31

what complications can arise from gonorrhea? treatment? 4 complications were discussed

Answer 31

dissemination to other parts of the body: 1. septic arthrits: spread throug blood to joints, esp. in knee. requires antibiotics AND joint washing/surgery 2. conjuctivitis: esp. of neonates infected during birth. can cause blindness. treat with topical antibiotics. 3. Pelvic inflammatory diseases: causes infertility and ectopic pregnancies. cervical motion tenderness observed (extreme pain during pelvic exam). 4. prostatitis and orchitis: perineal pain, difficult urinaiton, and male sterility

Question 32

How do you treat gonorrhea?

Answer 32

Ceftriaxone This is the ONLY remaining first line drug for gonorrhea, and we are very worried about resistance. treat ALL pts with gonorrhea as if they have chlamydia, too: oral azithromycin or doxycycline

Question 33

chlamydia trachomatis (C. trachomatis): characteristcs, growth

Answer 33

Gram negative, OBLIGATE INTRACELLULAR bacteria with no peptidoglycan cell wall. bacteria can't be grown with traditional methods: requires a giemsa stain.

Question 34

How is C. trachomatis transmitted?

Answer 34

contact with infected secretions and infects mucus membranes (urethra, cervix, throat, conjunctiva). mostly spread sexually but toching genitals and then eyes can also be a problem. Not easily spread by women: men are most common transmitters.

Question 35

Describe C. trachomatis infection/lifecycle

Answer 35

2 forms: elementary and reticulate body elementary is infectious and enters columnar epithelial cells via endocytosis. then, reticulate bodies replicate via binary fission.

Question 36

How is C. trachomatis diagnosed?

Answer 36

PCR of endocervical swab (women) first-catch urine (men) antigen dectection might be possible difficult culture requirements: don't use culture for diagnosis!

Question 37

What are the relevent serotypes of C. trachomatis?

Answer 37

A-C, D-K, L1-L3

Question 38

Serotypes A-C of C. Trachoma

Answer 38

cause chronic conjunctivitis in kids and is the leading cause of preventable blindness, esp. in developing world causes inflammation and scarring. spread via close contact with secretions

Question 39

Serotypes D-K of C. trachoma

Answer 39

non-gonococcal urethritis, cervicitis, and conjunctivitis. Causes CLEAR urethral or cervical discharge and dysuria (pain with urination). very very often asymptomatic but causes PID (pelvic inflammatory disease). again, conjunctivitis can be passed along to babies during birth: slighly more hemorrhagic than gonococcal conjunctivitis. neonatal conjunctivitis can lead to chlamydial pneumonia, so treat this with SYSTEMIC oral antibiotics (macrolide)

Question 40

Serotypes L1-L3: C. trachoma

Answer 40

causes lymphogranuloma venerum chronic, ulcerative infection of lymphatics, exp. in tropical/subtropical environments. 2 stages: 1. painless, self-healing genital ulcer 2. painful, swollen inguinal lymph nodes

Question 41

How do you treat C. trachoma?

Answer 41

NO BETA LACTAMS (no cell wall) | treat with macrolides or tetracyclines, exp. azithromycin or doxycycline

Question 42

Hemophilus ducyrei: characteristics, growth

Answer 42

gram negative bacillus/coccobacillus. grown on supplemented chocolate agar.

Question 43

what disease is caused by hemophilus ducyrei?

Answer 43

chancroid. asymmptomatic in women but causes a painful ulcer on the penis of infected men, accompanied by inguinal lympadenopathy. these sores are PAINFUL, SOFT, and PURULENT (unlike syphilis sores, which are pain-free, indurated, and not purulent)

Question 44

How is hemophilus ducyrei treated and transmitted?

