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Gastrointestinal infections Flashcards

1
Q

which pathogens produce acute diarrhea

A

rotavirus
e.coli
salmonella spp
vibrio cholerae

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2
Q

generalities of rotavirus

A

non-enveloped
segmented, double-stranded RNA
reovirus

its a common cause of viral gastroenteritis in infants and young children (daycares and kindergartens) → specially in the winter

leading cause of severe diarrhea world wide

fecal-oral route

short incubation period → 1-3 days

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3
Q

is there a vaccine for rotavirus

A

it’s vaccine is a live attenuated oral vaccine → RV1 and RV5

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4
Q

what’s the physiopathology of rotavirus

A

mucosal damage and villous atrophy in the gastrointestinal tract → impaired absorption of sodium and loss of potassium → non-bloody, watery diarrhea

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5
Q

symptoms of rotavirus

A

vomiting, watery diarrhea, high grade fever, malaise
- severe → >10 loose, watery stools within 24 hrs
- usually → 3-7 days
- mild to severe dehydration

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6
Q

how do you diagnose rotavirus?

A

diagnosis is clinical, if severe disease or no diagnosis you can do an ELISA to detect antigens in the stool (PCR and immunochromatography can also be used)

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7
Q

what’s the rotavirus treatment?

A

tx → supportive: fluid replacement, electrolyte repletion, antiemetics

** IV fluid resuscitation may be required on severe patients

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8
Q

generalities about e.coli

A

gram negative motile bacili

non-spore forming, encapsulated

lactose, glucose, and sorbitol fermenter

B-galactosidase

MacConkey Agar → pink colonies (because it’s a lactose fermenter)

Eosin-Methylene blue agar → green methallic sheen

Sorbitol-MacConkey Agar → selective for E.coli O157:H7 (does not turn medium pink)

facultative anaerobe

catalase positive, indole positive, oxidase negative, urease negative, bile resistant

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9
Q

Sorbitol-MacConkey Agar is selective for which type of E.coli ?

A

E.coli O157:H7 (does not turn medium pink)

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10
Q

how does the pathogenesis of e.coli work?

A

intestinal flora → UTI and GI infections

LPS endotoxin → bacteremia and septic shock

K antigen (capsule): K1 capsule → ⭣phagocytosis and complement activation → neonatal meningitis

H antigen (flagella)

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11
Q

1 cause of UTIs, most common in women

A

e. coli

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12
Q

e. coli can cause pneumonia and meningitis in which population

A

in immunocompromised people

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13
Q

name of the strain of e.coli O157:H7

A

EHEC

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14
Q

LPS role in e.coli

A

O-antigen: outer domain, target for host antibodies (TLR4, CD14)

core domain: linked between O-antigen and lipid A

lipid A → toxicity to host → septic shock

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15
Q

what’s ESLB e.coli

A

Extended-spectrum B-lactamase-producing E.coli

*resistance to B-lactamase antibiotics

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16
Q

general principles of Salmonella spp

A

S. enterica serotype Enteritidis, S. enterica serotyoe Typhimurium

gram negative motile bacilli

  • non-lactose fermenter
  • glucose fermenter
  • produces H2S

MacConkey agar → colorless colonies

triple sugar iron test → yellow base, black color above base, red slant

facultative anaerobe

  • catalase positive, oxidase negative, urease negative
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17
Q

pathogenesis of salmonella spp

A

reservoir: humans and animals

food contamination =
- undercooked poultry, eggs
- reptile pets (turtles)

fecal-oral transmission → bacteria destroyed in stomach → surviving bacteria multiply in intestine → endotoxin release → watery +/- bloody diarrhea

⭡⭡⭡ neutrophil inflammatory response → ⭡fecal WBC

not resistant to gastric acid, hematogenous dissemination

flagella

LPS endotoxin → septic shock

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18
Q

how do you expect to see a diarrhea caused by salmonella spp

A

inflammatory diarrhea = predominantly polymorphonuclear cells + WBC

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19
Q

characteristics of a gastroenteritis caused by salmonella spp

A

⭡risk in children, ⭡ID50

watery +/- bloody diarrhea

nausea, emesis, abdominal pain/cramping, malaise

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20
Q

management of salmonella spp

A
  • hydration, correct electrolyte derangements
  • typically self-limited
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21
Q

what’s the most common complication of salmonella spp

A

reactive arthritis (Reiter syndrome) → conjuctivitis, urethritis, oligoarthritis (lower extemities)

