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Immuno mikro eng > Intra-Abdominal Infections > Flashcards

Intra-Abdominal Infections Flashcards

1
Q

What is the main reservoir for introduction of bacteria into the GI tract?

A

Mouth, comprised of 99% anaerobes

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2
Q

Why are enterococcus different than other gram positive organisms?

A

They can live in the presence of bile salts -> highest concentration in duodenum

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3
Q

What is the purpose of M cells?

A

Aid in the presentation of antigens by phagocytosing bacteria and other antigens, and passing to underlying macrophages

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4
Q

What is the significance of crypts for enterocytes?

A

New enterocytes are produced in the crypt at a very high turnover rate, and are sloughed off at the tips of the villi

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5
Q

What is one major mechanistic difference between how bacterial flora are treated in the duodenum vs colon?

A

Small intestine: very fast movement of material which constantly washes bacteria out of it
Colon: Slow rate of flow allowing for dense bacterial population and protective flora

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6
Q

What are three major tests used in the identification of gram negative bacterial infections?

A
  1. Oxidase reaction - ability to oxidize cytochrome C
  2. Growth on MacConkey agar (gram negative and does it ferment lactose)
  3. Metabolism - Oxidative or fermentative growth based on oil / air above tubes of growth medium
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7
Q

What major family of bacteria is oxidase negative?

A

Enterobacteriacea - i.e. PEK + Salmonella, Shigella, Yersinia

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8
Q

What is secretory vs inflammatory diarrhea?

A

Secretory - watery, with no immune cells and no invasion

Inflammatory (dysentery) - Based on presence of leukocytes in the stool (inflammation)

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9
Q

What is invasive vs non-invasive?

A

Invasive - Organism can invade epithelial cells

Non-invasive - Bacteria stays in lumen but causes disease by secreting toxins

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10
Q

What is enterotoxin vs neurotoxin vs cytotoxin?

A

Enterotoxin - toxin released by microorganism in the intestine
Neurotoxin - acts directly on neurons
Cytotoxin - Has a specific toxic action on cells of special organs

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11
Q

What are the three classes of secretory diarrhea causes?

A
  1. Toxin-mediated - enterotoxin or neurotoxin
  2. Parasite-mediated - i.e. Giardia or Crypto
  3. Viral
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12
Q

What are the three types of invasive / tissue-damaging diarrhea, by etiology?

A
  1. Cytotoxin-mediated inflammation - i.e. C. difficile, EHEC
  2. Invasive-infection mediated - i.e. Shigella, EIEC, Salmonella
  3. Parasitic - i.e. E. histolytica
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13
Q

What two Vibrio cholerae serotypes cause pandemic cholera, and what is its morphology? Oxidase test?

A

O1 & O139 - gram negative (O antigens are on LPS), Comma-shaped motile rods. Oxidase positive

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14
Q

What is the mechanism of transmission of cholera? Can there be carriers?

A

Fecal-oral route, most commonly via water, fish, and shellfish

There can be carriers - important reservoir

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15
Q

What are the three main virulence factors of Vibrio cholera?

A
  1. Motility - Single polar flagellum to get close to mucosa
  2. Adherence - TCP (toxin co-regulated pili) which form bundles to adhere to mucosal epithelium of small intestine
  3. Cholera toxin - ADP-ribosylating AB type toxin
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16
Q

What is an AB toxin and how does cholera-toxin work?

A

AB = activity and binding.
B has 5 binding subunits, attaches to Ganglioside GM1. A is inactive until it enters the cell and becomes A1, enzymatically activating host adenylate cyclase.

Leads to chloride and fluid excretion via osmotic loss (up to 1 L / hr)

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17
Q

Why is the ID50 of cholera so high?

A

Need a large inoculum (>1 million) due to sensitivity to gastric acids

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18
Q

What special media is cholera grown on?

A

TCBS - Thiosulfate citrate bile sucrose

Think TCBY!~

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19
Q

What are the general virulence factors of E. coli?

A
  1. Bundle-forming pili- like TCP of Vibrio

2. Adhesins - bind to epithelial cells, “colonization factors” on pili

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20
Q

What are the two toxins produced by enterotoxigenic E. coli and how do you remember this?

A

“labile in the Air, stable on the Ground”

Heat labile toxin - raises cAmp levels, same mechanism as cholera-toxin (GM1 binding)

Heat stable toxin - raises cGmp levels, decreases the resorption of electrolytes and fluid

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21
Q

What does ETEC cause and how is it normally contracted?