Answer 44

transmission: sexual via skin abrasions treatment: macrolide (azithromycin or erythromycin) or ceftriaxone

Question 45

What are characteristics of a mycoplasma STI (growth, characheristics, 3 diseases)

Answer 45

lack a cell wall. intracellular and require media with cholesterol in order to grow 3 characteristics: mycoplasma genitalium causes nongonococcal urethritis ureaplasma urealyticum causes nongonococcal urethritis and prostatits mycoplasma hominis causes PID, postpartum fever and pyelonephritis

Question 46

characheristics of vibrio cholera (shape, gram, motility, reservoir, transmission)

Answer 46

gram negative rod and is a facultative anaerobe motile by means of a single polar flagellum transmission via contaminated water or food reservoir: water, world-wide

Question 47

cholera: symptoms, disease progression

Answer 47

can be rapidly fatal sudden onset of voluminous diarrhea. leads to dehydration, anuria, acidosis, and shock. people give off "rice water" stools: stools contain mucus and epithelial cells and are very watery. Some cardiac complications seen

Question 48

Describe the bichemical pathogenesis of cholera

Answer 48

mediated by the choleratoxin. Cholera is ingested in a relatively high infectious dose, since it is susceptible to stomach acids V. cholera colonizes the small intestine V. cholera produces its toxin the toxin activates adenylate cyclase enzymes, transfer of ADP ribose to Gs protein, leading to an increase in cAMP. this effect depends on monosialosyl ganglioside present on the surface of intestinal mucosal cells. Pathogen also makes neuraminidase, which degrades gangliosides to form the monosialosyl form. increased cAMP leads to secretion of H20, Na, K, Cl, and HCO3 into the lumen of the small intestine (starts with Cl pump; others follow Cl out).

Question 49

How is cholera treated?

Answer 49

either rapid IV fluid replacement or oral solutions, which contain water, electrolytes, and glucose. antibiotics are not generally used.

Question 50

What are the three relevant cholera serotypes?

Answer 50

O1, El tor (also produces hemolysins, heagglutination), and O139- first epidemic strain to not be of the O1 subtype. This was dangerous because nobody had any pre-existing immunity to this subtype.These serogroups describe the lipopolysaccharide O antigens.

Question 51

Describe cholera genetics for cholera toxin

Answer 51

The ctx gene is encoded as part of a larger genetic element of the V. cholerae chromosome. this element belongs to the genome of the CTX phi phage, which also includes genes for phage morphogenesis, replication of the phage, and integration of phage DNA. Therefore, it can be horizontally transferred. CTX phi receptor is the toxin-coregulated pili (TCP), which is also essential for colonization.

Question 52

What is important during V. cholera's colonization of the small intestine?

Answer 52

adhesins, neuraminidase, motility, resistance to bile salts. Adherence to the intestinal mucosa mediated by TCP.

Question 53

How are virulence factors regulated in vibrio cholera?

Answer 53

ToxR responds to environmental stimuli and cell density. ToxR is a TM protein that cand bind DNA and accessory proteins. ToxR increases toxT expression, which encodes the ToxT transcriptional activator. ToxT binds to the promoter of cholera toxin, the TCP gene, and genes for other virulence factors.

Question 54

vibrio parahaemolyticus: gram, asociated disease, pandemic strain, source

Answer 54

gram negative major cause of gastroenertitis in developed nations causes vomiting and diarrhea (possibly bloody diarrhea) pandemic strain is O3:K6. source: seafood

Question 55

What mediates the pathogenesis of vibrio hparahaemolyticus? What is one test/diagnostically relevant feature?

Answer 55

type III secretion system wherein a variety of toxins are inserted directly into host cells toxins are T3SS encoded proteins this has the kanangawa phenotype (diagnosticly)

Question 56

Vibrio vulnificus: gram stain? diseases? sources?

Answer 56

source: seafood, esp. oysters. 2 kinds of hazards: 1. wound contamination leading to edema, hemorrhagic lesions, and rapidly spreading necrotic regions 2. GI infection and possible septisemia

Question 57

How is Vibrio vulnificus treated when a wound is infected?

Answer 57

AGGRESSIVELY. debridement, possible amputation, and triple antibiotic therapy: tetracycline, 3rd gen cephalosporins, and imipenem

Question 58

What populations should not eat raw oysters, and why?

Answer 58

immunocompromised, ppl with liver disease, ppl with hemochromotosis, ppl with too much serum iron. they might get V. vulnificus infection, leading to septicemia and a 50% mortality rate.

Question 59

Shigella: what disease do they cause? Reservoir? Affected populations? Transmission?