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22
Q

general principles of vibrio cholerae

A

gram negative motile “comma-shaped” bacilli

growth in alkaline media (acid. labile)

thiosulfate citrate bile salts sucrose agar (TSCB)→ yellow colonies

non-lactose fermenter

sucrose fermenter

iron enrichment ⭡growth

facultative anaerobe

catalase positive, oxidase positive, urease negative

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23
Q

pathogenesis of vibrio cholerae

A

saltwater, brackish marine waters

water contamination or raw shellfish (oysters), travel to resource-limited regions

toxic mediated = cholera toxin → ⭡Gs → ⭡⭡⭡ adenylate cyclase activation → ⭡intracellular cAMP → ⭡Cl and H20 secretion into the lumen

polar flagella: monotrichous

LPS endotoxin

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24
Q

characteristics of an infection with vibrio cholerae (cholera)

A

⭡ID50

cholera-toxin mediated disease → profuse “rice-water” diarrhea, dehydration (”sunken” eyes)

non-inflammatory

isonatremic hypovolemia, hypokalemia, lactic acidosis

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25
what's the tx for cholera
aggressive rehydration, correct electrolyte derangements
26
which pathogen is associated with "rice-water" diarrhea
vibrio cholerae
27
general principles of helicobacter pylori
gram negative motile “spiral-shaped” bacilli silver stain microaerophile catalase positive, oxidase positive, urease positive
28
how does the pathogenesis of h. pylori work
antrum → body of stomach urease hydrolyzes urea to form ammonia → ammonia neutralizes gastric acid → H. pylori attaches to epithelial cells → destroys somatostatin-producing cells (D-cells) ⭣somatostatin release → ⭡gastrin, ⭡HCL, ⭡risk of PUD - this happens when the infection is acute, if it’s chronic eventually the cells that produce HCL in the body (parietal cells) will get destroyed decreasing the levels of HCL - somatostatin normally inhibits gastrin production flagella (lophotrichous) LPS endotoxin → septic shock
29
main characteristics does the h. pylori infection have
gastroenteritis and PUD
30
characteristics of gastroenteritis and PUD in a h. pylori infection
⭡risk with smoking and NSAID use epigastric pain/crampring, bloating, GERD gastric or duodenal ulcers - MMC of duodenal ulcers = S-cell damage in duodenum → ⭣secretin → ⭣production of HCO3 (bicarbonate) ** in an acute fase symptoms may improve when people eat because of this principle
31
how can you diagnose an h. pylori infection
- urea breath test → false negative when taking antibiotics - fecal antigen test - endoscopy → gastric biopsi
32
management of h. pylori infection
triple therapy: amoxicillin + clarithromycin + PPI (omeprazole) quadruple therapy: methronidazole + tetracycline + bismuth subcitrate + PPI antacid for symptomatic treatment avoid NSAID, tobacco, caffeine, alcohol
33
what are the complications of h. pylori
- gastric adenocarcinoma - MALT lymphoma → SOMETIMES you can resolve the cancer after the bacteria is gone - iron deficiency anemia → specially if the patient’s ulcer is bleeding
34
what pathogens produce dysentery
shigella spp enteroinvasive E. coli (EIEC) entamoeba hystolitica
35
general principles of shigella spp
S. dysenteriae > S. flexneri > S. boydii > S. sonnei gram negative non-motile bacilli non-lactose fermenter glucose fermenter does not produce H2S MacConkey agar → colorless colonies Triple sugar iron test → yellow base, red slant facultative anaerobe catalase positive (except S. dysenteriae type 1), oxidase negative, urease negative
36
pathogenesis of shigella spp
food contamination (undercooked meat) fecal-oral transmission → invasion of Peyer’s patches and M-cells (colon) → cell to cell transmission → phagosome evasion → bloody, mucous diarrhea resistance to gastric acid, no hematogenous dissemination (no flagella) shiga-toxin → inactivation of 60S ribosomal subunit **(minor pathogenicity vs EHEC)** LPS endotoxic → septic shock
