Study Notes on Microbial Diseases of the Cardiovascular and Lymphatic Systems
MICROBIAL DISEASES OF THE CARDIOVASCULAR AND LYMPHATIC SYSTEMS
Overview of Blood and Lymphatic Systems
Human Microbiome Project Findings
Recent data suggests that blood is not sterile.
The blood can tolerate or resist moderate numbers of pathogens without harm.
Blood is low in iron; bacterial growth requires iron.
Hemolysis liberates iron, increasing pathogen growth.
Defensive Mechanisms
Blood contains numerous defensive phagocytic cells.
Lymph vessels are very permeable, picking up microbes and their products and returning them to the blood.
In hospitals, invasive procedures (needles, catheters, tubes) can lead to frequent contamination.
Bacteremia, Septicemia, and Toxemia
Definitions
Bacteremia: Presence of bacteria within the bloodstream; a transient condition.
Can be introduced by flossing, catheter insertion, injection, etc.
Generally clears within days and is not considered a blood infection.
Septicemia (Sepsis): Uncontrolled proliferation of bacteria in the bloodstream.
Can be fatal.
Toxemia: Presence of toxins in blood, for example, tetanospasmin.
May arise from a focal infection of bacteria, spreading toxins through blood or lymph.
Signs and Symptoms of Sepsis
General Response
The inflammatory response to infectious agents in the blood typically results in the release of cytokines, leading to:
Fever, chills.
Vessels leaking fluid, resulting in decreased blood pressure (BP).
Increased heart rate (HR) and respiratory rates.
Severe Sepsis: Sepsis resulting in a drop in BP and dysfunction of at least one organ.
Septic Shock: Blood infection resulting in pathological low blood pressure, decreased blood flow to organs, leading to coma or death.
Lymphangitis: Inflammation of lymph vessels, often visible as red streaks under the skin running from the site of infection to the lymph node, where it often stops. Tender to touch.
Anthrax
Etiology: Caused by Bacillus anthracis, a Gram-positive, aerobic, endospore-forming bacterium.
Infects primarily grazing animals; humans can be infected through animal products.
Transmission: Endospores ingested with grass cause fatal animal sepsis.
Types of Anthrax:
Cutaneous Anthrax:
Accounts for 90% of cases; mortality rate of 10-20% if untreated.
Pathogenesis: Endospores enter through cuts, leading to exotoxin damage and ulceration.
Symptoms include a painless black eschar, low-grade fever, malaise.
Risk of developing septic shock if bacteria enter the blood from eschar area.
Inhalational Anthrax:
Can lead to severe illness or death within one day.
Symptoms initially may appear as mild pneumonia; untreated can lead to high fever, hemorrhagic lung complications, septicemia, and death within 1-3 days.
Identification (ID50): 2-9 spores.
Gastrointestinal and CNS Anthrax: Less common.
Virulence Factors:
Exotoxin (A-B type toxins) comprising edema toxin (causes local edema) and lethal toxin (kills host cells and impairs immune response).
Capsule made of amino acids that evade immune recognition.
Gangrene
Definition: Condition caused by loss of blood supply to a tissue, resulting in localized soft tissue necrosis.
Types of Gangrene:
Dry Gangrene: Caused by insufficient blood flow (e.g., atherosclerosis).
Symptoms: Tissue drying up, shriveling, blackening.
Wet Gangrene: Results from insufficient blood flow combined with bacterial infection (e.g., burns, frostbite).
Symptoms: Tissue appearing bruised, swollen, and decomposing.
Gas Gangrene: Caused by Clostridium perfringens
Combination of ischemia and anaerobic bacterial infection leading to extensive tissue damage and gas formation.
Symptoms include swelling, discoloration, severe pain, and the presence of gas-filled vesicles.
Treatment includes debridement, antibiotics, and in severe cases, amputation.
Plague
Overview
Etiology: Caused by Yersinia pestis, a Gram-negative rod.
Reservoirs and Vectors:
Commonly endemic in wild rodents (rats, squirrels).
Transmitted primarily by fleas (e.g., Xenopsylla cheopis).
Transmission:
Zoonotic transmission through flea bites, contact with infected fluids, and respiratory droplets from infected hosts.
Forms of Plague
Bubonic Plague:
Initial infection from flea to lymph nodes leading to buboes (painful, swollen lymph nodes).
Symptoms: High fever, buboes, and possible necrosis.
Septicemic Plague:
Occurs if bubonic plague is untreated, leading to bacteria in the blood, resulting in shock.
Symptoms include black spots on the skin, high fever, and shock.
Pneumonic Plague:
Develops from the septicemic form or direct airborne transmission.
Highly contagious with symptoms appearing 2 days post-inhalation; high mortality rate without treatment.
Control: Rapid recognition and treatment are crucial; vaccine development ongoing.
Lyme Disease
Etiology: Caused by Borrelia burgdorferi, a spirochete.
Vector: Transmitted primarily through the bite of black-legged ticks (Ixodes scapularis).
Transmission: Requires tick attachment for 24-48 hours before bacteria transfer occurs, making only 1% of bites lead to infection.
Symptoms:
Phase 1: Bull’s-eye rash at the bite site, flu-like symptoms.
Phase 2: Dissemination causing chronic complications like arthritis, cardiac irregularities, neurological issues.
Phase 3: Possible long-term neurological manifestations unrelated to persistent infection.
Prevalence: Approximately 30,000 cases annually in the U.S.
Filariasis and Elephantiasis
Etiology: Caused by Wuchereria bancrofti, a nematode.
Vector: Transmitted via mosquitoes, primarily in Africa and Asia.
Pathogenesis: Nematode larvae injected into the lymphatic system, leading to blockage and resulting in gross limb or scrotal swelling.
Septicemic Meningococcemia
Etiology: Caused by Neisseria meningitidis, which can lead to meningitis or septicemia.
Pathogenesis: Release of endotoxins promotes a severe inflammatory response, leading to vascular collapse and septic shock.
Symptoms: Sudden onset of high fever, petechial rash, rapid progression to shock and potential gangrene.
Ebola Virus Disease
Etiology: Caused by the Ebola virus, with zoonotic transmission from various animal reservoirs.
Transmission: Direct contact with infected blood or body fluids; not airborne.
Symptoms and Pathogenesis:
Incubation period of 3-21 days, initially presenting as severe weakness, fever, and digestive tract symptoms.
Hemorrhaging may occur, with the potential for multi-organ failure and shock.
Endotoxin Effects in Gram-Negative Sepsis
Mechanism: Gram-negative bacterial cell walls release the endotoxin Lipid A, triggering the immune response.
Cytokine Release: Endotoxin stimulates macrophages to release cytokines like TNF and IL-1, leading to vascular damage and septic shock.
Conclusion
Understanding these various microbial diseases affecting the cardiovascular and lymphatic systems is crucial for effective prevention, diagnosis, and treatment.