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Host Defense > bug parade > Flashcards

bug parade Flashcards

1
Q

staphlyococcus genus

A

round, gram positive cocci that are arranged like grapes. non-spore forming but hardy nonetheless: can survive for long periods on dry inanimate objects and is relatively resistant to heat.

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2
Q

S. aureus: coagulase results and color of colonies, catalase results?

A

coagulase pos and golden yellow colonies

catalase positive

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3
Q

what is the hallmark of stapholococcus infections? what are common sites for S. aureus coloniation in healthy ppl?

A

hallmark: abssess

reservoir; human nares and skin

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4
Q

what is USA300?

A

a hypervirulent strain of stapholococcus aureus that can cause disease in otherwise healthy individuals (esp. athletic teams and daycare centers)

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5
Q

what are five major features of the cell wall of staph aureus? how do they behave as virulence factors?

A
  1. peptidoglycans: leukocyce chemoattractant
  2. teichoic acid: adherence to mucosal surfaces
  3. protein A: bind Fc portion of IgG; inhibits phagocytosis and opsonization (process whereby a pathogen is marked for ingestion/phagocytosis)
  4. clumping factor: bound coagulase
  5. capsule: prevents phagocytosis
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6
Q

what are seven soluble virulence factors of S. aureus?

A
  1. leukocidin (damage to WBCs)
  2. catalase (reduces efficacy of phagocytes)
  3. coagulase: clot formation
  4. hemolysins (kills RBCs)
  5. hyaluronidase: hydrolyzes hyaluronic acid in tissue and allows for bacterial spread
  6. beta lactamase: inactivates penicillin
  7. exotoxins: may cause toxic shock toxins which are superantigens
    Also has staphylokinase, DNase, lipases, and proteiases
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7
Q

What are the main ways in which stapholococcus strains are typed?

A

MLST: multi-locus sequence typing: looks at the conservation of housekeeping genes.
may also use pulsed field gel electrophoresis (digest DNA and look how it runs on a gel) or spa typing (look at comparing the number and sequence of repeat sequences within the protein A/spa gene

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8
Q

chronic granulomatous disease

A

fatal disease characterized by frequen and serious S. aureus infection due to a genetic defect in phagocyte formation. neutrophils don’t make enough H2O2 to set off the killing pathway- staph wins

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9
Q

scalded skin syndrome

A

life threatening disease, esp. of kids, that leads to skin sloughing. exfoliatin toxin causes these synptoms. treat with antitoxin. produced by staph infections.

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10
Q

staphylococcal food poisoning

A

caused by intoxication rather than infection. results from the production of one of sixe serologcially distinct staphylococcal enterotoxins (a-f). very heat stable and not destroyed by cooking. causes acute vomiting and diarrhea within 1-5 hrs. superantigens.

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11
Q

toxic shock syndrome

A

life theatening. high fever, vomiting, diarrhea, sore throat, and muscle pain. may progress to severe shock with renal and hepatic damage within 48 hrs. cuased b toxin TSST-1, which is a superantigen. identical to enterotoxin F and pyrogenic toxin C.
Process:
vagina colonized with TSST-1 producing S. aureus.
2. tampon facilitates S aureus and TSST-1 growth.
3. toxin is absorbed. systemic effects may be because of toxin or because of cytokines released by the superantigen mechanism. toxin binds to the V beta protion of the Tcell recpetor and the class II MHC receptor. this causes production of IL1 and TNF cytokines.

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12
Q

what are two coagulase negative staphylococci?

A

S. epidermidis and S. saprophyticus
S. epidermidis rarely causes disease but may be found in pts with implanted artificail devices and IV catheters. biofilm formation is important in pathogenesis
S. saprophyticus: basically only causes UTIs in young women

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13
Q

streptococci genus

A

gram positive cocci arranged in pairs or chains, usually. many species in mouth and nasopharynx; some in GI tract.

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14
Q

in what three ways are streptococci species grouped?

A

by hemolysis pattern; biochem properties; serological properties (A, B, etc).