A

Travelers diarrhea

Normally contracted via contaminated food and beverages in th e tropics

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22
Q

How is ETEC identified?

A

ELISA or agglutination tests for presence of toxins, or DNA probes for the LT or ST (toxin) genes.

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23
Q

What is enteropathogenic E. coli known for (EPEC)

A

Causing a fatal, watery diarrhea in infants / children in developing countries (due to loss of absorptive capacity of mucosal surface)

EPEC = Pediatric (look at the P)

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24
Q

What is the major virulence mechanism of EPEC? What type of secretion?

A

Attachment and “effacement” of cell membrane by destroying the microvilli and sitting on an actin-like pedestal

Also uses Type 3 secretion to inject bacterial proteins

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25
Q

What are the three major bacterial species that create pre-formed toxins?

A
  1. Clostridium botulinum
  2. S. aureus
  3. Bacillus cereus
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26
Q

What is the structure of botulinum toxin, and what usually causes death?

A

AB toxin which binds to peripheral neurons. B portion binds the ganglioside receptors on nerve cells, and A toxin is internalized, blocking Ach release at neuromuscular junction = flaccid paralysis

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27
Q

Why is botulism an even bigger concern for children?

A

Floppy baby syndrome = infant botulism, can cause SIDS because honey often contains C. botulinum spores which cannot be fought off due to immature microbiota.

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28
Q

How is C. botulinum identified?

A

Gram + spore-forming bacillus, identified typically by immunoassay for toxin in food substance or gastric contents or blood

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29
Q

What is the most common bacterial form of food poisoning and what is its mechanism?

A

S. aureus, due to unrefrigerated foods. Uses enterotoxin B, not destroyed via reheating. (heat stable)

Stimulates neural receptors - leading to vomiting center stimulation in CNS = project vomiting

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30
Q

What are the two forms of Bacillus cereus food poisoning, and which one is associated with pre-formed toxin?

A
  1. Emetic / vomiting type - preformed toxin - reheated rice syndrome (from sitting at Chinese restaurant). Similar to S. aureus, short onset
  2. Diarrheal form - longer incubation, slower onset. Heat LABILE toxin which is formed in vivo, activates cAMP. Associated with GI pain and non-blood diarrhea from foods sitting above room temp.

Both resolve in <24 hours

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31
Q

What is one final bacterium that can release a heat-labile enterotoxin after ingestion?

A

Clostridium perfringens - much like B. cereus diarrheal form, produced in GI tract. From undercooked food

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32
Q

What is the virulence factor of Giardia?

A

Adhere to upper small intestine via ventral surface disk on trophozoite “sucking disk”

Although they have flagella for motility as well

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33
Q

What is the mechanism of Giardia infection?

A

Oral ingestion of cysts, commonly from drinking unfiltered water. Incubation is about 1 week, before acute onset of watery diarrhea.

Chronic giardia can lead to bloating, and fat-rich stool “Ghirardelli chocolate fat” stool

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34
Q

How is Giardia identified?

A

Antigens for it in stool, duodenal biopsy shows “old man face” or cysts in stool

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35
Q

What is a non-inflammatory protozoan which is of major concern to immunocompromised patients?

A

Cryptosporidium parvum - causes severe, watery, prolonged diarrhea in aids

Immunocompetent is a mild watery diarrhea

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36
Q

How does Cryptosporidium reproduce?

A

Invades the microvilli of the intestine, releases oocysts in the feces, and these are eaten (fecal-oral)

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37
Q

What is a protozoal diarrhea more severe in AIDS patients that can persist up to 7 weeks?

A

Cyclospora cayetanesis

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38
Q

What is an obligate intracellular spore-forming protist causing watery diarrhea?

A

Microsporidia

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39
Q

What is another protist causing watery diarrhea which is pretty much indistinguishable from the others?

A

Isospora belli - infects entire intestines

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40
Q

When does C. difficile infection typically occur?

A

In the 5% of healthy adults who carry it, follows clindamycin use

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41
Q

What are the two toxins produced by C. difficile and what does this cause overall?

A

Toxin A - Enterotoxin binding mucosa, causes altered membrane permeability, necrosis, and inflammation

Toxin B - Cytotoxin like diphtheria, disrupts actin cytoskeletal structure and decreases cellular protein synthesis

Results in pseudomembranous colitis

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42
Q

How is C. difficile clinically diagnosed?

