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Host Defense > bug parade week 2 > Flashcards

bug parade week 2 Flashcards

1
Q

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

A

small, non-motile gram-negative coccobacillus

hard to culture: requries Bordet-Gengou medium

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2
Q

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

A

whooping cough.

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

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3
Q

What happens during pertussis infection?

A

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.

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4
Q

what are the three stages of pertussis infection?

A
  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.
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5
Q

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

A

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)

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6
Q

How is pertussis diagnosed and treated?

A

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

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7
Q

How is pertussis prevented?

A

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.

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8
Q

N. meningitidis: characteristics, cultivation

A

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

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9
Q

what makes N. meningitidis unique among human pathogens?

A
  1. propensity to invate meninges

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

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10
Q

what happens during n. meningitidis infection?

A

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

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11
Q

what are the symptoms of meningitis?

A

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.

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12
Q

how does N. meningitidis attach and spread?

A

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.”

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13
Q

what are two critical virulence factors of N. meningitidis?

A
  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)
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14
Q

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

A

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

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15
Q

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

A

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

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16
Q

what diseases can be caused by H. influenzae?

A 
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
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17
Q

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

A
  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
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18
Q

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

A

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

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19
Q

What are the characteristics of mycoplasma pneumoniae: characteristics, growth

A

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

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20
Q

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

A

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.

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21
Q

what are the three virulence factors of mycoplasma pneumoniae?

A
  1. adherence: P1 protein
  2. toxicity: H2O2.
  3. inflammation: toxin causes pulmonary and lymphatic inflammation
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22
Q

how is mycolplasma pneumoniae diagnosed and treated?

A

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

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23
Q

chlamydioophila pneumoniae: characteristics

A

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)

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24
Q

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

A

person-to-person transmission of resp. secretions

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

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25
Q

What is the pathogenesis of chlamydophila pneumoniae?

A

EB attaches to host cell and gians entry through endocytosis. endosome changes to RB form

  1. RB form replicates via binary fission
  2. RBs transform into EBs which spread to neighboring cells
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26
Q

How is chlamydophila pneumoniae diagnosed, and treated?

A

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

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27
Q

neisseria gonorrheae: characteristics. growth features, reservoir, transmission

A

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

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28
Q

what is the pathogenesis of neisseria gonorrheae?

A

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)

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29
Q

how is gonorrhea diagnosed?

A

PCR, gram stain

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30
Q

what are the clinical manifestations of gonorrhea?

A

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.

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31
Q

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

A

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
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32
Q

How do you treat gonorrhea?

A

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

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33
Q

chlamydia trachomatis (C. trachomatis): characteristcs, growth

A

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

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34
Q

How is C. trachomatis transmitted?

A

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.

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35
Q

Describe C. trachomatis infection/lifecycle

A

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

36
Q

How is C. trachomatis diagnosed?

A

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

37
Q

What are the relevent serotypes of C. trachomatis?

A

A-C, D-K, L1-L3

38
Q

Serotypes A-C of C. Trachoma

A

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

39
Q

Serotypes D-K of C. trachoma

A

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)

40
Q

Serotypes L1-L3: C. trachoma

A

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

41
Q

How do you treat C. trachoma?

A

NO BETA LACTAMS (no cell wall)

treat with macrolides or tetracyclines, exp. azithromycin or doxycycline

42
Q

Hemophilus ducyrei: characteristics, growth

A

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

43
Q

what disease is caused by hemophilus ducyrei?

A

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)

44
Q

How is hemophilus ducyrei treated and transmitted?

A

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

45
Q

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

A

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

46
Q

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

A

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

47
Q

cholera: symptoms, disease progression

A

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

48
Q

Describe the bichemical pathogenesis of cholera

A

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).

49
Q

How is cholera treated?

A

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

50
Q

What are the three relevant cholera serotypes?

A

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.

51
Q

Describe cholera genetics for cholera toxin

A

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.

52
Q

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

A

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

53
Q

How are virulence factors regulated in vibrio cholera?

A

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.

54
Q

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

A

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

55
Q

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

A

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)

56
Q

Vibrio vulnificus: gram stain? diseases? sources?

A

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

57
Q

How is Vibrio vulnificus treated when a wound is infected?

A

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

58
Q

What populations should not eat raw oysters, and why?

A

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.

59
Q

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

A

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

60
Q

What happens during shigella infection?

A

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

61
Q

How is shigella prevented and treated?

A

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.

62
Q

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

A

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

63
Q

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

A

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

64
Q

typhoid fever: reservoir, causes/sources, prevention

A

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

65
Q

Characteristics of typhoid fever

A

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

66
Q

describe the pathogenesis of S. typhi

A
  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:
  8. death (GI hemorrhage and bowel perforation with peritonitis)
  9. resolution in 3-5 weeks
  10. Permanent carrier status: gall bladder.
67
Q

What happens during salmonella invasion?

A

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)

68
Q

PhoP/PhoQ

A

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

69
Q

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

A

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

70
Q

Sequelae of C. jejuni

A

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

71
Q

What factors contribute to C. jejuni virulence?

A

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.

72
Q

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

A

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

73
Q

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

A

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

74
Q

How can you treat an H. pylori infection?

A

tetracycline, metronidazole, and bismuth (pepto-bismal)

75
Q

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

A
  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
76
Q

What are the major virulence factors for H. pylori?

A

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

77
Q

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

A 
gram negative
motile
straight or slightly curvy rod
non-lactose fermenter
oxidase positive
78
Q

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

A

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

79
Q

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

A

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)

80
Q

Legionella pneumophila: characteristics, motility, growth

A

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!

81
Q

What is legionnaires’ disease?

A

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

82
Q

What is pontiac fever

A

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

83
Q

Where do you get legionnaire’s disease (source)

A

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

84
Q

How do legionella cause disease

A

legionella pneumophila are phagocitized by macrophages

  1. they multiply intracellularly until the macrophage ruptures
  2. they infect other cells
  3. 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.
85
Q

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

A

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.

Host Defense (38 decks)

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