Lecture 8 Flashcards
Communicable disease
Disease transmitted from person to person
Endemic
Communicable diseases in which a small number of cases are continually present in the population
Epidemic
Communicable diseases concurrently affecting large numbers of people in a population (contained to a defined geographic area)
Pandemic
Global, world-wide outbreak across several countries or continents
Direct Transmission
Direct physical contact (sex) and Droplet spread (coughing, sneezing)
Indirect transmission through an intermediary mechanism
Contaminated food or water
Insects (vector)
Methods of Disease Control
Immunization (Active), Plasma containing antibodies/Maternal transmission (Passive), Identification, Isolation, treatment, controlling means of transmission (mask wearing), controlling indirect transmission for contaminated food or water
Isolation
Promptly carried out to shorten the time in which others may be infected, Isolation prevents contact with susceptible persons and stops spread
Food or water contamination control
Chlorination of water supplies, Effective sewage treatment facilities, Standards for handling, manufacturing, and distributing commercially prepared foods, Eradication and/or control of animal sources and vectors, Physical barriers - nets
Bubonic Plague
The black death has a 70% death rate without treatment, and 10% with treatment, one of the most deadly diseases, carried by rodents
STIs
Spread primarily by sexual contact (examples: Syphilis, Gonorrhea, Herpes, Chlamydia)
Primary Syphilis
Penetrates mucous membranes of the genital tract, oral cavity, rectal mucosa, or through the break in skin; multiplies rapidly throughout the body; forms a chancre (small ulcer) found on the penis, vulva, vagina, oral cavity, or rectum; occurs for 4-6 weeks and can heal without treatment
Secondary Syphilis
Systemic infection with skin rash and enlarged lymph nodes (develops after 4-10 wks typically lasts 2-3 years); begins after the chancre has healed and is accompanied with fever, lymphadenopathy, skin rash, shallow ulcers on mucous membranes of oral cavity and genital tract; can subside without treatment
Tertiary Syphilis
Late destructive lesions in internal organs (3-15y develops in 15-40% of cases); not generally communicable, Organisms remain active, causing irreparable organ damage due to chronic inflammation; Neuro and ocular syphilis are common in this stage
How to diagnose syphilis
Microscopic exam (Detection of Treponema from fluid squeezed from chancre) and Serologic tests (antigen–antibody reactions; Turns positive soon after chancre appears and remains positive for years)
Congenital Syphilis
Transmission from mother to child could cause the death of the fetus
Gonorrhea
Neisseria gonorrhoeae infection; Primarily infects mucosal surfaces: Urethra, genital tract, pharynx, rectum (symptoms appear about a week after exposure)
Gonorrhea in females
Infects mucosa of the uterine cervix and urethral mucosa; profuse vaginal discharge from cervical infection; can be asymptomatic; Infection may spread to fallopian tubes (Salpingitis)
How does gonorrhea manifest
Abdominal pain and tenderness, Fever, Leukocytosis
Gonorrhea in males
Acute inflammation of the mucosa of anterior urethra, Purulent urethral discharge, Pain on urination, Less likely to be asymptomatic in males than females
Extragenital gonorrhea
In the rectum; Pain and tenderness; purulent bloody mucoid discharge (anal sex) or Pharynx and tonsils (Oral-genital sex acts)
Disseminated gonococcal infection
Organisms gain access to the bloodstream and spread throughout body; Fever; joint pain; multiple small skin abscesses; infections of the joints, tendons, heart valves, meninges
Gonorrhea Diagnosis and treatment
Culture swab (Suspected sites: Urethra, cervix, rectum, pharynx, Blood in disseminated infections)
Nucleic acid amplification test: Based on the identification of nucleic acids in the organism
Treatment: Antibiotics - cefriaxone (some strains are penicillin resistant
Type 1 Herpes simplex virus infection
Infects oral mucous membrane and causes blisters; usually infected in childhood, most adults have antibodies to the virus; It may cause genital infections
Type 2 Herpes simplex virus infection
Infects genital tract and infections usually occur after puberty; Causes 80% of infections – a higher rate of recurrence, 20% of type 1 due to oral-genital sexual practices and may infect oropharyngeal mucous membranes
Herpes Manifestation
Vesicles (Small external painful blisters) and shallow ulcers following sexual exposure, Men (Glans or shaft of the penis), Women (Vulva - painful, Vagina or cervix - little discomfort)
Herpes diagnosis
Intranuclear inclusions in infected cells, Viral cultures from vesicles or ulcers most reliable diagnostic tests, and Serologic tests in some cases
Herpes Treatment
Antiviral drug shortens the course and reduces the severity, but does not eradicate the virus (orally, per IV, or topically), Cold compress and pain relievers, Deliveries should be done by cesarean section
Chlamydia trachomatis infection
Most common STD, 3 to 4 million cases per year
Chlamydia clinical manifestations
Similar to gonorrhea (infection can spread to fallopian tubes to have similar effects), many are asymptomatic
Chlamydia in Women
Cervicitis and urethritis, involving the uterine cervix, and urethra; moderate vaginal discharge (Major complications: sterility)
Chlamydia in Men
Nongonococcal urethritis, acute urethral inflammation with frequency and burning on urination (Major complications: epididymitis)
Chlamydia Diagnosis
Detection of chlamydial antigens in cervical or urethral secretions, Fluorescence microscopy
Cultures (swabs), Nucleic acid amplification tests: based on chlamydial nucleic acids
Chlamydia Treatment
Antibiotics (azithromycin/doxycycline)
Condylomata
Anal and genital warts - HPV
Trichomonal vaginitis
Trichomonas vaginalis infection (protozoan parasite)
Scabies and crabs
Microscopic mites
HIV Virus
Attacks the immune system, specifically destroying CD4 T cells, leads to the development of Acquired Immuno Deficiency Syndrome which increases susceptibility to pathogens and opportunistic infections.