Answer 59

primary cause of bacterial dysentery, wherein dysentery descripbes stools of relatively small volume that contain blood, mucus, and inflammatory cells. Shigellosis causes lower abdominal cramps and tenesmus with abundant pus and blood in the stool. Reservoir: humans and "higher apes" Transmission: HIGHLY communicable- infectious dose as low as 10 organisms. oral-fecal route Affected pops: kids, 6 mo-10 yrs. or populations suffering from overcrowding, poor sanitation, and poor nutrition

Question 60

What happens during shigella infection?

Answer 60

Person-to-person transmission. VERY low infectious dose (as low as 10 organisms!) oral-fecal route. Critical step: colonization of the colon and penetration of the colonic epithelium (esp. M cells) visible disruption of the brush border follwed by endocytosis organism gets free in the cytoplasm and multiplies. leads to cell death and infection of adjacent cells forms a micro-abscess with form larger abscesses with form mucosal ulcerations. lesions also the result of persistant inflammation and epithelial necrosis

Question 61

How is shigella prevented and treated?

Answer 61

proper sanitation, proper feces disposal, potable water, hand washing with potable water. treatment: fluid and electrolyte balance; infection generally self-limited. antibiotics used to prevent spread to family members and close contacts of infected individuals. Amp and/or tetracycline might work, but shigella is fairly antibiotic resistant.

Question 62

Salmonella: gram, motility, shape, daignostic/growth characteristics. two types.

Answer 62

gram neg motile rod-shaped facultative anaerobes that don't use lactose but produce H2S. facultative intracellular pathogens that can live inside macrophages and epithelial cells. typhoid and non-typhoid types

Question 63

non-typhoid salmonella: causes/sources, incubation, symptoms, treatment

Answer 63

symptoms: vomiting and diarrhea and nausea lasting 2-5 days incubation: 8-48 hrs after exposure causes: contaminated food, esp. poultry and poultry products; or food handlers treatment: supportive. generally no antibiotics given

Question 64

typhoid fever: reservoir, causes/sources, prevention

Answer 64

causes: fecal-oral route of infection (salmonella typhi) reservoir: all human Prevention: hygiene, oral/intramuscular vaccination, don't travel

Question 65

Characteristics of typhoid fever

Answer 65

sustained fever lasting 2-4 wks, bacteremia, abdominal tenderness, and leukopenia

Question 66

describe the pathogenesis of S. typhi

Answer 66

1. ingest contaminated food or water 2. bacteria penetrate the small intestine 3. Bacteria invade the lymphatci tissues and multiply 4. Bacteria enter the blood stream and to to many organs, including kidneys and intestines (7-14 days) 5. Patient feels sick! Malaise, headache, fever, detectable bugs in blood) 6. Organisms get to gall pladder and stool cultures become positive 7. Rose spots rash apears in the 2nd or 3 rd week 3 outcomes: 1. death (GI hemorrhage and bowel perforation with peritonitis) 2. resolution in 3-5 weeks 3. Permanent carrier status: gall bladder.

Question 67

What happens during salmonella invasion?

Answer 67

penetration through M cells of the Peyer's patches. Host cell membrane "ruffling" ruffled cells wrap around bacteria and pull them in Similarly, macrophages will eat up these organisms then, macrophages carry them to the lymphatic system. get to the liver and spleen. bacteria replicate there and enter the blood (septicemia) also go to the gall bladder, replicate, and go back to the intestines cause inflammation and ulceration of the intestine (diarrhea, hemorrhage, perforation)

Question 68

PhoP/PhoQ

Answer 68

-Salmonella species -P is the transciptional regulaor Q is the membrane sensor required for virulence regulate gene expression

Question 69

Campylobacter jejuni: disease, reservoirs, sources, primary symptoms of infection. gram

Answer 69

gram negative rod disease: primary cause of food-borne illness in US. causes abdominal cramps, fever, diarrhea, and dysentery source: many animals, esp. poultry/avian species (not pathogenic in birds) source: contaminated food

Question 70

Sequelae of C. jejuni

Answer 70

reactive arthritis, Reiter syndrome, and Guillain Barre syndrome these may be due to cross-reactivity

Question 71

What factors contribute to C. jejuni virulence?

Answer 71

LPS, capsule, flagella, and toxins that induce inflammation may play a role best characterized: cytolethal distending toxin: -AB toxin. A binds, B goes to the nucleus and causes cell cycle arrest, possibly by inducing DNA damage. cytotoxic and possibly also pro-inflammatory.