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15
Q

S. pyrogenes: hemolysis, cell wall polysaccharide, surface protein, diseases, diagnostic features

A

beta hemolysis
lancefield group A
80+ M proteins
associated with pharyngitis, impetigo, rheumatic and scarlet fever, and glomerulonephritis. it is bacitracin sensitive

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16
Q

S. agalactiae: hemolysis, cell wall polysaccharide, diseases, diagnostic features

A

beta hemolysis
B is the lancefield cell wall polysaccharaide
causes neonatal sepsis and meningitis
it is bacitracin resistant

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17
Q

S. bovis: hemolysis, cell wall polysaccharide, diseases, diagnositic features

A

alpha or gamma (non) hemolytic
D (cell wall polysaccharide)
generally not very virulent but can cause endocardidtis. frequently isolated from the blood of pts with colon cancer
doesn’t grow on 6.5% NaCl plates

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18
Q

S. pneumoniae: hemolysis, diseases, diagnostic features

A

alpha hemolytic, causes pneumonia, meingitis, and otitis media. it is bile-soluble and is inhbitied by optochin. they are oval.lancet shaped and often arranged in diplococci or short chains.

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19
Q

viridans (green): hemolysis, disease, diagnostic features

A

alpha or gamma hemolytic
low virulence but can cause endocarditis when protected from host defenses. they are the most common cause of subacute bacterial endocarditis of abnormal heart valves. S. mutans causes dental caries
not bile-soluble and not inhibited by optochin

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20
Q

enterococci: hemolysis, lancefield cell wall polysaccharide, diseases, diagnosis
(E. faecalis is an example)

A

alpha or non-hemolytic
D
causes UTIs; often vancomycin resistant
grows in 6.5% NaCl and is bile esculin-positive

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21
Q

Name ad explain 7 diseases caused by group A strep. know what these diseases are.

A
  1. pharyngitis (strep throat)
  2. Impetigo (epidermis infection often seen on face and lower limbs)
  3. erysipelas: infection of skin and subq tissues (epidermis and upper dermis). It is characterized by a spreading area of erythema and edema with rapidly advancing, well-demarcated edges, pain, and systemic manifestations. Treat immediately with antibiotics.
  4. Cellulits: infection of lower dermis
  5. wound/burn infection
  6. necrotizing fasciitis: invasive GAS disease that can lead to bacteremia and sepsis
  7. puerperal infection: postpartum infection of the uterus- “childbed fever.” can be lethal.
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22
Q

What are two diseases associated with strep. pyrogenes exotoxins

A
  1. Scarlet fever (pharyngitis with arast that is due to erythrogenic exotoxin
  2. toxic shock-like syndrome (TSLS). you see shock, renal impairment, rash, resp failure, and diarrhea- systemic toxin. due to SPE toxins (streptococcal pyrogenic exotoxins), esp. SPE A. SPEs are superantigens: bind directly to antigen processing cell so we get a huge cytokine storm.
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23
Q

What is acute rheumatic fever/acute glomerulonephritis?

A

these are immune-mediated sequelae of streptococcal infection. it is basically an autoimmune disease that occurs 2-3 wks after pharyngitis due to cross-reactivity btw streptococcal antigens and human heart and jt antigens. AGN can occur 1 wk after impetigo or pharyngitis becasue antigen/antibody complexes are deposited in the basement membrane of the nephron and cause inflammation. you get bloody urine (hematuria)

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24
Q

What is the role of M protein?

A

it is an anti-phagocytic factor of S. pyrogenes and is the centralthrem in sptretococcal pathogenesis. there are more than 80 serotypes based on antigenic differences in epitopes of the M protein. Immunity to gropu A strep is mediated by type-specific antibody to the given M protein. Without M proteins, strep A is not infectious.

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25
Q

What is the role of F protein in strep infections>

A

it has a receptor for fibronectin, which is a matrix protein on eukaryotic cells and may be important for adhesion of bacteria to epithelial cells of the pharynx and skin.