37
if you start to get dysentery symptoms after eating an undercooked hamburger, which pathogen do you suspect caused your symptoms
shigella
38
characteristics of dysentery/gastroenteritis caused by shigella
- ⭡risk in children, ⭣ID50 - watery → bloody and mucoid diarrhea - nausea, emesis, abdominal pain/cramping, malaise
39
what should the management of a shigella infection look like?
- hydratation, correct electrolyte derangements *ceftriaxone, ciprofloxacin, trimethoprim-sulfamethoxazole → severe patients
40
complications of a shigella spp infection
reactive arthritis (Reiter syndrome) → conjunctivitis, urethritis, oligoarthritis (lower extremities) hemolytic uremic syndrome (similar to EHEC)
41
which GI infections can cause Reiter syndrome and what is it?
its a mix of conjunctivitis, urethritis, oligoarthritis (lower extremities) pathogens: shigella spp, salmonela spp, yersinia, campylobacter jejuni
42
there are 6 types of e.coli, what are them
enterohemorragic = EHEC enterotoxigenic = ETEC enteroinvasive = EIEC enterophatogenic = EPEC enteroaggregative = EAEC urophatogenic = UPEC
43
how does EHEC work?
transmitted via undercooked meat, raw leafy vegetables, and unpasteurized dairy products does NOT ferment sorbitol shiga-like toxin → inactivation of 60S ribosomal subunit → ⭣protein formation → enterocyte necrosis → bloody diarrhea
44
which type of e.coli have the O157:H7 strain
EHEC
45
what's the main complication of EHEC
hemolytic uremic syndrome (HUS): hemolytic anemia, thrombocytopenia, acute renal failure - this happens because the inflammatory cascade, the platelets in circulation will built up causing microthromby = ⭣platelets - acute renal failure → because there will be less oxygen carrying capacity to the kidneys **ALMOST ALWAYS IN CHILDS**
46
what's the management of EHEC
supportive management (antibiotics may⭡ risk of development HUS)
47
what type of e. coli causes traveler’s diarrhea
ETEC
48
what types of toxins does ETEC have and how do they work
heat-labile (LT) enterotoxin → ⭡Gs → ⭡⭡⭡ adenylate cyclase activation → ⭡intracellular cAMP → ⭡Cl ion secretion into lumen heat-stable (ST) enterotoxin → ⭡⭡⭡Guanylate cyclase → ⭡intracellular cGMP → ⭡Cl ion secretion into lumen
49
how does ETEC present itself and what's it's management
- watery diarrhea, abdominal pain, nausea, emesis - supportive management
50
how does EIEC work and what's it's maagement
enterotoxin → watery diarrhea enterocyte invasion → enterocyte necrosis → bloody diarrhea supportive management
51
how does EPEC work and which population is more susceptible to this infection
effacement and destruction of microvilli of enterocytes → ⭣absorption → ⭡permeability of tight junctions does not produce toxin ** more common in children
52
how does EAEC work
aggregation and adherence to enterocytes (”stacked brick” pattern) → ⭡inflammation → persistent diarrhea (watery → bloody +/- pus)
53
MCC of cystitis/UTI
UPEC
54
what's the mechanism of pathogenesis of UPEC? how does it present itself ?
P fimbriae (pili) → pyelonephritis dysuria, urinary frecuency/urgency, +/- costovertebral tenderness
55
what's the tx for UPEC
trimethoprim-sulfamethoxazole, fosfomycin, nitrofurantoin
56
what's the complication e. coli can have in neonates
neonatal meningitis (NMEC)
57
how does NMEC work?
K1 capsular polysaccharide → ⭣phagocytosis and complement activation
58
how does NMEC present itself
hypotonia, neck stiffness, lethargy, bulging fontanelle, hyperthermia/hypothermia, kerning sign, brudzinski sign
59
how do you diagnose NMEC and what's the treatment for it
- lumbar punture - ampicilin
60
what are the life cycles of entamoeba histolytica
2 lifecycle stages: trophozoite (active) and cyst (infectious)
61
what's the pathophysiology of Entamoeba histolytica