Question 72

why is C. jejuni a people pathogen but a chicken commensal?

Answer 72

In humans, C. jejuni invades epithelial cells and causes inflammation. In chickens it stays in the mucus layer and doesn't cause inflammation.

Question 73

What are some characteristics of H. pylori (gram, shape, growth conditions).

Answer 73

Gram negative micro rod that colonizes the gastric mucosa hard to culture

Question 74

How can you treat an H. pylori infection?

Answer 74

tetracycline, metronidazole, and bismuth (pepto-bismal)

Question 75

What three factors are essential for H. pylori survival and pathogeneis?

Answer 75

1. buffering of pH: H. pylori secres urease to buffer the pH of immediate surroundings 2. swimming through the mucus: highly motile because of a bundle of 6-8 unipolar flagella. 3. bacterial surface components that allow for adherence to the grastric epithelial cells

Question 76

What are the major virulence factors for H. pylori?

Answer 76

VacA cag pathogenicity island that uses a type IV secretion system and helps deliver CagA to host cytoplasm CagA induces host cytoskeletal rearrangment, which gives it a pedestal on which to sit. Inflammation is also important for pathogenesis and can lead to ulcers or adenocarcinoma

Question 77

Pseudomonas aeruginosa: gram, motility, shape, diagnostic/growth stuff

Answer 77

``` gram negative motile straight or slightly curvy rod non-lactose fermenter oxidase positive ```

Question 78

What are some diseases that can be caused by pseudomonas aeruginosa? What is the common feature of these diseases?

Answer 78

These diseases occur following the breakdown of innate body defenses endocarditis (IV drug users, pts with prosthetic heart valves) respiratory infections (imminocompromised pts, pts on ventilators, CF) bacteremia and septicemia (AIDS, neutropenia, burns- immunocompromised ppl) CNS infections (direct innoculation from head trauma or invasive diagnostic procedures, or spread from a UTI. Which, terrifying) ear infections eye infections if there is a break in the integrity of the corneal epithelium bone and jt infections from direct inoculation or spread from other parts of the body (esp. seen in IV drug users) UTIs, esp. from catheterizaion GIs:esp. in immunocompromised ppl skin and soft tissue infections following burns

Question 79

What are the main virulence factors of P. aeruginosa/factors that affect colonization and invasion?

Answer 79

largely oppurtunistic- not very virulent! most pathogenesis linked to regulation of virulence factors via quorum sensing: pili (adherence) exotoxins A and S, elastase, phospholipase C (cell destruction) flagella (motility) siderophores (sequester iron) type III secretion system (injection of virulence factors) and mucoid exoppolysaccharide/antibiotic tolerance in biofilms.(evasion of immune response/therapy)

Question 80

Legionella pneumophila: characteristics, motility, growth

Answer 80

pleomorphic aerobic faintly gram neg in culture may appear filamenouts, in clinical specimens may look like coccobacilli single polar flagellum slow growing (3-5 days) tel lab that you're looking for legionella!

Question 81

What is legionnaires' disease?

Answer 81

severe form of pneumonia often in elderly or immunocompromised high fever, chills, cough (2-14 days after exposure).

Question 82

What is pontiac fever

Answer 82

mild diseases caused by legionella. symptoms for 2-5 days with fever, headaches, and muscle aches but no pneumonia. no treatment needed

Question 83

Where do you get legionnaire's disease (source)

Answer 83

from water- can live in many water environments and are resistant to high temps and chlorine. they parasitize amoebas and also form biofilms.

Question 84

How do legionella cause disease

Answer 84

legionella pneumophila are phagocitized by macrophages 2. they multiply intracellularly until the macrophage ruptures 3. they infect other cells 4. monocytes and polymorphonuclear leukocytes can't always help, but hopefully the immune system eventually wins. Much of the damage is done by a vigorous host inflammatory response due to the fact that infected macrophages release lots of cytokines.

Question 85

How is legionnaire's disease diagnosed and treated? how is it prevented?

Answer 85

diagnosis: pneumonia plus: positive urinary antigen test OR legionella culture from a clinical specimen OR increased antibody levels in blood (paired) treat with antibiotics Prevention: check for legionella in the water.