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S4M2 > Other Micro > Flashcards

Other Micro Flashcards

1
Q

Features of H.pylori, reservoir, transmission

A

Gram(-), Motile w/flagella, Microaerophilic, Cat(+), Ox(+)

Human reservoir, fecal-oral transmission

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2
Q

Virulence Factors of H. pylori!!!!!!!!

A

Urease (Urea -> NH3 + CO2)
Cytotoxin (VacA)
CagA (cell signaling in epithelial cells– affects actin, cytokines)

**A mutant lacking any ONE of these virulence factors will NOT be pathogenic!

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3
Q

Pathogenesis of H.pylori

A
  1. Attracted to hemin & urea– penetrate mucous layer lining gastric eptihelium
  2. H.pylori recruit & activate inflammatory cells & release urease, producing NH3, which neutralizes stomach acid
  3. H.pylori cytotoxin & NH3 destroy mucus-producing cells, exposing underlying CT to stomach acid –> ulcers
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4
Q

Consequences of H.pylori infection

A
  1. Atrophic gastritis (2*- occurs in months) -> gastroadenocarcenoma
  2. Hyperacidity -> duodenal ulceration
  3. Antigenic stimulation -> B-cell lymphoma
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5
Q

Marker for inflammation & cancer from H.pylori

A

CagA

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6
Q

Diagnosis & Treatment of H.pylori infection

A

Dx:
Bx + culture of gastric mucosa
Urease breath test– radioactive urea, test breath for radioactive CO2

Tx: PPI + Amoxicillin & Metronidazole
helps prevent recurrence

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7
Q

Candida albicans

A

Part of normal flora– overgrowth with abx or IC pts

Causes ORAL THRUSH or ESOPHAGITIS (in IC pts only)

See pseduohyphae & true hyphae in overgrowth; (yeast normally)

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8
Q

Clinical presentation of H.pylori

A

acquisition asymptomatic

pain, belching, vomiting
hypochlorhydria

Peptic ulcers: epigastric pain @ night or after meals- relieved by milk/antacids
(can cause bleeding or perforation)

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9
Q

Clinical presentation of viral diarrheas

A

Stool NOT BLOODY or MUCOID.
Usually fecal-oral
No anti-viral tx

Usually seen with Childhood diarrhea (rotavirus) or Outbreaks (Caliciviruses)

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10
Q

Rotavirus characteristics

A

dsRNA (segmented, naked)
DOUBLE-shelled

5 serotypes (usually type A for infx)

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11
Q

Rotavirus infection presentation

A

self-limiting, 48h incubation
Sudden onset of vomiting –> watery diarrhea @ 5 days –> abdominal cramps, low fever, dehydration

Infx restricted to ENTEROCYTES on small intestinal microvilli –> incr secretions + malabsorption

Vaccine available

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12
Q

Demographics of Rotavirus infx

A

Nov-march in temperate climates

Children <2y, elderly, institutionalized, healthcare personelle

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13
Q

Calicivirus:

A

+ssRNA (naked)
All ages, fecal-oral (airborn possible), mostly winter
<48h incubation, vomiting +/- watery diarrhea for 1-3 days.
NO vaccine

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14
Q

Helminths: groups, stages, characteristics

A

Tapeworm, fluke, roundworm

Egg -> larva -> adult (multi-cell, does not need microscope)

Do NOT multiply in humans
(Intermediate host– where eggs develop -> larvae)

Humans get infected by ingestion/penetration of eggs or larvae

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15
Q

Pinworm / Enterobius vermicularis

  • Susceptibility
  • life cycle
  • location
A
  • usually in young children but doesn’t discriminate
  • In GIT: ingest egg -> larva -> adult -> lay eggs
    • adults migrate at night thru anus, lay eggs outside, & die
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16
Q

Pinworm / enterobius

  • S/S
  • Dx
  • Tx
A
  • Mostly asymptomatic, but PERIANAL ITCH
  • mild dz– no invasion, no eosinophilia
  • eggs NOT in stool, only see adults @ night
  • Tx pt AND fam w/ anti-parasitic to control spread
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17
Q

Ascaris: lifecycle

A
  1. ingest eggs –> larvae
  2. hatch in intestine -> blood
  3. enter lung –> trachea –> swallowed
  4. larvae –> adult in intestine & eggs in feces (fecal-oral)
  5. Eggs mature in soil (faster in warmer temp)
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18
Q

Ascaris: epidemiology

A
  • Warm climates (1/3 of world infected)
  • Children in developing nations
  • In US: latino immigrants
  • Fecal-oral (veg contaminated)
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19
Q

