Chapter 21: Rickettsias, Chlamydias, Spirochetes, and Vibrios Flashcards

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1
Q

What are two types of relapsing fever in the genus Borrelia including their causes and vectors

A

1) Louse-borne relapsing fever
- Caused when Borrelia recurrentis is transmitted between humans by the human body louse
- Lice become infected with B. recurrentis when they feed on infected humans, the only reseroir for this spirochete

2)** Tick-borne relapsing fever**
- Several Borrelia species can cause this disease
- Transmitted to humans by soft ticks of genus Ornithodorus
- Ticks and rodents are common reservoirs of infections

Spirochetes: Borreila

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2
Q

What are both types of relapsing fever characterized by and treatment

A
  • Characterized by recurring episodes of septicemia and fever
  • Due to the body’s repeated efforts to remove the spirochetes
  • Successful treatment is with doxycyline or erthromycin

Spirochetes: Borrelia

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3
Q

Describe Leptospira

A
  • Motile by means of two axial filaments
  • Obligately aerobic bacteria
  • Found in numerous wild and domestic animals (ex. rats, raccons, foxes, horse, cattle, pigs)
  • Grows in kidney tubules
  • Grown on special media enriched with bovine serum albumin or rabbit serum

Spirochetes: Leptospira interrogans

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4
Q

Describe Leptospriosis

A
  • Caused by L. interrogans
  • Zoonotic in nature
  • One end of the spriochete is hooked like a question mark
  • Humans contract disease via contact with infected urine or environment
  • Leptospira enters cuts/abrasions in skin and mucous membranes
  • Travels via bloodstram throughout the body
    • Infection may lead to kidney dysfuntion
    • Bacteremia eventually resolves; spirochetes found only in kidneys
  • Eradication impractial due to the varous animal reservours
  • Vaccine available for animals

Spirochetes

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5
Q

How do humans contract Leptospirosis

A
  • Via contact with infected urine or enviroment
  • Leptospira enters cuts/abrasion in skin mucous membranes

Spirochetes: Leptospira

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6
Q

How does Leptospira travel?

A
  • Travels via the bloodstream throughout the body
  • Infection may lead to kidney dysfunction
  • Bacteremia eventually resolves then the spirochetes will only be found in the kidneys

Spirochetes: Leptospira

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7
Q

What are three genera of the more pathogenic vibrios

A
  • Vibrio
  • Campylobacter
  • Helicobacter

Vibrios

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8
Q

Contrast Vibrio with enteric bacteria in terms of their flagella and biochemical properties.

A

Compare: Vibrios and enteric bacteria both have O polysacharide antigens
Contrast: Vibrios are oxidase positive with polar flagellum

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9
Q

Describe the action of cholera toxin in causing cholera

A

Step 1) Cholera toxin binds to membrane of epithlial cell
Step 2) Portion of toxin (part A) enters the cell
Step 3) A1 activates adenylate cyclase (AC)
Step 4) Cyclic AMP (cAMP) is synthesized
Step 5) Cyclic AMP stimulates cell to secrete Cl-, Na+, and other electrolytes
Step 6) Water follows electrolytes into lumen

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10
Q

Name three species of Vibrio and describe the resulting diseases

A
  • Vibrio cholerae causes cholera (particularly O1 El Tor strain)
  • Vibrio parahaemolyticus results from ingestion of shellfish; causes cholera-like gastroenteritis
  • Vibrio vulnificus causes spepticemia due to consumption of contaminated shellfish, and wound infections can result from washing wounds with contaminated seawater
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11
Q

List several possible reserviors of Campylobacter jejuni

A

Campylobacter jejuni is zoonotic - many animals serve as reservoirs for the bacteria including:
- Poultry
- Dogs
- Cats
- Pigs
- Cattle
Humans become infected by consuming contaminated food, milk, or water
Poultry is the most common source of infection

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12
Q

What is the most common source of infection for Campylobacter jejuni bacteria

A

Poultry is the most common source of infection

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13
Q

Describe the pathogenesis of Campylobacter jejuni

A
  • Bacteria possesses adhesins, cytotoxins and endotoxins
  • Infections produce self-limiting bloody and frequent diarrhea that may last 7-10 days
  • Appears to colonize and invade jejunum, ileum and colon producing bloody lesions
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14
Q

Describe the pathogenesis of Helicobacter pylori

A
  • Produces numerous virulence factors that enable it to colonize the stomac
  • Proteins that inhibits acid production in stomach
  • Flagella help the pathogen to burrow through the stomach lining
  • Adhesins facilitate binding to gastric cells
  • Exotoxins - Cytotoxin-associated gene A product (CagA)
  • Enzymes like urease that help neutralize stomach acid
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15
Q

Discuss the major change in medical opinion concerning the cause of peptic ulcers

A
  • H. pylori causes gastritis and most peptic ulcers, erosions of the mucus membrane of the stomach or small intestine
  • Prevailing viewing that - stress, alcohol consumption, spicy food, or excess stomach acid production cause peptic ulcers
  • Robin Warren and Barry Marshall detected Helicobacter colonizing the majority of their patients’ stomachs

Pathogenic Gram negative Vibrios: Helicobacter pylori

Dr. Marshall drank one of his cultures of Helicobacter. He developed painful gastritis and was able to isolate H. pylori in his stomach.

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16
Q

Define peptic ulcers

A
  • Erosions of the mucous membrane of the stomach or small intestine
17
Q

Describe the effect of Helicobacter pylori on the lining of the human stomach.

A

The formation of a peptic ulcer begins when H. pylori (protected by urease) burrows through the stomach’s protective layer of mucus to reach the underlying epithelial cells
1) Where the bacteria attach to the cells’ cytoplasmic membranes and multiply. A varitey of factors - the triggering of inflammation by bacterial exotoxin and destruction of mucus producing cells by the bacteria- causes the layer of mucus to become thin
2) Allowing acidic gastric jusic to digest the stomach lining, H. pylori gains access to the underlying muscle tissue and blood vessels
3) Those bacteria that are phagocytized survive in part through the actions of catalase and superoxide dismutase, enzmes that neutralize part of the phagocytes’ killing mechanism

1) Bacteria invade mucus and attach to gastric epithelial cells 2) Helicobacter, its toxins, and inflammation cause the layer of mucus to become thin 3) Gastric acid destroys epithelial cells and underlying tissue
18
Q

Prevention of Helicobacter pylori

A
  • Good hygiene
  • Adequate sewage treatment
  • Proper food handling
  • Water purification
19
Q

Treament of Helicobacter pylori

A

Treat with antimicrobial drugs in combination with drugs that inhibit acid production

20
Q

Helicobacter pylori

A
  • Slightly helical, motile bacterium that colonizes in the stomach of its hosts
  • Urease positve, a characteristic that is essential for colonizing the stomach (degrades urea to produce ammonia which neutralizes tomach acid)
  • Causes gastritis and most peptic ulcers
  • Long term infection with Helicobacter is a significant risk factor for stomach cancer