Other Micro Flashcards
Features of H.pylori, reservoir, transmission
Gram(-), Motile w/flagella, Microaerophilic, Cat(+), Ox(+)
Human reservoir, fecal-oral transmission
Virulence Factors of H. pylori!!!!!!!!
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!
Pathogenesis of H.pylori
- Attracted to hemin & urea– penetrate mucous layer lining gastric eptihelium
- H.pylori recruit & activate inflammatory cells & release urease, producing NH3, which neutralizes stomach acid
- H.pylori cytotoxin & NH3 destroy mucus-producing cells, exposing underlying CT to stomach acid –> ulcers
Consequences of H.pylori infection
- Atrophic gastritis (2*- occurs in months) -> gastroadenocarcenoma
- Hyperacidity -> duodenal ulceration
- Antigenic stimulation -> B-cell lymphoma
Marker for inflammation & cancer from H.pylori
CagA
Diagnosis & Treatment of H.pylori infection
Dx:
Bx + culture of gastric mucosa
Urease breath test– radioactive urea, test breath for radioactive CO2
Tx: PPI + Amoxicillin & Metronidazole
helps prevent recurrence
Candida albicans
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)
Clinical presentation of H.pylori
acquisition asymptomatic
pain, belching, vomiting
hypochlorhydria
Peptic ulcers: epigastric pain @ night or after meals- relieved by milk/antacids
(can cause bleeding or perforation)
Clinical presentation of viral diarrheas
Stool NOT BLOODY or MUCOID.
Usually fecal-oral
No anti-viral tx
Usually seen with Childhood diarrhea (rotavirus) or Outbreaks (Caliciviruses)
Rotavirus characteristics
dsRNA (segmented, naked)
DOUBLE-shelled
5 serotypes (usually type A for infx)
Rotavirus infection presentation
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
Demographics of Rotavirus infx
Nov-march in temperate climates
Children <2y, elderly, institutionalized, healthcare personelle
Calicivirus:
+ssRNA (naked)
All ages, fecal-oral (airborn possible), mostly winter
<48h incubation, vomiting +/- watery diarrhea for 1-3 days.
NO vaccine
Helminths: groups, stages, characteristics
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
Pinworm / Enterobius vermicularis
- Susceptibility
- life cycle
- location
- 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
Pinworm / enterobius
- S/S
- Dx
- Tx
- 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
Ascaris: lifecycle
- ingest eggs –> larvae
- hatch in intestine -> blood
- enter lung –> trachea –> swallowed
- larvae –> adult in intestine & eggs in feces (fecal-oral)
- Eggs mature in soil (faster in warmer temp)
Ascaris: epidemiology
- Warm climates (1/3 of world infected)
- Children in developing nations
- In US: latino immigrants
- Fecal-oral (veg contaminated)
Ascaris: disease
- 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.
Ascaris: Diagnosis
Thick sell, ruffled, wavy mammilated surface (looks like nipples lol)
Look for Ova & Parasite in stool
Hookworms:
- types
- life cycle
- diagnosis
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
Tenia Solium
- Definitive & intermediate hosts
- Location of cysts
- Infectious cycle
- Types
- definitive: human, intermediate: human, pig
- Cysts in muscle, brain
- Eggs in human poo -> other humans -> form larval cysts (only pigs can form larval cysts)
- Adult tapeworm = NO SX;
Cysticercosis = brain inflammation
Cysticercosis: diagnosis
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)
Schistosomiasis:
- life cycle
- epidemiology
Swimming larvae -> skin -> lung, liver -> GIT -> poop -> larvae -> snails -> water
Humans bathing/swimming in fresh water w/proper snails
– increased risk with Dams
Schistosomiasis: S/S
- Dermatitis (larva penetrates)
- Hematuria (eggs in bladder)
- Fibrosis & inflammation of liver -> portal HTN -> esophageal varices -> vomit blood
Stool has ova w/ characteristic spine
Protozoal biology
- 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
Forms of protozoa
Trophozoites: metabolically active, replicate, motile, PATHOGENIC
Cysts: dormant– double membrane -> resistant to dessication & osmotic swelling; DON’T replicate– survive & spread to new host
Giardia lamblia: cyst vs. trophozoite
Cyst: 4 Nuclei & infective
Trophozoite: flagellated, 2 nuclei, motile, “heart shaped” :)
Giardia: demographics
- children 0-5y; backpackers from streams/lakes– most from human cysts in H2O
