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SEM 3 Bacteria, Parasites, Viruses GI > Bacteria > Flashcards

Bacteria Flashcards

1
Q

Enteric fever

A

Typhoid fever - Salmonella typhi

Paratyphoid fever - Salmonella typhi A,B,C

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2
Q

Pathophysiology: Salmonella typhi

A

penetrate gut mucosa via Peyer’s patches in jejunum/distal ileum (could lead to ulceration/ perforation) –> multiply within macrophages –> enter mesenteric lymph nodes –> thoracic duct –> bloodstream –> invade reticuloendothelial system (multiply in Kupffer cells) –> reinvade blood –> gallbladder infection

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3
Q

Clinical features: typhoid fever

A
  • constipation then diarrhea
  • rose spots
  • fever, malaise, flu-like illness
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4
Q

Lab Diagnosis: Salmonella typhi

A
  • serotyping (O,H, Vi antigens)
  • WIDAL test - detects rise in antibodies against H and O antigens

Checking blood, stool, urine

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5
Q

Treatment: Salmonella typhi

A

Ceftriaxone/ Ciprofloxacin

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6
Q

Prevention: Salmonella typhi

A

good hygiene, typhoid carriers excluded from food handling

Vaccination

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7
Q

Salmonellosis

A

include all salmonellas except typhi and paratyphi

  • found in poultry and diary products
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8
Q

Salmonellosis: Pathogenesis

A

ingested-> absorbed to epithelial cells in small intestine –> penetrates to lamina propria layer –> multiply in lymphoid follicles –> reticuloendothelial hyperplasia –> confined to GI tract –> inflammatory response (release of prostaglandins) –> stimulates cAMP and active fluid secretion –> diarrhea

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9
Q

Salmonellosis: clinical manifestations

A

Bacteremia: blood cultures positive

Enterocolitis
-low grade fever
- nausea, headache, vomiting, diarrhea
- stool cultures positive

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10
Q

Salmonellosis: Treatment

A

no need antibiotics, just fluid and electrolyte replacement

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11
Q

Vibrio cholerae: Pathogenesis

A

ingested –> sensitive to stomach acid, some make it to intestines –> toxin production –> diarrhea

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12
Q

Vibrio cholerae: clinical manifestations

A

due to enterotoxin
- rice water stool
- marked dehydration
- metabolic acidosis
- hypokalemia
- hypovolemic shock

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13
Q

Vibrio cholerae: lab diagnosis

A

culture

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14
Q

Vibrio cholerae: Treatment

A

rehydration with fluids and electrolytes

  • tetracycline MAY be given
    (erythromycin in children)
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15
Q

Vibrio cholerae: prevention

A

good hygiene
clean water and food
vaccination

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16
Q

Vibrio parahaemolyticus

A

consumption of uncooked seafood
pathogenesis unclear

17
Q

Shigellosis: pathogenesis

A

fecal- oral route, limited to GI tract
invades mucosal epithelial cells -> multiplies and spreads within epithelial cell cytoplasm–> microabscesses leading to necrosis –> ulceration, bleeding

heat labile exotoxin affects gut and central nervous system

18
Q

Shigellosis: clinical manifestations

A

due to exotoxin:
- abdominal pain, fever, watery diarrhea
- number of stool increases, contains mucus and blood (dysentery)
- tenesmus (Rectal spasms)

19
Q

Shigellosis: treatment and prevention

A

mild: only symptomatic treatment
sever: ciprofloxacin

Prevention: good hygiene, no handling food until negative

20
Q

Clostridium difficile: Pathogenesis

A

pseudomembranous colitis
-usually caused by disruption to normal gut flora (e.g. antibiotics)

Toxin A (enterotoxin) – binds to brush border membranes of gut receptor sites

Toxin B (cytotoxin_

21
Q

Clostridium difficile: Clinical manifestations

A
  • watery/bloody diarrhea
  • abdominal pain
  • low grade fever
  • leukocytosis
  • plaques and microabscesses (endoscopic findings)
  • biopsy -> inflammation in lymphoid tissue, mucosa (destruction and inflammation exudates produce thick pseudomembrane)
22
Q

Clostridium difficile: lab diagnosis

A

feces:
- cycloserine cefotixin fructose agar (CCFA)
+ detection of toxins in feces

histological changes on affected colonic mucosa

23
Q

Clostridium difficile: Treatment

A

metronidazole/ oral vancomycin –> discontinue offending antibiotic initially

24
Q

Campylobacter: pathogenesis

A
  • unpasteurised milk, untreated water

killed in stomach, but may be protected in milk —> invade epithelium of small intestine –> inflammation –> red, white blood cells in stool

enterotoxin produced causes fluid accumulation in ileal loops

25
Q

Campylobacter: clinical manifestations and treatment

A
  • abdominal pain, bloody diarrhea, headache, malaise, fever

usually resolves without antibiotic therapy: erythromycin sensitive

26
Q

Campylobacter: lab diagnosis

A

feces:
- -ve “sea gull wing” shape organism
- grows on skirrow’s medium
oxidase positive

27
Q

Campylobater: treatment and prevention

A

erythromycin, ciprofloxacin

prevention: good hygiene, public health measures for milk

28
Q

Helicobacter pylori: pathogenesis

A

chronic gastritis
peptic ulcer
mucosa-associated lymphoid tissue lymphoma (MALT)
gastric carcinoma

  • grows optimally at pH 6-7, found in mucus layer near epithelial surface
  • produces protease that modifies gastric mucus, reducing ability of HCl to diffuse through mucus
  • potent urease acitivty–> yields production of ammonia (alkaline
  • motile in mucus
29
Q

Helicobacter pylori: clinical manifestations

A

nausea, pain, vomiting, fever
organism: spiral shaped, gram -ve

30
Q

Helicobacter pylori: diagnosis

A

Urea breath test:
- patient swallows urea orally, broken down by urease in stomach, measures CO2

Biopsy:
rapid urease test
histology
Skirrow’s medium culture

31
Q

Helicobacter pylori: Treatment

A

Triple therapy
proton pump inhibitor + clarithromycin + amoxicillin + (bismuth compound)

32
Q

Escherichia coli: EPEC pathogenesis

A
  • belongs to O serotypes
  • attaches to epithelial cells, disrupts microvillus causing diarrhea
33
Q

Eshcerichia coli: ETEC pathogenesis

A
  • fimbrial adhesions
  • enterotoxins: heat labile, heat stable
  • commonly causes traveler’s diarrhea
34
Q

Escherichia coli: EHEC pathogenesis

A
  • serotype O157:H7
  • produces verotoxin, binds to verotoxin receptors on renal epithelium
  • causes haemorrhagic colitis (destruction of mucosa)
  • causes haemorrhagic uremic syndrome
35
Q

Escherichia coli: EIEC

A
  • tissue destruction, inflammation, necrosis, ulceration, blood and mucus in stools
  • due to poor hygiene
36
Q

Escherichia coli: EAEC

A
  • produces heat labile toxin
37
Q

Escherichia coli: DAEC

A
  • produces a-haemolysin, cytotoxic necrotizing factor
38
Q

Escherichia coli: Treatment and prevention

A

no specific antibiotic
- fluid replacement
- treat hemolytic uremic syndrome

clean water, adequate sewage disposal

SEM 3 Bacteria, Parasites, Viruses GI (3 decks)

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