fecal-oral transmission (water or food contamination) ingestion of cyst → colon → excystation of trophozoites → trophozoites and cysts in feces trophozoites invade colonic mucosa → proteolytic enzymes → cell lysis in mucosa - Gal/GalNAc receptor in colonic mucosa trophozoite invade bloodstream → liver → abscess
62
how does amebiasis by entamoeba histolytica present itself
more common in tropical areas with poor sanitation mostly asymptomatic intestinal: dysentery (bloody diarrhea), tenesmus, abdominal pain, weight loss, fever amebic liver abscess: RUQ pain, fever, chills - first cause of hepatic abscess
63
how do you diagnose entamoeba histolytica
- stool sample → trophozoites with engulfed RBCs, cysts with up to 4 nuclei - colonoscopy + biopsy → flask shaped ulcers on histology
64
if you have a liver abscess caused by entamoeba histolytica what do you spect ti find upon aspiration of it? how do you spect to find your hepatic markers?
aspiration of abscess: “anchovy paste” pustular fluid liquefactive necrosis ⭡AST, ALT, ALP and bilirubin
65
what do you spect to see in a CT and US of a liver abscess caused by entamoeba histolytica
- US: hypoechoic solitary lesion, right lobe of liver - CT: well-defined, circular contrast-enhancing lesion
66
what's the treatment of entamoeba histolytica
asymptomatic: paromomycin OR iodoquinol symptomatic: tinidazole OR metronidazole → paromomycin OR iodoquinol liver abscess: needle aspiration
67
what pathogens cause enteric fever
Yersinia Campylobacter jejuni Salmonella Parathyphi A and B
68
Yersinia generalities and principles:
Y. enterocolitica, Y. pseudotuberculosis gram negative non-motile cocobacilli (pleomorphic) bipolar staining (”closed safety pin”) - non-lactose fermenting - glucose fermenter - iron and cold enrichment ⭡ growth (siderophilic) **can become motile at cold temperatures** - does nor produce H2S MacConkey agar → colorless colonies facultative anaerobe catalase positive, oxidase negative, **urease positive**
69
pathogenesis de Yersinia
food contamination (undercooked pork, unpasteurized milk), pet feces fecal-oral transmission → bacteria proliferative in terminal ileum and invade Peyer’s patches and M-cells → enterotoxin release → bloody diarrhea migration to mesenteric lymph nodes → Lymphadenopathy enterotoxin → ⭡⭡⭡ guanylate cyclase → ⭡intracelular cGMP → ⭡Cl iron secretion into lumen → watery diarrhea type III secretion system → inject Yops → forms pores in host cell membranes, ⭣phagocytosis, ⭣host cytokine production LPS endotoxin → septic shock
70
if you get a fever after consuming uncooked pork, what do you suspect cause your infection?
Yersinia
71
gastroenteritis characteristics of a Yersinia infection
⭡risk in children, day-care centers, and iron-overload states (hemochromatosis) watery +/- bloody diarrhea nausea, emesis, abdominal pain/cramping, malaise pseudoappendicitis, RLQ abdominal pain + mesenteric lymphadenitis abdominal CT: no imaging evidence of appendicitis
72
which bacteria causes a pseudoappendicitis
Yersinia
73
what type of secretion system does Yersinia have?
type III secretion system → inject Yops
74
what's the management of a Yersinia infection
hydration, correct electrolyte derangements typically self-limited severe cases → gentamycin, doxyclycine, ceftriaxone, trimethoprim-sulfamethoxazole
75
posible complications of a Yersinia infection
reactive arthritis (Reiter syndrome) → conjuctivitis, urethritis, oligoarthritis (lower extremities) - HLA-B27 intussusception → bowel ischemia
76
which GI infection is associated with bowel ischemia
Yersinia
77
gram negative non-motile cocobacilli that can become motile in cold environments
Yersinia
78
reactive arthritis (Reiter syndrome) is associated with a particular HLA variant, which variant is it?
HLA-B27
79
generalities of Campylobacter Jejuni
gram negative motile “corkscrew-shaped” bacilli “darting” motility growth at high temperatures (37-42ºC) microaerophile catalase positive, **oxidase** positive, **urease negative**