- MCC protozoal-induced diarrhea
- Improper chlorination– cysts don’t die
Giardia: S/S
Diarrhea, cramps, bloating, flatulence, anorexia
CHRONIC = >1week: weight loss, malabsorption (->steatorrhea), lactose intolerance
NO fever, NO blood in stool
Giardia: pathogenesis
- 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 **
Giardia: diagnosis
- Stool: ova + parasite (fresh liquid stool may have trophozoites)
- –Need 3 specimens (not always shedding)
- ELISA + Ag detection w/Immuno is better
Giardia: immunity
- formed in infection
- IgA is protective & helps recovery
- Gain abs from breast feeding
- Immunodeficiency -> predisposition to giardia
Cryptosporidium: reservoir, demographics
Cattle
AIDS pts, or immunocompetent but in developing nations
Cryptosporidium: pathogenesis, morphology
Path:
- Ingest oocysts -> sporozoites
- Invade surrounding cell membrane
- asexual division (SOME for sexual gametocytes to become oocysts)
Chlorine-resistant (pools)
“Nipple” appearance on cells in intestinal bx
Cryptosporidium: epidemiology, clinical features
- 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)
Cryptosporidium: diagnosis
Stool cysts
- ACID FAST
- auramine
- immunofluorescence
- ag detection
Microsporidium: Location, demographics, morphology
- Water (pig, dog, chicken, rabbit)
- AIDS pts
- Little vacuoles within cells
Microsporidium: life-cycle
Like fungi:
Ingest spores - use polar tube to inject sporoplasm into host cell -> proliferate -> form spores that rupture cells to release more cells
Microsporidium: Clincal features, S/S
- Diarrhea (watery), ad pain, fever
- some malabsorption
- @ distal duodenum, prox jejunum
- in AIDS pts– disseminate to liver, brain, etc **spreads more than cryptosporidium
Isosporabelli: demographics, incubation, S/S
- AIDS pts (“AIDS Assoc Chronic Diarrhea)
- 1 week incubation, lasts 2-3weeks
- Watery diarrhea
Isosporabelli: Life cycle, Dx
- Ingest oocyst -> sporozoites
- Enter epithelial cells -> trophozoites
- reproduce –> oocysts
Dx: oocysts AUTOFLUORESCE in stool!
Enantomoeba Histolytica: Demographics, Incubation, S/S, Complications
- 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
Enantomoeba histolytica: life cycle
- Ingest cyst
- Form trophozoite
- Penetrate intestinal wall
- Multiply in colon wall
- Liver invasion via portal vein
- Discarded in feces
Enantomoeba histolytica: morphology
Flask-shaped deep ulcers that bleed but rarely enter peritoneum
Wheel & spoke appearance of trophozoites
INGET RBCs
Cyst has 4 nuclei
Enantomoeba histolytica: diagnosis
Stool smear: ova + parasite
Fresh stool will have trophozoites
If you have a patient with no symptoms but culture indicative of significant bacteremia, would you treat them with antibiotics?
NO if person is NOT pregnant
YES if person is pregnant or has a known obstruction (kidney stone)
If you have a male patient with Acute Hemorrhagic Cystitis… what is the cause?
VIRUS
- Adenovirus
- BK virus
Staph sprophyticus:
- characteristics
- demographics
Staph saprophyticus:
- G(+), cat(+), coag(-), nitrite(-), novobiocin resistant.
- causes lower UTIs in YOUNG SEXUALLY ACITVE FEMALES (Honeymoon Cystitis) or Postmenopausal women.
Which microorganism is associated with UTIs in BPH patients?
Enterococcus faecalis (G+ cocci in chains, Group D strep, cat -, Nitrite -)
Which microorganisms are Nitrate (+)?
- E.coli
- Proteus
- Klebsiella penumoniae
What are the virulence factors that help E.coli to be uropathogenic?
Type 1 pili, P. fimbriae
Lower UTI: types
- Cystitis
- Urethritis
- Prostatitis
Upper UTI: types
- Pyelonephritis
- Intrarenal Abscess
- Perinephric Abscess
- Emphysematous Pyelonephritis
Cystitis: S/S
- Dysuria, frequency, urgency
- Bladder fullness/pressure
- NO abnormal vag discharge
- Suprapubic discomfort/pain
- Hematuria in 50%, bacteriuria, pyuria
Pyelonephritis: S/S
- Fever, chills, sweats
- N/V
- Flank pain or abd pain
- Dehydration, Hypotension
- Hematuria, bacteriuria, pyuria
- May see WBC casst
Common causes of Upper UTI? (general)
- Untreated cystitis or other lower UTI infection
- Hematogenous spread from abscess or infection elsewhere
What can you determine if the Leukocyte Esterase test is negative?
Patient does NOT have infection
How do you determine “significant bacteremia”?
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
