Diseases :P Flashcards
The Berlin patient
-first person cured of HIV (stem cell transplants)
-London patient, city of hope, and New York patient followed
stem cell transplants
-aka bone marrow transplant
-high risk
-used to treat blood cancer, received HIV-resistant mutation from donors
-deletes protein virus uses to enter blood
cells
1920 (HIV)
-Democratic Republic of Congo
-HIV cross species from chimps to humans
HIV-1
-primary HIV
-worldwide
-99% cases genetically related to Simian Immunodeficiency Virus (SIV) carried by chimps
HIV-2
-weakly contagious
-not often found outside Africa
-closely related to SIV (SIVcpz infects chimps)
-only 1% of people with HIV in the US have this type
HIV origin
-In chimps in Central Africa may have crossed to humans in the 1800s
-SIV is chimp version of HIV
-crossover when hunted chimps and contact infected blood
-HIV spread over Africa and then to other parts of the world
-in US since mid/late 1970s
HIV classification and virus description
-family: Retroviridae
-genus: Lentivirus
-enveloped with ssRNA
HIV virions have
-2 identical ssRNA
-reverse transcriptase, integrase, protease, and an envelope
-envelope spikes termed gp120 (combine with CD4 receptor on T helper cells, target of HIV)
reverse transcriptase
-enzyme
-RNA template to synthesize DNA
-high error rate
HIV resistance
-resistance to HIV-1 is rare
-“exposed-uninfected”: despite repeated exposure may still be uninfected
-long-term non-progressors: infected but disease doesn’t/slowly progresses
HIV resistance theory
-host traits preventing HIV-1 entry into cells reduce chance of infection/slow or eliminate the development if infection occurs
HIV stages
-1: acute HIV infection
-2: chronic HIV infection
-3: acquired immunodeficiency syndrome (AIDS)
HIV stage 1 (acute HIV infection)
-large amount HIV in blood
-very contagious
-flu-like symptoms
HIV stage 2 (chronic HIV infection)
-aka asymptomatic HIV infection/clinical latency
-HIV still active and reproducing in body
-may not have symptoms or get sick but can still transmit
-if HIV in blood increases, can move to stage 3
-without treatment can last a decade or progress even faster
HIV stage 3 (AIDS)
-may never reach this stage with proper HIV treatment
-high viral load, easily transmit to others
-damaged immune system, prone to opportunistic infections or serious illnesses
-without treatment only survive 3 years
HIV symptoms
-flu-like 2-4 weeks after infection
-symptoms last for a few days or weeks
-can be asymptomatic
-fever, sore throat, night sweats, mouth ulcers, chills, rash, swollen lymph nodes, muscle aches, fatigue
HIV early symptomatic stage other possible infections
-decrease in CD4+ T cells
-unusual infections, high fever, diarrhea more than a month, some cancers, peripheral neuropathy
-susceptible to secondary infections: thrush (oral candidiasis), persistent vaginal candidiasis, listeriosis, shingles
HIV AIDS other possible infections
-opportunistic infection: pneumocystis jirovecii or candidiasis of esophagus, trachea, bronchi, lungs
-unusual cancers: Kaposi’s sarcoma
HIV targets
-CD4+ T cells and replicates rapidly
-viral load: concentration of virus in the blood
HIV clinical progression four stages
-primary (including seroconversion)
-clinical latency (slow steady loss of T cells)
-early symptomatic disease
-AIDS (acquired immunodeficiency syndrome)
HIV transmission
-incubation period: 9 months to 20+ years (average 12 years)
-through sexual contact (vaginally, orally, anally) or direct contact with body fluids (blood transfusion or sharing drug needles)
HIV tests
-antibody test
-antigen/antibody test
-nucleic acid test (NAT)
HIV antibody test
-tests for antibodies to HIV in blood or oral fluid
-only HIV self-test approved by FDA
HIV antibody/antigen test
-looks for HIV antibodies and antigens
-recommended for testing in lab
-uses blood from finger
HIV nucleic acid test (NAT)
-look for actual virus in blood
-detect HIV sooner than other tests
-for those with recent exposure and early symptoms of HIV but test negative with other 2 tests
HIV treatment
-antiretroviral drugs
-target important points in replication cycle
HIV treatment
-antiretroviral drugs
-target important points in replication cycle
HIV most common in
men (80%)
HIV decrease
-17% from 2019 to 2020
-due to disruption in care services,hesitancy to go to care services and shortages in materials for testing due to COVID
HIV and reemerging diseases
-global spread of HIV/AIDS has increased number of immunocompromised persons -> reemergence of infectious disease once “under control”
-AIDS patients highly susceptible to many organisms (mycobacterium tuberculosis included)
microbiome risks
-microbiota may escape from niche and cause disease
-opportunistic pathogens among microbiota cause disease in immunocompromised hosts
s agalactiae (streptococcus)
-vaginal flora
-infections: septicemia, meningitis, pneumonia, osteomyelitis
-common population: newborns (especially vaginal birth)
s pneumoniae (streptococcus)
-upper respiratory tract
-infections: meningitis, otitis media, pneumonia, sepsis
-common population: children, elderly, immunocompromised, asplenic
s pyogenes (streptococcus)
-skin, throat
-infections: pyogenic infections, toxin-mediated infections, autoimmune sequelae, necrotizing fasclitis
-common population: children
viridans group streptococci
-oral cavity
-infections: s mutans and s mitis: dental caries, subacute bacterial endocarditis, s sanguinis: subacute endocarditis on damaged heart valves
-common population: damaged heart valve patients
first infections of streptococcus
-described by Hippocrates
-description by Theodor Billroth, associated with wound infections and erysipelas (more surface layers of skin)
streptococcus epidemiology
-carrier state: nasopharynx
-s. pyogenes or s. agalactiae: 5-15%
-s. pneumoniae: 20-40%
s. pyogenes respiratory disease peak
-6 years old and 13 years old
-most common late winter and early spring
streptococcus infectious agent description
-streptococcus spp.
