Special Topics Vocabulary

Immune Disorders

• Acquired immunodeficiency syndrome (AIDS) is caused by the human immunodeficiency virus (HIV).

• HIV progressively destroys the immune system.

• HIV is found in blood and some body fluids and is transmitted through blood or body fluid transfer.

• HIV is a retrovirus: an RNA-based virus that converts into viral DNA within a host.

HIV Structure

• HIV contains:

  • Envelope

  • Lipid bilayer

  • Glycoproteins

  • Protein coat (capsid)

  • Reverse transcriptase

  • RNA (single-stranded)

• Size: 100-140 nm

HIV Progression and Treatment

• HIV itself does not directly cause death; it weakens the immune system, making the individual susceptible to other infections.

• Treatment options include:

  • Reverse transcriptase inhibitors: Block viral RNA conversion to DNA.

  • Protease inhibitors: Block the assembly of HIV protein capsids.

  • Integrase inhibitors: Prevent viral DNA from inserting into cellular DNA.

HIV Infection Phases

• Phase 1: Asymptomatic or chronic lymphadenopathy

  • About 2 months post-infection, the HIV population in the blood peaks at approximately 10 million per ml.

  • The CD4+ T cell population decreases during the acute phase but recovers as the immune response appears.

  • Seroconversion occurs, detectable antibodies against HIV appear, causing a rapid decline in the HIV population.

  • HIV in blood stabilizes at a steady rate of 1000 to 10,000 per ml.

• Phase 2: Symptomatic; early indications of immune failure.

  • CD4+ T cell population declines steadily.

  • Clinical latency or chronic HIV infection can last for 10 years or longer, during which HIV continues to multiply.

• Phase 3: Clinical AIDS

  • CD4+ T cell population drops to 200 cells/μl.

  • HIV levels in the blood rise as the immune system weakens.

Common Diseases Associated with AIDS

• Protozoa:

  • Cryptosporidium hominis: Persistent diarrhea

  • Toxoplasma gondii: Encephalitis

  • Isospora belli: Gastroenteritis

• Viruses:

  • Cytomegalovirus: Fever, encephalitis, blindness

  • Herpes simplex virus: Vesicles of skin and mucous membranes

  • Varicella-zoster virus: Shingles

• Bacteria:

  • Mycobacterium tuberculosis: Tuberculosis

  • M. avium-intracellulare: May infect many organs; gastroenteritis and other variable symptoms

• Fungi:

  • Pneumocystis jirovecii: Life-threatening pneumonia

  • Histoplasma capsulatum: Disseminated infection

  • Cryptococcus neoformans: Disseminated, especially meningitis

  • Candida albicans: Overgrowth on oral and vaginal mucous membranes (phase 2 stage of HIV infection); Overgrowth in esophagus, lungs (phase 3 stage of HIV infection)

• Cancers or precancerous conditions:

  • Kaposi's sarcoma: Cancer of skin and blood vessels (caused by human herpesvirus 8)

  • Hairy leukoplakia: Whitish patches on mucous membranes; precancerous

  • Cervical dysplasia: Abnormal cervical growth

Skin Disorders

• A skin lesion is a superficial growth of skin that does not match the surrounding skin.

  • Vesicle: Small fluid-filled lesion less than 1 cm in diameter.

  • Bulla: Fluid-filled lesion larger than 1 cm in diameter.

  • Macule: Flat, reddish lesion.

  • Papule: Elevated lesion.

  • Pustule: Papule containing pus.

Skin Infections

• Impetigo:

  • Highly contagious infection of the epidermis.

  • Causes pustules that rupture and form light-colored crusts.

  • Commonly caused by Staphylococcus aureus, less commonly by Streptococcus pyogenes.

  • Transmission: Direct physical contact, usually through breaks in the skin.

  • Treatment: Topical antibiotics; lesions often heal without treatment.

• Erysipelas:

  • Infection of the dermis by Streptococcus pyogenes.

  • Lesion: Reddish and hardened appearance with elevated edges.

  • Caused by beta-hemolytic exotoxins from S. pyogenes.

  • Symptoms: Fever and chills.

  • May progress to local tissue destruction and sepsis.

  • Treatment: Antibiotics, including penicillins.

• Necrotizing Fasciitis:

  • Advanced streptococcal infection resulting in inflammation of connective tissue, leading to necrosis.

  • Exotoxins may cause direct tissue damage or act as superantigens.

  • Another species contributing to cases is methicillin-resistant S. aureus.

  • Treatment: Broad-spectrum antibiotics, removal of necrotic tissue, and amputation.

• Ringworm:

  • Caused by a mycosis (fungal infection), not a parasitic worm.

  • Transmission: Fomites (clothes, utensils, furniture) and animal vectors.

  • Treatment: Azoles (miconazole and clotrimazole) and allylamines (terbinafine, naftifine, and butenavine).

  • These antifungal drugs can be toxic to humans as they target eukaryotes.

• Dermatomycosis (Tinea):

  • Mycosis (fungal infection) of the skin.

  • Ringworm is also known as tinea barbae; location of infection can change the name.