Genetic material and Proteins in the HIV virus
9 kb Genome, ssRNA retrovirus (+ve), codes for 9 proteins, 2 structural proteins (Gag and Env), 1 enzymatic protein (Pol), 6 regulatory proteins (Tat, Rev, Nef, Vif, Vpr, and Vpu)
HIV Transmission
Sexual contact, Blood and body fluids (seminal, vaginal), Mother to infant (HIV primarily infects CD4 T-cells through interactions with CD4 receptors on the cell surface and GP120 spikes on virus
HIV Direct inoculation
Intimate sexual contact, linked to mucosal trauma from rectal intercourse
HIV Transfusion
Contaminated blood or blood products, lessened by routine testing of all blood products, Sharing of contaminated injection needles, Transplacental or postpartum transmission via cervical or blood contact at delivery and in breast milk
HIV steps of infection
- HIV cannot multiply alone. It must be inside a cell before it can make copies of itself.
- When HIV infects a cell, it hijacks its machinery.
- In the host cell, HIV makes copies of itself.
- These newly created virus particles can then go infect other cells.
HIV life cycle
Binds to CD4 and enters the cell, reverse transcriptase converts RNA into DNA (errors and mutations occur in this step), DNA is then transported into the nucleus, intergrase integrates the viral DNA into the host cell’s genome (can be inactive), once activated genes are transcribed and viral RNA is transported to the cytoplasm, proteins are translated and cleaved by a protease, virions are released at the membrane, T-cells are activated and support the infection
HIV replication and Genetic Variability
Fast replication and high mutation rate (1/cycle). This provides an adaptive advantage to HIV
What mutants are immune to infection with HIV
CCR5 (highly expressed in macrophages)
CD4 T-cells abnormalities
Depletion/cell death, reduced proliferation /regeneration, destruction by infection, indirect and direct destruction by viral proteins
HIV to AIDS
A healthy individual has between 800 and 1500 CD4T cells in 1 µL of blood. Immune deficits start to emerge below 500 (HIV/other autoimmune diseases), Once this number drops below 200, the individual is described as having AIDS.
Cytopathic effects of HIV
Cell-cell fusion, accumulation of unintegrated viral DNA, alteration of cell permeability lipids, apoptosis, the release of toxic cytokines by infected cells, destruction of immune responses, inhibition of growth factors, degradation of RNA which reduces protein synthesis
CD8 T-cells are destroyers using…)
Cell-to-cell contact and secreted factors destroy infected cells (Perforin/Granzyme A, B) and inhibit virus production/promote immune activation (IFNy, TNFa, IL-2, MIP1a/b, RANTES)
What is CTL dysfunction caused by
Cytokine/ receptor dysregulation, Direct effect of HIV soluble factors, Cell death/ apoptosis, Other immune cell dysfunction, Anergy
What is Anti-HIV CTL (CD8) activity associated with
LTNP/Elite controllers (some control of the HIV infection and slower disease progression)
Early vs. Late Manifestations of HIV infection
Early (Asymptomatic, mild febrile illness) and Late (Generalized lymph node enlargement, nonspecific symptoms, fever, weakness, chronic fatigue, weight loss, thrombocytopenia, AIDS)
Antibody response to HIV
Antibodies are formed within 1 to 6 months, Detection of antibodies provides evidence of HIV infection, Antibodies do not eradicate virus, Virus is detectable by laboratory tests (viral RNA)
Signs and Symptoms of AIDS
An infected person usually experiences a mononucleosis-like syndrome that may be attributed to the flu or another virus (may be asymptomatic for years)
Non-specific symptoms
Weight loss, fatigue, night sweats, and fever
Viral replication
Measure the amount of viral RNA in the blood (Virus replicates in lymph nodes, but the amount of viral RNA in blood reflects extent of viral replication in lymphoid tissue)
Treatment for HIV and AIDS
No cure for AIDS, antiretroviral agents inhibit HIV viral replication
HIV Treatment groups
Nonnucleoside reverse transcriptase inhibitors, Nucleoside reverse transcriptase inhibitors (nucleoside analogs), Protease inhibitors, Integrase inhibitors
Protease Inhibitors
Block the action of viral protease in viral replication; cut viral protein into short segments to assemble around viral RNA to form infectious particles
PrEP
HIV prevention treatment