A

Detection of toxin in stool, as it is anaerobic but technically can be cultured on CCFA agar

43
Q

What are the three H’s of EHEC?

A

Hemorrhagic
Hamburger
Hemolytic-uremic syndrome

44
Q

What does Hemolytic uremic syndrome cause? Why?

A

Triad:
Anemia
Thrombocytopenia
Acute renal failure

Due to microthrombi forming on damaged endothelium of renal glomeruli

45
Q

What is the mechanism of the EHEC toxin?

A

It is Shiga-like. AB toxin which is is carried by bacteriophage.

B binds Gb3 ganglioside on host cell. A toxin modifieds 28S ribosome of 60S subunit, leading to decreased protein synthesis and cell death.

46
Q

In what way is EHEC similar to EPEC?

A

Uses type 3 secretion and causes attaching and “effacement” of colonic mucosa

47
Q

What is the infectious dose of EHEC? What type of diarrhea does it cause?

A

Really low (10 or fewer), found in hamburgers, raw milk, or apple cider

48
Q

What is the OHK serotyping of E. coli?

A

O - outer region 1 of LPS
H - flagellar protein
K - capsular polysaccharide (like E. coli K1 of meningitis)

49
Q

What is the major causative serotype of EHEC? How is it identified in the lab?

A

O157:H7

identified on MacConkey sorbitol agar - does not ferment sorbital in most cases

Can also probe for toxin genes or anti-O157:H7 serum

50
Q

How does Shigella invade?

A

Enters through M cells. Uses Type 3 secretion modification to enter macrophages from M cells and multiples in cytoplasm. Uses listeria-like mechanism to invade adjacent cells by actin repolymerization

51
Q

How does Shigella cause bacillary dysentery? Do they all produce Shigatoxin?

A

Uses local inflammation produced by PMNs to induce more epithelial damage and allowing more invasion by bacteria, although it typically does not cause sepsis.

Only Shigella dysenteriae produces Shigatoxin, which is a cytotoxin killing more intestinal epithelium (like EHEC).

52
Q

What is the symptomatic progression of Shigella? What is the composition of the stool?

A

Early - abdominal pain, cramping, fever (in small intestine)
Later - 12-72 hours - fever drops but pain is more severe as organism is in large intestine (lower quadrant). Tenesmus, cramps, and lethargy.

Causes large numbers of PMNs in mucoid stool.

53
Q

What is tenesmus?

A

The feeling that you need to poop, very uncomfortable

54
Q

What is the route of infection + identification of organism?

A

Fecal-oral
ID is via oxidase-negative gram negative bacillus with NO FLAGELLA (only Salmon swim). Also will be lactose negative (nonfermenter) unlike EIEC

55
Q

What are the properties of EIEC?

A

EnteroInvasive = invasive just like Shigella, just without Shigatoxin.

Also, it will be lactose positive

56
Q

How does the ID50 differ between Salmonella and Shigella, and which Salmonella only affects humans?

A

ID50 of Salmonella is much higher, since it is not resistant to gastric acids

Salmonella typhi only affects humans

57
Q

What are the major membrane changes that occur with Salmonella infection? How is it internalized?

A
  1. Organism binds microvilli, invading M cells or mucosa, and replicating inside the phagosome
  2. Ruffle-like appearance of microvilli due to actin-rearrangement via Type 3 secretion
  3. Lipid A release upon cell lysis will cause mucosal damage
58
Q

What are common sources of Salmonella?

A

Poultry meat or eggs

59
Q

What are the three clinical diseases inducible by Salmonella?

A
  1. Gastroenteritis - most common from non typhi, due to increased cAMP from prostaglandin inflammation. Some diarrhea and vomiting.
  2. Bacteremia - often follows gastroenteritis, causes spiking fever, because organism can invade bloodstream
  3. Enteric fever - typically only associated with S. typhi or paratyphi
60
Q

What is enteric fever?

A

Typhoid fever - Malaise, swollen lymph nodes (as bacteria migrate to mesenteric nodes), hepatosplenomegaly, and 1/3 of patients have ROSE SPOTS on abdomen.

61
Q

How do people carry typhoid?

A

In their gallbladder (Mary Mallon)

62
Q

Since Shigella and Salmonella are both lactose negative, how do you tell them apart?

A

Hektoen enteric agar - Salmonella appears black as a result of H2S production. Can grab from a stool sample in gastroenteritis

63
Q

How are bacteremia and enteric fever told apart?

A

Bacteremia - rarely a positive stool culture. Rapid, spiking fever.

