EXAM 2 STUDY GUIDE (COMPREHENSIVE
NOTES)
Bacterial Diseases and Key Characteristics
Bartonella henselae
Disease Caused: Cat-scratch disease – a zoonotic infection presenting with lymph
node inflammation.
Description: A Gram-negative intracellular bacillus transmitted through cat
scratches or bites. The infection typically remains confined to the skin and nearby
lymph nodes.
Timeline of Infection:
Animal scratch or bite → formation of small papule/pustule → enlargement of
nearby lymph nodes → gradual resolution.
Prognosis: Excellent, especially in children (90–95% recovery rate).
Diagnosis: Primarily clinical—based on exposure history and typical presentation.
Culture Use: Rare, since it requires specialized laboratory methods and takes time.
Biopsy Findings: Stellate granulomas with central necrosis surrounded by
epithelioid histiocytes.
Treatment:
Mild cases: Supportive care.
Moderate cases: Azithromycin for 5 days.
Severe infections: Azithromycin combined with rifampin, trimethoprim-
sulfamethoxazole (Bactrim), or ciprofloxacin.
Vaccine Availability: None.
Clostridium botulinum
,Disease Caused: Botulism – characterized by descending flaccid paralysis.
Description: Anaerobic, Gram-positive, spore-forming bacillus that blocks
acetylcholine release at the neuromuscular junction.
Toxin: Botulinum neurotoxin – the most potent biological toxin known; as few as
1–5 spores can be lethal.
Types of Botulism:
Foodborne (contaminated or improperly preserved foods)
Wound botulism (commonly in injection drug users)
Infant botulism (due to intestinal colonization by spores)
Important Note: No honey should be given to infants under 12 months, as it can
cause infant botulism.
Symptoms:
Early (Cranial Nerves): Diplopia, ptosis, dysphagia, and dry mouth.
Progression: Gastrointestinal symptoms (6–36 hrs), neurological involvement (18–
36 hrs), followed by descending paralysis and respiratory failure (24–72 hrs).
Pathophysiology: Prevents acetylcholine release, leading to symmetrical decending
paralysis (contrast with Guillain-Barré Syndrome, which ascends).
Emergency Management:
Maintain airway.
Administer antitoxin immediately—do not delay for lab results.
Continuous ICU monitoring.
Antitoxin:
,Adults: Heptavalent Botulinum Antitoxin (HBAT).
Infants: Botulism Immune Globulin (BIG-IV).
Wound Botulism Management:
Surgical debridement.
Antitoxin administration before starting antibiotics.
Antibiotics (Penicillin G or Metronidazole) after antitoxin.
Note: Starting antibiotics before antitoxin can worsen symptoms by releasing more
toxin.
When to Avoid Antibiotics: In foodborne and infant botulism—they offer no
benefit and may worsen paralysis.
Mortality Rate: Less than 5% with prompt antitoxin and intensive care (historically
over 50%).
Campylobacter jejuni
Disease Caused: Gastroenteritis with potential post-infectious complications.
Description: Spiral-shaped, motile, Gram-negative bacterium; the leading bacterial
cause of diarrheal disease in the U.S. and responsible for millions of global cases
annually.
Symptoms:
Watery or bloody diarrhea
Severe abdominal cramps
Nausea and vomiting
Fecal urgency and tenesmus (painful sensation of needing to defecate).
, Haemophilus ducreyi
Disease Caused: Chancroid – a painful sexually transmitted genital ulcer.
Chlamydia trachomatis
Disease Caused: The most common bacterial sexually transmitted infection (STI)
worldwide.
What is the critical complication (40%) of Campylobacter jejuni that we are
usually most concerned about?
Guillain-Barre syndrome (GBS) due to molecular mimicry
What is the gold standard diagnosis method for Campylobacter?
Stool Culture on selective media
NAAT (PCR) panel is used as well
What is the cornerstone for campylobacter treatment?
REHYDRATION (& electrolytes)
C. jejuni is self-limited, so supportive care first!
In oral rehydration, what needs to be in the concentration?
Solution with sodium and glucose