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26
Q

What role do lipoteichoic acid and capsules play in group A strep infections?

A

Lipoteichoic acid: binds to fibronectin. may help with adhesion to epithelial cells
capsule: hyaluronic acid capsule of group A strep is non-immunogenic and protects against phagocytosis

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27
Q

What are the wto hemolysins responsible for the hemolysis with group a strep.

A

streptolysin O and S. O lysis PMN

S lyses RBCs, leukocytes, and platelets. this is responsible for observed beta hemolysis.

28
Q

What is streptokinase?

A

it is an exotoxin that cuases lysis of fribrin clots and facilitates the rapid spread of bacteria in tissue. also used to treat stroke bc it is a clot buster.

29
Q

What is the main virulence determinant of group b strep?

A

the polysaccharide capsule, which can be typed and which all contain sialic acid.

30
Q

Tell me about the bacillus genus. What are the two species with which we are most concerned?

A

gram positive
rod shaped
large
aerobic spore formers; spore formation occurs in response to stress
species of concern: b. anthracis (causes ANTHRAX), and B. cereus (causes food poisoning)

31
Q

What are the three types of anthrax?

A

cutaneous (through epithelial barrier breaches)
gastrointestinal (through contaminated uncooked meat)
pulmonary (through inhalation of spores and lunch infection. 60% mortality).

32
Q

What are some drugs that can be used to treat anthrax?

A

penicillin, doxycycline,a nd ciprofloxacin

33
Q

What are the virulence factors of B. anthracis?

A
  1. capsular polypeptide (D0glutamic acid) that interferes with phagocytosis. also, antrax toxins are critical virulence factors
34
Q

what are the three components of anthrax toxins?

A

protective antigen: works with capsular polysacchraide to confer protection to the anthrax bug.
EF or OF edema factor: adenylate cyclase activated by host cell calmodulin
Lethal factor: required for lethathality. it is a protease that cleaves the amino terminus from MAP kinase kinases and disrupts cell signaling. PA can combine with either EF or LF.

35
Q

What diseases are caused by B. cereus? Anything important to know about B. cereus? Drug resistance/susceptibility?

A

gram pos. spore forming bacteria found in soil, animal intestines, and plants. it is a major foodborne bacterial pathogen in industrialized nations. disease is usually mild and self-limiting. many strains are resistant to penicillin and cephalosporin but susceptible to vancomycin, chloramphenicol, gentamycin and ciprofloxacin.

36
Q

emetic disease vs. diarrheal disease for B. cereus

A

emetic disease: associated with rice and is rare. due to a backerial toxin called cereulide. also usually accompanied by diarrhea. incubation of 1-5 hrs.
diarrheal disease: meats, veggies, dairy, and sauce. 4-16 hrs. toxins disrupt the integrity of epithelial cell membranes in the small intestine.

37
Q

Corynebacteria diphtheria: features, toxin, prevention

A

gram pos, non-motile aerobic bacteria that can cause resp. one or both poles have ablublous or enlarged shape. disease called diphtheria. humans are the only reservoir. disease due to the diphtheria toxin.
prevention possible with vaccination (diphtheria toxoid) at 2,4,6 and 15-18 months of age plus boosters every 10 yrs. tellurite blood agar medium is selective

38
Q

diphtheria pathogenesis

A

nasopharyngeal and throat colonization. multiplying organisms produce diptheria toxin that inhibits protein synthesis leading to local tissue necrosis and formation of a pseudomembrane. toxins distributed throughout the body cause resp paralysis and heart failure. takes about 2-5 days for symptoms to appear.

39
Q

types of diphtheria and different disease characteristics

A

anterior nasal diphtheria: like the common cold; relatively mild bc toxin is poorly absorbed
pharyngeal and tonsillar diphtheria: early on, present with malaise, sore throat, and fever, but progress with the formation of a bluish white membrane that covers the tonsils and extends across the small palate, it changes color and can cause resp obstruction. neck swelling present. rapid pulse, coma, and death in 6-10 days possible.
laryngeal diphteria: like pharyngeal, plus a barking cough.
cutaneous diphtheria through direct contact: scaling rash and non-toxigenic strains

40
Q

how is diphtheria treated?

