Infectious Diseases (IRAT 10)

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86 Terms

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Which bacteria is a gram negative bacilli with motile polar flagellum?

Campylobacter Jejuni

<p><span style="color: rgb(16, 5, 146);"><strong>Campylobacter Jejuni </strong></span></p>
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How is Campylobacter Jejuni transmitted?

  1. Fecal—> oral

  2. Food Borne ( unpasteurized milk, contaminated water, undercooked poultry)

  3. Contact with infected animal ( pigs, dogs, cats)

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What’s the incubation period for Campylobacter Jejuni?

INCUBATION PERIOD: 2-4 days

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At what temperatures does Campylobacter Jejuni grow best?

high temperatures

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What are the initial clinical findings seen with Campylobacter Jejuni?

Initial watery diarrhea —> progress to BLOOD DIARRHEA (enterocolitis) with fever, muscle pain, malaise, HA.

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What abdominal presentation can mimic appendicitis in Campylobacter Jejuni infection?

What GI condition can Campylobacter also present as?

Pseudoappendicitis; Colitis.

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Is Campylobacter Jejuni usually self-limited? How long does it last?

Yes — lasts about 5–7 days. Will get better on its own 

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Which group is more likely to have complications from Campylobacter Jejuni?

HIV patients

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What high-yield neurologic complication is associated with Campylobacter Jejuni?

Guillain-Barré syndrome (GBS).

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What autoimmune complication can follow Campylobacter Jejuni infection?

Reactive arthritis.

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What severe GI complication can occur, especially in immunocompromised patients with Campylobacter Jejuni?

Toxic megacolon.

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What are the two main virulence factors of Campylobacter Jejuni?

Flagellar filaments (flagellin)
Cytolethal distending toxin (CDT)

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What is the MOA of Campylobacter Jejuni

Antiganglioside abs attack peripheral organ—> Guillain-Barré syndrome (GBS).

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What would you use to diagnose Campylobacter Jejuni?

PCR OR Stool culture (Skirrow’s agar) Which

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How do you treat a Campylobacter Jejuni?

  1. Supportive Care (hydration)

  2. SEVERE: Antibiotics:

    • (Azithromycin or Fluoroquinolones)

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🦞Which bacteria is a gram negative rod with a motile polar flagellum and causes high volume fluid loss with electrolyte derangements

🦞Vibrio cholerae

(Severe dehydration → can cause hypovolemic shock) 

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How is Vibrio cholera transmitted?

💩👄 Fecal–oral route

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What are the two main sources of cholera infection?

🚰 Contaminated water
🦪 Uncooked seafood (esp. raw shellfish)

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Where do cholera outbreaks commonly occur?

🌍 Areas with poor sanitation
👥 Overcrowded regions (refugee camps, disaster zones)

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What is the incubation period (exposure to developing infection) for cholera?

0–2 days (very rapid onset)

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What are the key symptoms of Cholera?

Key Symptoms

🌡 Low-grade fever
🤮 Vomiting + abdominal pain
💦 Profuse non-bloody watery diarrhea (“rice-water stool”)

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Major Risk with Cholera?

Hypovolemic shock from massive fluid + electrolyte loss

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What is the pathophysiology of Vibrio cholera?

🦠 Cholera toxin activates adenylate cyclase → ↑ cAMP → stimulates CFTR channels → massive Cl⁻ secretion + inhibited Na⁺/Cl⁻ absorption → huge water loss into the intestinal lumen (“rice-water diarrhea”).

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What the Diagram Shows (Simplified)1⃣ Cholera toxin enters the intestinal cell

The toxin binds → activates a G-protein inside the cell.

2⃣ G-protein turns ON adenylate cyclase

Adenylate cyclase → increases cAMP levels.

📈 More cAMP = cell becomes a salt-secreting machine

3⃣ High cAMP forces CFTR channels to pump OUT chloride (Cl⁻)

The purple channel → CFTR
It starts secreting HUGE amounts of Cl⁻ into the GI lumen.

Cl⁻ goes OUT into the gut

4⃣ When Cl⁻ is pushed out… Na⁺ and water follow it

Opposites attract → the body must keep charges balanced.

So:

  • 🧂 Na⁺ follows Cl⁻

  • 💧 Water follows Na⁺ + Cl⁻

  • Result = massive watery diarrhea

5⃣ Why you wrote “H⁺” and “pH↑”?

In MASSIVE diarrhea:

  • You lose lots of H⁺ from the GI tract

  • Losing acid (H⁺) → makes the blood more alkalotic

  • This causes metabolic alkalosis → pH increases

So your arrow 🡅 pH ↑ = blood becomes more alkaline.