Ascaris: disease

A
  • Mostly asymptomatic
  • More bugs/larger -> obstruction -> jaundice, pain, distention (due to blocked biliary/pancreatic ducts), and malnutrition
  • Exit thru anus– not painful but nasty
  • When moving in LUNG –> eosinophilia / dyspnea / pneumonitis / cough can occur.
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20
Q

Ascaris: Diagnosis

A

Thick sell, ruffled, wavy mammilated surface (looks like nipples lol)
Look for Ova & Parasite in stool

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21
Q

Hookworms:

  • types
  • life cycle
  • diagnosis
A

7-13mm- have biting plates
- Types: Ancyclostoma duodonae, necutor americanus (children walking barefoot)

  • eggs -> stool -> soil/water -> larvae (molt 2x) — 5-10 days later are infective:
    larvae -> skin -> lung -> swallow -> adult in GIT
  • Ova, stool with SMOOTH SHELL
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22
Q

Tenia Solium

  1. Definitive & intermediate hosts
  2. Location of cysts
  3. Infectious cycle
  4. Types
A
  1. definitive: human, intermediate: human, pig
  2. Cysts in muscle, brain
  3. Eggs in human poo -> other humans -> form larval cysts (only pigs can form larval cysts)
  4. Adult tapeworm = NO SX;
    Cysticercosis = brain inflammation
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23
Q

Cysticercosis: diagnosis

A

endemic in some countries

Larval cysts in several organs, but BRAIN & SC most severe.

Years later, causes focal seizures, mental impairment, meningitis, psych illness

Dx with Serology (no ADULT in intestine in Cysticercosis)

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24
Q

Schistosomiasis:

  • life cycle
  • epidemiology
A

Swimming larvae -> skin -> lung, liver -> GIT -> poop -> larvae -> snails -> water

Humans bathing/swimming in fresh water w/proper snails
– increased risk with Dams

25
Q

Schistosomiasis: S/S

A
  • Dermatitis (larva penetrates)
  • Hematuria (eggs in bladder)
  • Fibrosis & inflammation of liver -> portal HTN -> esophageal varices -> vomit blood

Stool has ova w/ characteristic spine

26
Q

Protozoal biology

A
  • Unicellular, diploid, nuclear membrane
  • Most are larger than bacteria
  • NO cell wall (thus no gram stain)
  • *are able to form Double-Membraned Cysts to survive outside the body
27
Q

Forms of protozoa

A

Trophozoites: metabolically active, replicate, motile, PATHOGENIC

Cysts: dormant– double membrane -> resistant to dessication & osmotic swelling; DON’T replicate– survive & spread to new host

28
Q

Giardia lamblia: cyst vs. trophozoite

A

Cyst: 4 Nuclei & infective
Trophozoite: flagellated, 2 nuclei, motile, “heart shaped” :)

29
Q

Giardia: demographics

A
  • children 0-5y; backpackers from streams/lakes– most from human cysts in H2O
  • MCC protozoal-induced diarrhea
  • Improper chlorination– cysts don’t die
30
Q

Giardia: S/S

A

Diarrhea, cramps, bloating, flatulence, anorexia

CHRONIC = >1week: weight loss, malabsorption (->steatorrhea), lactose intolerance

NO fever, NO blood in stool

31
Q

Giardia: pathogenesis

A
  • Ingest cysts -> trophozoites
  • Use ventral disk to attach to SI mucosa
  • 1-2 week incubation (incr. in #)
  • -> disrupt brush borders (dissacharideases, lose absorptive surface–flat villi)

** NO INVASION. NO EXOTOXIN **

32
Q

Giardia: diagnosis

A
  • Stool: ova + parasite (fresh liquid stool may have trophozoites)
  • –Need 3 specimens (not always shedding)
  • ELISA + Ag detection w/Immuno is better
33
Q

Giardia: immunity

A
  • formed in infection
  • IgA is protective & helps recovery
  • Gain abs from breast feeding
  • Immunodeficiency -> predisposition to giardia
34
Q

Cryptosporidium: reservoir, demographics

A

Cattle

AIDS pts, or immunocompetent but in developing nations

35
Q

Cryptosporidium: pathogenesis, morphology

A

Path:

  1. Ingest oocysts -> sporozoites
  2. Invade surrounding cell membrane
  3. asexual division (SOME for sexual gametocytes to become oocysts)

Chlorine-resistant (pools)

“Nipple” appearance on cells in intestinal bx

36
Q

Cryptosporidium: epidemiology, clinical features

A
  • 4% of diarrhea in US, 2% traveler’s diarrhea
  • Higher incidence in developing nations
  • Watery diarrhea + steatorrhea
  • @ terminal ileum, prox colon (but disseminate in AIDS pts –> lung, pancreatitis, cholangitis)

Incubation: 1week
Lasts 5-10 days (14+ in dev. nations)