A
  1. anti-toxin to neutralize DT. is begun even without confirmed diagnosis (disease can be lethal before we can get diagnostic confirmation)
    antibiotics: penicillin or erythromycin
41
Q

characteristics of listeria monocytogenes

A

gram pos
non-spore forming
rod shaped
facultative anaerobe

found everywhere (soil, decaying plant matter, sewage, vegetation) and can grow in the fridge. mostly a food bourne pathogen. immune status of the patient is critical in determining outcome of listeria monocytogenes infection.

42
Q

clinical presentation and treatment of listeria monocytogenes.

A

healthy ppl: self-limited gastroenteritidis with flu-like symptoms (nausea, vomiting, cramps, diarrhea, fever). 2-70 days after food consumption.

pregnant women: mild symptoms. but, with symptoms of sepsis, you should get blood and urine samples and treat with ampicillin. can cause abortion/delivery of septic baby (death withing minutes/hrs of delivery). (early onset listeriosis)
late onset listeriosis: baby is grumpy, feeds poorly, and may get meningitis within 1-4 wks of delivery. 50% mortality of the baby. treat with amp and gentamicin.

immunocompromised adults (neoplasms, CV disease, TB, HIV, diabetes): septic shock, meingitis, and encephalitis

43
Q

what is the pathogenesis of listeria monocytogenes?

A

ccan survive inside host cells and replicate and spread cell to cell. thus, they avoid the humoural immune response. transcrptional regulator PrfA is critical)

44
Q

gastroenteritis: definition

A

GI symptoms of nausea, vomiting, diarrhea, and abdominal pain

45
Q

dysentery definition

A

inflammatory disorder of the GI tract associated with blood and pus in the feces and ccompanied by pain, fever, abdominal cramps. ususally becasue of large intestine disease

46
Q

enterocolitis definition

A

inflammation involving the mucosa of the small and large intestine

47
Q

E. coli: gram, shape

A

gram negative enteric rod

48
Q

E. coli serotypes and disease

A

somatic, flagellar, and capsular antigens. concept: clonal nature of bacterial pathogens: isolates from the same same serotype from adefinied disease may be descendants of one or a few clones of bacteria.

49
Q

Eneterotoxic E coli (ETEC)

A

causes traveler’s diarrhea and diarrhea in kids.
these strains produce a toxin similar to the cholera toxin: either heat stable enterotoxin (ST) or a heat labile eneterotoxin (LT). both a plasmid encoded. they bind at the apical membrane and affect secondary messengers.
most strains also have plasmid-encoded conlonization factor antigens
symptom: watery diarrhea

50
Q

ETEC toxins: how do they work?

A

heat labile: AB toxin. B subunit binds host cell gangliosides, leading to increased cAMP levels: increased fluid secretion
heat stable: pre-pro-toxins. then cleaved and bind to guanylate cylcase C leading to increased cGMP levels of increased Ca levels: increased fluid secretion.

51
Q

what are three additional ETEC toxins?

A

EatA: serine protease
EAST1: heat stable doxin
ClyA is a hemolysin

52
Q

enteropathogenic e. coli (EPEC)

A

infantile gastroeneteritis and infantile diarrhea, esp. in developing world. they adhere to the intestinal mucosa: attaching and effacing lesion in the brush border. cause dysentery.

53
Q

what genes are involved in EPEC?

A

plasmid-encoded bundle forming pilus, plasmid encoded transcriptional regulator, and a chromosomal pathogenicity island that encodes type III secretion apparatus, intimin for adhesion, and Tir, which is a translocated intimin receptor.. we see attachement of bacteria to the cell surface and a reorganization of the cytoskeleton of the underlying host cell. (attaching/effacing lesion). this forms a pedestal.

54
Q

describe the five steps of the attaching effacing lesion of epec.