Putting it all together (super clear)

Cholera toxin → ↑ cAMP → ↑ CFTR → Cl⁻ pumped into gut → Na⁺ + water follow → huge water loss → “rice-water diarrhea” → dehydration + ↑ blood pH (alkalosis).

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🔍 How is cholera diagnosed?

  • 👀 Clinical presentation

  • 💧 Dipstick rapid test (initial)

  • 🧫 Stool culture (confirmatory)

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💧 What is the most critical treatment for cholera?

Aggressive fluid + electrolyte replacement

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💊 Which antibiotics are used for cholera?

  • Doxycycline (preferred)

  • Azithromycin

  • Ciprofloxacin
    (Used to shorten course; reserved for severe cases)

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🧫 Which species cause non-typhoidal Salmonellosis?

  • S. enteriditis

  • S. typhimurium

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🔬 What type of bacteria are non-typhoidal Salmonella?

  • Gram-negative bacilli

  • Encapsulated

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🚩 Do Salmonella have flagella?

Yes — they contain flagella (motile).

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🍗 What is Salmonella (*hint: animals) a common cause of in the U.S.?

Foodborne disease (poultry, raw eggs, milk products) OR Contact with reptiles (i.e. turtles, snakes) 

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Whats the incubation period for NON-typhoidal Salmonella?

0-2 days

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🤒 What are the common symptoms of non-typhoidal Salmonella?

  • Fever

  • Nausea

  • Vomiting

  • Myalgia

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💩 What type of diarrhea occurs in Salmonella?

  • Brown-green “pea soup” diarrhea

  • Can be bloody

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What complications occur (esp. in immunocompromised patients)?

  • Reactive arthritis

  • Systemic disease: osteomyelitis, myocarditis, aortitis

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Where does Salmonella colonize?

📍 Ileum and colon

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How does Salmonella invade cells?

🧬 Uses Type III Secretion System (T3SS) to inject proteins and invade intestinal epithelial cells

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How does Salmonella cross the mucosa?

Penetrates M cells and is taken up by macrophages

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What immune response does Salmonella trigger?

🔥 Releases pro-inflammatory cytokines, recruiting neutrophils

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What causes tissue injury in a Salmonellosis (non-typhoidal infection?

🧨 Neutrophil influx → injury + disruption of tight junctions

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How do we diagnose Salmonellosis *non-typhoidal infection?

Stool culture

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How do you treat a Salmonellosis infection? 

  1. Mild-Moderate: supportive care ONLY( hydration)

  2. Severe: Immunocompromised or invasive disease: Abx

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💊 Should antibiotics be used?

Generally NO — they can prolong carriage
Use ONLY if:

  • Invasive disease

  • Immunocompromised patient

  • Severe infection (systemic, hospitalized, ≥9 diarrheal episodes/day)

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Which bacteria is a Gram-negative bacilli, encapsulated. It contains flagella and causes🤒 Typhoid fever.

Salmonella Typhi

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How does Salmonella Typhi spread?

👤 Human host ONLY
🍽🚰 Spread through contaminated food or water (fecal-oral route)

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What are the clinical findings associated with Salmonella Typhi?

🤒 Enteric Fevers: Persistent fever + headaches + myalgias
🚽 Constipation → non-bloody “pea-soup” diarrhea”

Rose spots

🌹 Faint pink macules on abdomen/trunk (classic sign)

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What are the complications of Salmonella Typhi (Typhoid fever)?

Complications

🫀 Hepatosplenomegaly
🩸 GI bleeding (ulceration)

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❤‍🩹 What is “relative bradycardia” associated with Salmonella Typhi?

Fever with a slow pulse, classic for Typhoid. (high temp, low HR)

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🚪 How does Salmonella Typhi enter the body?

Penetrates via M-cells in the intestinal epithelium

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🧫 What intestinal structure becomes hypertrophied in Typhoid?

Peyer’s patches (in the submucosa)

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🩸 How does Salmonella Typhi disseminate?

Through lymphatics + bloodstream

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🏥 Where does Salmonella Typhi replicate?

Reticuloendothelial system (RES)
(liver, spleen, bone marrow)

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🫀 What major finding results from RES involvement?

Hepatosplenomegaly

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Pathophysiology of Salmonella Typhi?

Salmonella Typhi enters through M-cells → infects and hypertrophies Peyer’s patches → spreads via lymphatics + bloodstream → replicates in the reticuloendothelial system (liver, spleen, bone marrow) → causes hepatosplenomegaly.