Typhoid - positive culture only later in disease. Also has an INSIDIOUS onset rather than acute. That is, a slowly rising fever rather than a rapid, spiking fever. Blood diarrhea will occur later.

64
Q

What are the virulence factors associated with Campylobacter?

A

Flagella - motility through intestinal mucus layer, where it multiples.

Enterotoxin / cytotoxins which destroy intestinal cells.

Protein S - surface protein = capsule, resist complement and phagocytosis

65
Q

What is campylobacter pathologically associated with?

A

Guillain-Barre syndrome - an acute autoimmune demyelinating disease.

Results from hurmoral response to surface antigen of C. jejuni and its cross-reactivity to myelin protein.

66
Q

What is the source of campylobacter?

A

Undercooked chicken, although milk, water, and other meats have been known.

67
Q

How is Campylobacter identified / cultured?

A

Camp = Hot Campfire, 42 degrees Celsius incubation.

It is microaerophiic and capnophilic (good for intestinal growth).

Importantly, it is oxidase-positive (otherwise the same as the other Enterobacter).

68
Q

How does one get Vibrio parahaemolyticus?

A

Consuming raw seafood, especially salty (halophilic).

Major problem in Japan - produces Cytotoxin and invades epithelial cells

69
Q

How do humans get Yersinia enterocolitica?

A

Transmitted from pet feces, or livestock / rodents, and humans consume contaminated food, water, or blood products.

Blood products a real issue - grows at lower temps and can multiple in refrigerated stored blood

70
Q

What does Yersinia enterocolitica cause?

A

Pseudoappendicitis - due to Mesenteric lymphadenitis, common in young children. Also necrosis of Peyer’s patches in terminal ileum (lasts 1-2 weeks).

71
Q

What is the causative agent of amoebic dysentery? How does it adhere to the host? What enzymes?

A

Entamoeba histolytica

Adheres via galactose receptors on bowel wall, while using proteolytic enzymes to dissolve extracellular matrix

72
Q

What microbe commonly causes ulcerative colitis?

A

Shigella, as invaded cells die and slough off, resulting in erosion of gut wall and formation of shallow ulcers

73
Q

How does Entamoeba histolytica excyst and where does it cause damage?

A

Excystation occurs in small intestine, trophozoites will invade mucosal surface and invade crypts, leading to undermining of submucosa and formation of

“flask-shaped lesions.” in the crypts, on histology
Liver abscesses can also form if it enters veins - extraintestinal involvement

74
Q

Where does E. histolytica form cysts?

A

In the colon, which are excreted in feces.

These can be diagnostically detected in stool, along with organism

75
Q

What is H. pylori pre-disposing for?

A

Chronic gastritis, 70-80% of gastric ulcers, 90% of duodenal ulcers, and gastric cancer (gastric adenocarcinoma)

76
Q

What are two unique virulence factors of H. pylori? How does this relate to gastric ulcer formation?

A
  1. Urease - converts urea to ammonia for local protection from acid, establishing in mucin layer
  2. Mucinase - local destruction and stimulation of inflammatory cells. Used to penetrate gastric mucus.

Inflammation and mucosal death will ultimately lead to gastric ulcer formation?

77
Q

How is H. pylori clinically identified?

A

The urease test or gastric biopsy - it is “campylobacter-like”, microaerophilic, gram negative, oxidase positive

78
Q

What is the morphology and growth characteristics of L. monocytogenes? How do you get it?

A

Gram POSITIVE - facultative intracellular bacillus, oxidase negative, beta-hemolytic

Has tumbling motility at room temperature, but non-motile at human temp

Mostly get it from food, because it can survive in refrigerators

79
Q

Who typically gets Listeria?

A

Immunocompromised, infants, or pregnant women who have not developed an immune response

It is cleared by macrophages in healthy people

80
Q

How does Listeria get into the CNS / placenta?

A

Enters through intestines, through M cells, and moves through bloodstream. Has a predilection towards the CNS and placenta

81
Q

List the three types of Nematodes of human significance?

A
  1. Roundworms - i.e. Ascaris
  2. Pinworms -i.e. Enterobius
  3. Hookworms - i.e. Necator or Ancylostoma
82
Q

List the Cestodes of human significance? How do you get them?

A
  1. Beef tapeworm
  2. Pork tapeworm

You get them from eating both of those uncooked

83
Q

Where does Ascaris lumbricoides live and what does it cause? They are roundworms, how are they transmitted?