80
pathogenesis de Campylobacter Jejuni
food contamination (undercooked poultry or meat, unpasteurized dairy), contact with infected domestic animals, travel to resource-limited regions fecal-oral transmission → invasion of intestinal mucosa → watery diarrhea → bloody diarrhea cytolysins → to destroy intestinal epithelium cells polar flagella (amphitrichous) LOS endotoxin → septic shock - harder to detect antigen
81
gastroenteritis, dysentery characteristics of a Campylobacter Jejuni infection
MCC of bacterial diarrhea in the US ⭡risk in children, ⭣ID50 bloody, mucoid diarrhea **fever**, nausea, emesis, abdominal pain/cramping, malaise
82
management of a Campylobacter Jejuni infection
- hydratation, correct electrolyte derangements - azithromycin (severe infections)
83
complications of a Campylobacter Jejuni infection
reactive arthritis (Reiter syndrome) → conjunctivitis, urethritis, oligoarthritis (lower extremities) - man with the HLA-B27 are predisposed to this reaction Guillain-barre syndrome → ascending (symmetric) muscle weakness, ⭣DTRs (Deep tendon reflexes) - treated with IVIG
84
bacteria that grows in a 37-42ºC temperature
Campylobacter Jejuni
85
MCC of bacterial diarrhea in the US
Campylobacter Jejuni
86
general principles of Salmonella Paratyphi
S. enterica serotype Typhi S. enterica serotype Paratyphi gram negative motile bacilli encapsulated → Vi capsule - non-lactose fermenter - glucose fermenter - produces H2S MacConkey agar → colorless colonies triple sugar iron test → yellow base, black color above base, red slant - facultative anaerobe - catalase positive, oxidase negative, urease negative
87
pathogenesis of Salmonella paratyphi
reservoir: GI tract travelers to resource-limited regions and areas of poor sanitation fecal-oral transmission → bacteria destroyed in the stomach → surviving bacteria invade Peyer’s patches and M-cells (small intestine) → hematogenous spread +/- gallbladder colonization in chronic carriers not resistant to gastric acid, hematogenous dissemination flagella LPS endotoxin → septic shock Vi capsule (vaccine target) → ⭣phagocytosis → ⭣⭣⭣neutrophil response → ⭡intracellular replication → spread to reticuloendothelial system → monocyte-mediated response
88
bacteria that commonly spreads to the reticuloendothelial system
Salmonella paratyphi
89
which bacterias aim to infect the Peyer patches and M cells
Salmonella paratyphi Yersinia Shigella spp
90
characteristics of gastroenteritis/typhoidal fever
⭡risk in children, ⭡ID50 progressively worsening fever over several days, high fever, pulse-temperature dissociation (relative bradicardia) faint erythematous maculopapular lesions (”rose spots”), chest and abdomen are classic, trunk to extremities nausea, emesis, abdominal pain/cramping, malaise constipation → watery “pea-soup” diarrhea hepatosplenomegaly, anemia, leukopenia osteomyelitis in sickle cell disease
91
bacteria associated with a "pea-soup diarrhea"
Salmonella paratyphi
92
management of a salmonella paratyphi infection
- hydration, correct electrolyte derangements antibiotic tx: ceftriaxone, ciprofloxacin, azithromycin FIRST LINE OF TX ARE ANTIBIOTICS
93
which vaccines are given for salmonella paratyphi
vaccination: - oral vaccine: live-attenuated S. thypi - IM vaccine: Vi capsular polysaccharide
94
which vaccine is given for salmonella paratyphi when people plan to go to endemic regions
oral vaccine: live-attenuated S. thypi
95
complications of salmonella paratyphi
ulceration, hemorrhage → bowel perforation
96
if your patients presents himself with faint erythematous maculopapular lesions (”rose spots”) that apear from the trunk to extremities, which bacteria suspect caused this
Salmonella paratyphi

Infectious Disease Pathophysiology (5 decks)

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