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How do you diagnose Salmonella Typhi?

  1. Blood or bone marrow culture

  2. Bloodwork Findings: mild normocytic anemia and leukopenia

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What is the treatment for Salmonella Typhi?

Fluoroquinolones (☆Cipro) OR Azithromycin

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🔬 What type of bacteria is Shigella?

Gram-negative rods

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🇺🇸 Which Shigella species is most common in the U.S.?

S. sonnei

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Which Shigella species produces the most toxin?

S. dysenteriae

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How does Shigellosis spread?

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How is Shigella transmitted?

🍽 Foodborne (unpasteurized milk, raw unwashed vegetables)
💩👄 Fecal-oral

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🍑 Can Shigella spread through sexual contact?

Yes — oral-anal sexual contact

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How infectious is Shigella?

Highly infectious — very low inoculum required

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What is the incubation period?

0–2 days

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What are the Classic Symptoms of Shigellosis?

🤒 High fever
🤕 Abdominal cramps
🚽 Tenesmus (painful urge to poop)

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What is the diarrhea pattern of Shigellosis?

💦🩸 Explosive watery diarrhea → progresses to bloody, mucoid diarrhea (dysentery)

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What are the major complications of Shigella?

Major complications of Shigella:

  • 🔥 Reactive arthritis

  • 🩸 HUS (hemolytic uremic syndrome)

  • 💥 Toxic megacolon

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Shigella — Pathophysiology?

🦠 Shiga toxin (Shiga toxin → vessel damage → microclots → RBC destruction → kidney failure)
🔹 Inactivates 60S ribosome → stops protein synthesis
🔹 Endothelial damage → hemorrhage
🔹 ↑ Cytokines → HUS ( hemolytic uremic syndrome)

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How would you diagnose and treat a Shigellosis infection?

☆Diagnose: Stool Culture💩

☆Treatment:

  1. Supportive Care: Hydration

  2. Antibiotics: Azithromycin or Cipro—> used to shorten duration and reduce spread.

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Which gram-negative rod commonly causes traveler’s diarrhea and is transmitted through contaminated food and water?

☆Enterotoxigenic E. coli (ETEC)

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What are the Clinical Findings of ETEC?

Abrupt onset abdominal cramps—> vomiting—> watery, NON-bloody diarrhea

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How does Enterotoxigenic Escherichia coli attach to the intestine?

🧲 Using fimbriae to stick to intestinal epithelium

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What toxins does Enterotoxigenic Escherichia coli produce?

LT (heat-labile) + ST (heat-stable) enterotoxins

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What does heat-labile (LT) toxin do?

It activates adenylate cyclase, which increases cyclic adenosine monophosphate (cAMP)

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What does the heat-stable (HT) toxin do?

💥 It activates guanylate cyclase, which increases cyclic guanosine monophosphate (cGMP).

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What is the result of increased cAMP and cGMP?

💦 They cause increased chloride secretion and decreased sodium and chloride absorption → leading to major water loss → watery diarrhea.

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What condition is Enterotoxigenic Escherichia coli (ETEC) known for causing?

🌎 Traveler’s diarrhea.

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Which bacteria is the 0157:H7, gram-negative rod due to contaminated beef products?

⊹ ࣪ ˖Enterohemorrhagic E. coli⊹ ࣪ ˖

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Enterohemorrhagic E. coli — Transmission?

🍽 Foodborne:

  • Ingestion of undercooked meat

  • Contaminated water

  • Raw leafy vegetables

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What are the clinical findings of Enterohemorrhagic E.coli?

Bloody stool, low grade fever, cramping, & vomiting

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How does Enterohemorrhagic Escherichia coli enter the intestinal tissue?

🚪 Enterohemorrhagic Escherichia coli crosses the intestinal lining by passing through M cells.

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What does Enterohemorrhagic Escherichia coli do once it reaches the lamina propria?

🧫 Once in the lamina propria, the bacteria produce a shiga-like toxin that induces cell death.

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What is the main virulence toxin produced by Enterohemorrhagic Escherichia coli?

The main virulence toxin is the shiga-like toxin, also called verotoxin.

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How does the shiga-like toxin cause cellular injury?

🛑 The shiga-like toxin inactivates the 60S ribosome, which stops protein synthesis and leads to cell death.

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How does the shiga-like toxin damage blood vessels?

💥 It causes endothelial cell injury, which results in hemorrhage.

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What life-threatening complication can result from shiga-like toxin?

The toxin increases cytokine release, which can trigger hemolytic-uremic syndrome (HUS).