Pathogens and Bacterial Diseases Lecture Notes

Borrelia burgdorferi and Lyme Disease

Microbial Characteristics * Borrelia burgdorferi is a spirochete characterized by having internal flagella. * It is the causative agent of Lyme disease.
Vectors and Transmission * Northeast United States: Transmitted to humans by Ixodes scapularis, commonly known as the deer tick. * Pacific Coast: Transmitted to humans by Ixodes pacificus, known as the dusky footed woodrat tick. * Transmission occurs through the bite of the tick.
Clinical Presentation and Symptoms * Primary Stage ( $7$ to $10$ days after the bite): * Development of a "bull's eye" rash, medically termed erythema migrans, at the site of the bite. * Flu-like symptoms including malaise, fatigue, headache, fever, and chills. * Secondary Stage (Weeks or months after untreated infection): * Neurological abnormalities. * Inflammation of the heart. * Arthritis. * Tertiary Stage (Years after untreated infection): * Demyelination of neurons. * Significant behavioral changes.
Diagnosis and Laboratory Identification * Demonstration of spirochetes in the blood using dark-field microscopy. * Polymerase Chain Reaction (PCR) to identify microbial DNA within urine samples. * Serological testing using ELISA or Western Blot to detect IgM or IgG antibodies against the microbe.
Treatment and Clinical Management * Early Illness: Administration of amoxicillin or tetracycline. * Neurologic and Arthritic Disorders: Administration of ceftriaxone.
Prevention and Vector Control * Control of the vector through habitat destruction and application of insecticides. * Use of tick repellents containing DEET. * Prompt inspection of the skin and removal of ticks. Infection typically requires the tick to be attached for at least $24$ to $36$ hours.
Tick Removal Procedure * Use tweezers to grasp the tick near the mouth parts, as close to the skin as possible. * Pull the tick in a steady, upward motion away from the skin. * Prohibited Methods: Do not use kerosene, matches, or petroleum jelly to remove the tick. * After removal, disinfect the site with soap and water, rubbing alcohol, or hydrogen peroxide. * Record the date and location of the bite for medical tracking.

Helicobacter pylori and Gastric Disease

Microbial Characteristics * Helicobacter pylori is a Gram-negative, nonsporulating, microaerophilic, spiral bacillus. * It selectively colonizes gastric mucus-secreting cells.
Pathophysiology and Disease Association * It is the leading factor in Peptic Ulcer Disease, found in $95\%$ of patients. * It causes chronic gastritis, which serves as a risk factor for the development of gastric carcinoma. * Urease Production: The bacterium produces urease, which allows for urea hydrolysis. This process releases ammonia ( $NH_3$ ), creating a localized alkaline environment to survive gastric acidity.
Transmission * Transmission is likely person-to-person, noted by clusters of infection within families or nursing homes.
Laboratory Identification * Culture of gastric biopsy material. * Detection of serum IgG using tests such as Pyloriset EIA-G. * Detection of urease activity within cultures. * Urea breath test.
Treatment Regimens * Regimen 1: Bismuth subsalicylate (Pepto-Bismol), metronidazole, and either tetracycline or amoxicillin. * Regimen 2: Clarithromycin (Biaxin), ranitidine, and bismuth citrate. * Regimen 3: Clarithromycin, amoxicillin, and lansoprazole (Prevacid).
Historical Significance * The $2005$ Nobel Prize in Physiology or Medicine was awarded to Barry J. Marshall and J. Robin Warren for discovering Helicobacter pylori and its role in gastritis and peptic ulcer disease.

Clostridium perfringens and Gas Gangrene

Microbial Characteristics * Clostridium perfringens is a Gram-positive, anaerobic, spore-forming rod. * Naturally occurs in soil and as part of the normal microflora of the human large intestine.
Etiology of Gas Gangrene * Occurs when wounds—resulting from abortions, automobile accidents, military combat, or frostbite—come into contact with spores in the soil. * Pathogenesis: Bacteria grow within the wound and secrete $\alpha$ -toxin. This leads to gas accumulation and the breakdown of muscle tissue.
Clinical Symptoms * Severe localized pain. * Edema and drainage from the wound. * Muscle necrosis caused specifically by the $\alpha$ -toxin.
Diagnosis and Treatment * Diagnosis: Based on clinical symptoms and the recovery of Clostridia from the wound site. * Treatment Measures: * Extensive surgical debridement of infected tissue. * Administration of polyvalent antitoxin. * Antibiotic therapy using penicillin and tetracycline. * Hyperbaric oxygen therapy. * Amputation of a limb is often necessary to stop the spread of the disease.
Prevention * Thorough debridement of contaminated wounds. * Antibiotic prophylaxis. * Prompt medical treatment of all wound infections.

Mycobacterium leprae and Leprosy

Epidemiology and Reservoirs * Causes leprosy, also known as Hansen’s disease. * Reservoirs: Humans are the proven reservoir. The nine-banded armadillo is an animal reservoir, though it does not transmit the disease to humans. * Prevalence: Most common in tropical countries ( $14$ million cases globally); approximately $4,000$ cases exist in the United States.
Transmission * Occurs in children exposed for prolonged periods to infected individuals shedding bacteria. * In family settings, nasal secretions are considered the primary infectious material. * Chemoprophylactic drugs are recommended for family members of infected individuals.
Multi-Drug Therapy (MDT) Regimens * Treatment is administered via blister packs designed for $4$ -week intervals. * PB (Paucibacillary) Adult Treatment: * Day 1 (Once a month): $2$ capsules of rifampicin ( $300\,mg \times 2$ ) and $1$ tablet of dapsone ( $100\,mg$ ). * Days 2-28 (Once a day): $1$ tablet of dapsone ( $100\,mg$ ). * Duration: Full course requires $6$ blister packs. * MB (Multibacillary) Adult Treatment: * Day 1 (Once a month): $2$ capsules of rifampicin ( $300\,mg \times 2$ ), $3$ capsules of clofazimine ( $100\,mg \times 3$ ), and $1$ tablet of dapsone ( $100\,mg$ ). * Days 2-28 (Once a day): $1$ capsule of clofazimine ( $50\,mg$ ) and $1$ tablet of dapsone ( $100\,mg$ ). * Duration: Full course requires $12$ blister packs. * PB Child Treatment ( $10$ - $14$ years): * Day 1 (Once a month): $2$ capsules of rifampicin ( $300\,mg + 150\,mg$ ) and $1$ tablet of dapsone ( $50\,mg$ ). * Days 2-28 (Once a day): $1$ tablet of dapsone ( $50\,mg$ ). * Duration: Full course requires $6$ blister packs. * MB Child Treatment ( $10$ - $14$ years): * Day 1 (Once a month): $2$ capsules of rifampicin ( $300\,mg + 150\,mg$ ), $3$ capsules of clofazimine ( $50\,mg \times 3$ ), and $1$ tablet of dapsone ( $50\,mg$ ). * Days 2-28 (Once a day): $1$ capsule of clofazimine every other day ( $50\,mg$ ) and $1$ tablet of dapsone ( $50\,mg$ ). * Duration: Full course requires $12$ blister packs. * Note for Children: For patients younger than $10$ , doses must be adjusted based on body weight.