A

Lives in lumen of small intestine.

Causes asymptomatic infection in most, with possible loss of appetitite. Heavy infection causes a physical instruction (biliary or at ileocecal valve).

Transmission is fecal-oral via eggs

84
Q

Where do pinworms live? What is the species? What is the symptom?

A

They live in the cecum, spread via fecal-oral route, Enterobius vermicularis

Cause anal pruritis (due to egg deposition), especially in children

85
Q

What are the species of hookworms? how are they transmitted? What do they cause?

A

Necator americanus and Ancylostoma duodenale

Transmitted via larvae penetrating skin (barefeet), or drinking contaminated water

Cause cutaneous larvae migrans (itchy rash) or ANEMIA from them blood-sucking your intestinal wall.

86
Q

What are the two tapeworms and which is worse?

A

Taenia saginata - beef tapeworm

Taenia solium - pork tapeworm (pork is salty / sodiumy)

Solium is worse because it can migrate to varius tissues causing cystericerocosis

87
Q

What is peritonitis? How does it occur?

A

Inflammation of the peritoneum, a cavity extending from the undersurface of the diaphragm to the floor of the pelvis

Occurs via contamination of the peritoneal cavity by micro-organisms

88
Q

What are the three types of peritonitis?

A
  1. Primary - spontaneous bacterial
  2. Secondary - most common, spillage
  3. Dialysis-associated
89
Q

What is the most common cause of primary peritonitis?

A

Advanced liver disease, leading to ascites + cirrhosis of liver.

Most often a monomicrobial infection of unknown source via facultative anaerobe (since ascitic fluid has a relatively high oxygen content). Typically E. coli or Klebsiella from GI tract.

90
Q

What is a secondary peritonitis?

A

Infection caused because of spillage of GU or GI organisms into the cavity. Much larger than primary infection.

Anaerobes will predominate (endogenous source) and polymicrobial

91
Q

What is a dialysis-associated peritonitis? Is it poly or mono microbial? What are some common microbes

A

A complication of peritoneal dialysis (CAPD), in which skin / oral flora infect the catheter. Often monomicrobial, with P. aeruginosa being the most common pathogen!!

but others include S. epidermitis, E. coli, or S. aureus.

ALSO C. albicans is frequently associated with CAPD

92
Q

What are symptoms of peritonitis?

A

Abdominal distension, pain, absence of bowel sounds, and nausea / vomiting / fever.

93
Q

What is a major concern with E. coli peritonitis?

A

Lipid A toxicity, since any E. coli can colonize.

Leads to LPS-activated cytokine / complement activation

94
Q

What are the predominant aerobes in peritonitis?

A

Gram negative: E. coli, Klebsiella, Enterobacter

Gram positive: E. faecalis, Viridans Strept

95
Q

What are the prominent anaerobes in peritonitis?

A

AGNB - Anaerobic gram negative bacilli

B. fragilis, others

96
Q

What causes intraperitoneal abscess?

A

A polymicrobial complication secondary to local or generalized peritonitis / other GI / GU inflammatory disease

97
Q

What is a common causative agent of intraperitoneal abscess? How is it identified?

A

Bacteroides fragilis, a gram-negative encapsulated anaerobic bacillus.

Identified via foul-smelling discharge and broad antibiotic resistance (i.e. aminoglycosides because they are oxygen-dependent)

98
Q

Why are obligate anaerobes typically missed with facultative anaerobes in abscesses?

A

So that the facultative anaerobes will use all the oxygen so they can live. This is why most abscesses are polymicrobial

99
Q

What is the source of most pancreatic abscesses?

A

Penetration due to peptic ulcers, or due to necrotizing pancreatitis in the late stage

100
Q

What accounts for the majority of hepatic abscesses?

A

Biliary tract disease or gall bladder inflammation

Can also be as a result of portal system infection, but really anywhere where the liver gets blood from or a penetrating wound

101
Q

How does the source of splenic abscess determine the causative organism?

A

Since the spleen sees all types of infections, the organism will relate to the site of derived infection

I.e. Endocarditis can lead to S. aureus splenic abscess frequently, or abdominal infection leads to Bacteroides splenic abscess. Blood cultures will be positive in 70% of cases.

102
Q

What causes appendix rupture in appendicitis?

A

Gangrene and pus-filled rupture, leading to peritonitis

103
Q

What is it called when herniation of mucosa and submucosa ruptures, leading to peritonitis?

A

Diverticulitis

Immuno mikro eng (56 decks)

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