  • Ringworm of the foot is also known as athlete’s foot or tinea pedis.

Nervous System Infections

• Encephalitis: Infection of the brain itself.

• Meningitis: Infection of the meninges of the central nervous system.

  • Viral meningitis: Relatively mild, often caused by enteroviruses.

  • Bacterial meningitis: Often results in significant neurological damage.

  • Diagnosis: Spinal tap to obtain cerebrospinal fluid.

  • Treatment: Third-generation cephalosporins (class of antibiotics).

• Bacterial Meningitis Causes:

  • Haemophilus influenzae: Less prevalent since the introduction of an effective vaccine in 1988.

  • Neisseria meningitidis: Produces endotoxin rapidly, potentially leading to death in a few hours.

  • Streptococcus pneumoniae: Now the leading cause of bacterial meningitis.

  • Listeria monocytogenes: Can grow in refrigerated conditions.

• Leprosy:

  • Progressive disease that damages nervous tissue through a cell-mediated immune response.

  • Caused by Mycobacterium leprae and Mycobacterium lepromatosis.

  • Secondary infections can cause numbness and tissue loss.

  • M. leprae was one of the first bacteria identified as pathogenic for humans.

  • Treatment: Multidrug regimen including clofazimine, dapsone, and rifampicin.

Cardiovascular Infections

• Rheumatic Fever:

  • Streptococcal infections can lead to rheumatic fever, a cell-mediated attack against connective tissue in joints and the myocardium.

  • Symptoms: Migratory arthritis, inflammation of heart tissue, and formation of subcutaneous nodules (firm lumps under the skin).

  • Streptococcus species produce M protein, a virulence factor that induces the cell-mediated response.

  • Treatment: Anti-inflammatory drugs and low-dose antibiotics.

• Anthrax:

  • Caused by two A-B exotoxins released by Bacillus anthracis.

    • Edema toxin: Causes swelling and interferes with phagocytosis.

    • Lethal toxin: Targets and kills macrophages.

  • Infection occurs through direct contact, inhalation, or ingestion of anthrax endospores.

  • The capsule of B. anthracis is protein-based, allowing it to elude immune responses.

  • Anthrax is a zoonosis.

  • Direct contact:

    • Endospores enter through damaged skin.

    • Symptoms include low-level fever and distinctive black scab; sepsis is rare.

  • Ingestion:

    • Endospores cause lesions in the GI tract.

    • Symptoms include nausea, abdominal pain, and bloody diarrhea; sepsis is common.

  • Inhalation:

    • Endospores often enter the cardiovascular system; death through septic shock (without antibiotics) occurs in two to three days.

  • Treatment options:

    • Ciprofloxacin (a fluoroquinolone).

    • Doxycycline (a tetracycline).

    • Raxibacumab (a monoclonal antibody).

  • Vaccination:

    • Animals: Live attenuated (a weakened or attenuated/modified version) anthrax cultures.

    • Humans: Subunit vaccine based on the binding component (protective antigen) of edema toxin and lethal toxin.

• Plague (Black Death):

  • Caused by the bacterium Yersinia pestis.

  • Transmission: Arthropod vectors (fleas), but can spread via direct contact.

  • After entering the bloodstream, Y. pestis can survive in phagocytes after phagocytosis.

  • Septicemia may occur if the bacteria proliferate in the bloodstream.

  • Symptoms: Hemorrhage, fever, swelling of lymph nodes, and necrosis.

  • Mortality rate without treatment: Over 50%.

  • Pneumonic plague (infection spreads to the lungs):

    • Mortality rate is almost 100% without treatment.

  • Natural reservoirs: Rats, cats, squirrels, and prairie dogs.

  • The disease is zoonotic.

  • Treatment: Antibiotics and vaccines are readily available; drugs must be administered before the infection overwhelms the host.

• Lyme Disease:

  • Caused by the bacterium Borrelia burgdorferi, a spirochete.

  • Symptoms: Distinctive rash, heart disorders, arthritis, and neuropathy.

  • Diagnosis is difficult due to overlapping symptoms with other disorders and hard-to-interpret diagnostic tests.

  • Primary reservoirs: Field mice and deer.

  • Vector: Deer ticks.

  • Treatment: Antibiotics may be effective when administered early.

• Viral Hemorrhagic Fevers:

  • Caused by four families of viruses:

    • Arenaviridae: Lassa fever.

    • Bunyaviridae: Hantavirus (hemorrhagic fever with renal syndrome).

    • Filoviridae: Ebola and Marburg viruses.

    • Flaviviridae: Yellow fever, dengue, and West Nile viruses.

  • Symptoms: Fever, excessive bleeding (due to inability to clot), and shock.

  • Vaccines exist for yellow fever, Dengue fever, and Argentinean hemorrhagic fever (an arenavirus).

  • Ribavarin (antiviral drug, nucleoside agent) is effective against some strains of viral hemorrhagic fever, especially flaviviridae members.

  • Convalescent plasma (plasma from patients who have survived hemorrhagic fever) has seen some success.

  • Note: Ribavarin and convalescent plasma and interferon have not been certified by the FDA.