37
Q

Cryptosporidium: diagnosis

A

Stool cysts

  • ACID FAST
  • auramine
  • immunofluorescence
  • ag detection
38
Q

Microsporidium: Location, demographics, morphology

A
  • Water (pig, dog, chicken, rabbit)
  • AIDS pts
  • Little vacuoles within cells
39
Q

Microsporidium: life-cycle

A

Like fungi:
Ingest spores - use polar tube to inject sporoplasm into host cell -> proliferate -> form spores that rupture cells to release more cells

40
Q

Microsporidium: Clincal features, S/S

A
  • Diarrhea (watery), ad pain, fever
  • some malabsorption
  • @ distal duodenum, prox jejunum
  • in AIDS pts– disseminate to liver, brain, etc **spreads more than cryptosporidium
41
Q

Isosporabelli: demographics, incubation, S/S

A
  • AIDS pts (“AIDS Assoc Chronic Diarrhea)
  • 1 week incubation, lasts 2-3weeks
  • Watery diarrhea
42
Q

Isosporabelli: Life cycle, Dx

A
  1. Ingest oocyst -> sporozoites
  2. Enter epithelial cells -> trophozoites
  3. reproduce –> oocysts

Dx: oocysts AUTOFLUORESCE in stool!

43
Q

Enantomoeba Histolytica: Demographics, Incubation, S/S, Complications

A
  • Rare in US (sanitation)– in refugees, immigrants
  • 1 week incubation, 1-3 week duration
  • MCC diarrhea & dysentery (blood/mucus) in the WORLD
  • Cause deep ulcers in colon –> perforation
  • Liver/ Brain /Lung/ Subdiaphragm abscess
  • toxic megacolon
44
Q

Enantomoeba histolytica: life cycle

A
  1. Ingest cyst
  2. Form trophozoite
  3. Penetrate intestinal wall
  4. Multiply in colon wall
  5. Liver invasion via portal vein
  6. Discarded in feces
45
Q

Enantomoeba histolytica: morphology

A

Flask-shaped deep ulcers that bleed but rarely enter peritoneum

Wheel & spoke appearance of trophozoites
INGET RBCs

Cyst has 4 nuclei

46
Q

Enantomoeba histolytica: diagnosis

A

Stool smear: ova + parasite

Fresh stool will have trophozoites

47
Q

If you have a patient with no symptoms but culture indicative of significant bacteremia, would you treat them with antibiotics?

A

NO if person is NOT pregnant

YES if person is pregnant or has a known obstruction (kidney stone)

48
Q

If you have a male patient with Acute Hemorrhagic Cystitis… what is the cause?

A

VIRUS

    • Adenovirus
    • BK virus
49
Q

Staph sprophyticus:

  • characteristics
  • demographics
A

Staph saprophyticus:

  • G(+), cat(+), coag(-), nitrite(-), novobiocin resistant.
  • causes lower UTIs in YOUNG SEXUALLY ACITVE FEMALES (Honeymoon Cystitis) or Postmenopausal women.
50
Q

Which microorganism is associated with UTIs in BPH patients?

A

Enterococcus faecalis (G+ cocci in chains, Group D strep, cat -, Nitrite -)

51
Q

Which microorganisms are Nitrate (+)?

A
  • E.coli
  • Proteus
  • Klebsiella penumoniae
52
Q

What are the virulence factors that help E.coli to be uropathogenic?

A

Type 1 pili, P. fimbriae

53
Q

Lower UTI: types

A
  • Cystitis
  • Urethritis
  • Prostatitis
54
Q

Upper UTI: types

A
  • Pyelonephritis
  • Intrarenal Abscess
  • Perinephric Abscess
  • Emphysematous Pyelonephritis
55
Q

Cystitis: S/S

A
  • Dysuria, frequency, urgency
  • Bladder fullness/pressure
  • NO abnormal vag discharge
  • Suprapubic discomfort/pain
  • Hematuria in 50%, bacteriuria, pyuria
56
Q

Pyelonephritis: S/S

A
  • Fever, chills, sweats
  • N/V
  • Flank pain or abd pain
  • Dehydration, Hypotension
  • Hematuria, bacteriuria, pyuria
  • May see WBC casst
57
Q

Common causes of Upper UTI? (general)

A
  • Untreated cystitis or other lower UTI infection

- Hematogenous spread from abscess or infection elsewhere

58
Q

What can you determine if the Leukocyte Esterase test is negative?

A

Patient does NOT have infection

59
Q

How do you determine “significant bacteremia”?

A

Quick & dirty: >1 organism per oil immersion field (in uncentrifuged urine)
>1 = >10ˆ5 = >100’000 CFU/mL

Long: uncetrifuged urine - count CFU
CFU x 10ˆ3 = CFU/mL
>100 colonies = >100’000 CFU/mL = significant

S4M2 (10 decks)

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