A
  1. activation of type III secretion
  2. injection of Tir and binding to intimin
  3. loss of microvilli
  4. actin rearrangements
  5. pedestal formation
55
Q

EHEC (enterohemorrhagic E coli)

include 4 steps of pathogensis

A

this causes hemorrhagic colitis and hemolytic uremic syndrome. it inolves the LEE pathogenicity island.
pathogenesis:
1. bacterial binding and colonization of the large intestine (attaching and effacing lesions)
2. toxin (shiga toxin) production causing microvilli disruption and hemorrhagic colitis
3. toxin dissemination, causing endothelial damage
and 4. acute renal failure and other severe sequellae

56
Q

EIEC: enteroinvasive e coli

A

some cross over in virulence plasmids with shigella (“invasiveness plasmids”)
important causes of morbidity and mortality in kids and cause dysentery like diarrhea in tropical countries.

57
Q

UPEC: uropathogenic E coli

virulence factors?

A

most common cause of UTIs (big prob, esp. for women)
ascend up and cause recurrent infections. UPECs express alpha-hemolysin, proteins that sequester iron for in vivo growth despite the presence of high affinity iuron binding proteins in the host, and pillli to allow for attachment and colonization. FimH also critical for colonization (binds mannose)
FimH expressing and/or type 1 pilli can form biofilms and infect bladder (bad news)

58
Q

E. coli K1 capsule

A

very commonly seen in e coli infections that cause neonatal bacterial meningitis (infection occurs at birth)
K1 is a capsular polysaccharide
also seen in septicemia and UTIs
this polysacchride is similar to that seen in Neisseria meningitides,\

59
Q

spirochetes: what are they?

A

thin gram negative tightly coilded helical bacteria that have an endoflagella located in the periplasmic space. flagella are anchored at each end of the cell and sprial around the organism. this protects the flagella from recognition by the innate immune system

60
Q

treponema pallidum

A

causes syphilis

too thin to be seen directly by light microscopy

61
Q

what are the three stages of syphilis?

A
  1. primary syphilis: chancre forms in the area where the infection was initiated (genitals, rectum, mouth). chancre is painless and resolves on its own in 3-6 wks (but it’s SUPER infectious. note to self: avoid sex with people who have CHANCERS).
  2. 2-4 wks after chancre stage. organisms have spread throughout the body and cause scaly papular rash on trunk and extremities, esp. on soles of feet and palms of hands. also, fever, headache, loss of appetite, weight loss, sore throat, muscle aches, jt pain, malaise, large lymph nodes.
  3. latent/tertiary syphilis: little sexual transmission but destruction of tissue is seen as a result of immune response to treponemal antigens. granulomatous necrotic regions called gumma seen in eyes, blood vessles, heart, bones, and CNS. we see impaired mental function, probs with walking, balance, bladder control, vision, impotence, and loss of sensation. Can’t be treated with antibiotics at this stage.
62
Q

what causes lyme disease?

A

borrelia burgdorferi (spirochete)

63
Q

what are the stages of lyme disease>

A
  1. early: red rash at the tick bite site. rash is called erythema migrans. only seen in 60-80% of individuals. seen 3 days to 1 month after bite; lasts 3-4 wks
  2. spirochetes are in other tissues: fatigue, chills and fever, headache, muscle and joint pain, swollen lymph nodes, arthritis
  3. intermittent episodes of joint pain, meningitis, Bell’s palsy, cardiac probs, migratory pain in jts, tendons, muslces and bones. also neuro complications (depression, memory probs, mood and sleep probs)
64
Q

how is lyme disease diagnosed and treated?

A

diagnosed by detection of serum antibodies- but you can’t tell the difference btw active and past infections.
treated with antibiotics. persistant lyme symptoms following antibiotics may be caused by autoimmune mechanisms.

65
Q

what causes relapsing fever and why?

A

Borrelia recurrentis. they have 8-10 periplasmic flagella!
relapsing fever: two forms: tick-borne and louse borne. this is due to variation i nthe surface protein antigens and the ability to evade the antibody response.

Host Defense (38 decks)

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