-non motile
-gram +
-chains/pairs
Streptococcus has
-varied pathogenic potential
-may infect respiratory or skin
streptococcus transmission
-s pyogenes: respiratory droplets, contact with fomites
-skin infections may have irritation
-may be traced to rectal carriers, food borne
lipoteichoic acid (streptococcus)
-cell wall component
-facilitates adherence to host
streptolysins
lyse blood cells
streptococcal enzymes that degrade
-DNA (DNAses)
-fibrin (streptokinase)
-connective tissue (hyaluronidase)
m protein streptococcus
-antiphagocytic function
-critical to survival in human tissues and fluids
SPEs (streptococcal pyogenic exotoxins)
-formerly erythrogenic toxins
-scarlet fever, streptococcal toxic shock syndrome, and necrotizing fasciitis
s sequelae (streptococcus)
-pathological conditions result after a primary disease has run its course
-antibodies cross-react with host cells in autoimmune reaction -> serious sequelae
s pyogenes cytoplasmic membrane
-antigens similar to human cardiac, skeletal, and smooth muscle, heart valve fibroblasts, neuronal tissues -> molecular mimicry
post streptococcal sequelae
-acute rheumatic fever (ARF)
-young kids (4-9)
-high fever
-damage to heart, joints, skin, nervous system
-cross reactive antibodies
-glomerulonephritis (kidney disease)
streptococcal pharyngitis
-strep throat
-contagious spread through: person to person contact, indirect contact with contaminated items
-symptoms: sudden fever and sore throat, tender lymph nodes, exudate on tonsils, no cough
-treatment: antibiotics
scarlet fever
-SPEs cause
-rash and fever starting on head and neck, spread to trunk and then limbs
-may also have bumpy red tongue (strawberry tongue)
erysipelas (streptococcus skin infection)
-s pyogenes
-acute infection: small erythematous patch becomes fiery-red shiny plaque (upper layer dermis but spreads to superficial lymphatics), swollen lymph nodes, fever, systemic symptoms
-rash: most commonly on lower body, covers face and bridge of nose, butterfly appearance
cellulitis (streptococcal skin infection)
-non-necrotizing inflammation of dermis, related to acute infection
-localized pain, swelling, tenderness, erythema, warmth
-develops slow and moves deeper into dermis (including subcutaneous fat and connective tissue)
-often a complication of a wound infection
-commonly from s pyogenes but can be other
-deeper than erysipelas
cellulitis diagnosis
-base on symptoms
-remove aspirates from advancing edge of cellulitis
-site of trauma
-skin biopsies
-blood
impetigo (streptococcus skin infection)
-highly contagious
-can be from s pyogenes or staphylococcus aureus
necrotizing fasciitis (streptococcus skin infection)
-flesh eating
-polymicrobial
-usually s pyogenes and sometimes s aureus
-fatal
-therapy antibiotics
streptococcus spp. diagnosis
-serology: detection of antibodies (antibodies against streptococcal m protein, ELISA, fluorescent antibody, direct bacterial agglutination)
-bacterial culturing
-throat or skin cultures
ARF long term complications
-2 weeks after infection
-most common in 5-15 year olds
-can cause valvulitis of mitral and aortic valve leading to valvular regurgitation and heart murmur
ARF diagnosis JONES criteria
-joints (migratory polyarthritis)
-O (carditis)
-nodules on extensor surfaces
-erythema marginatum rash
-sydenham chorea (neurological symptoms)
rheumatic heart disease (RHD) (streptococcus long term complication)
-long term sequelae
-single or repeat acute RF episodes, cumulative damage to heart valves
-symptoms: ARF symptoms and chest pain, swelling, short breath
-develops 4-8 weeks after first ARF episode in 3-19 year olds
-peak prevalence in third and fourth decades of life
-autoimmune reaction triggered by untreated s pyogenes throat infection -> severe valvular damage in genetically susceptible individuals
pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) (streptococcus long term complication)
-symptoms: OCD, motor or vocal tic disorder, moodiness, irritability, anxiety attacks and separation anxiety
-symptoms appear or worsen following strep
-first appear age 3 to puberty
-treatment: treat strep infection and if still present use antibiotics
-may benefit from standard medications (therapists)
streptococcus prevention
-vaccines: PCV13 (pneumococcal conjugate) and PPSV23 (pneumococcal polysaccharide vaccine
pharyngitis (superficial)
-sore throat
-malaise
-fever
scarlet fever (superficial)
-deep red rash
-strawberry tongue
-exudative pharyngitis
impetigo (superficial)
-skin pustules mature into honey colored scabs
acute rheumatic fever (sequelae)
-polyarthritis, carditis, rapid and jerky movements, rash, subcutaneous nodules
rheumatic heart disease (sequelae)
mitral and or aortic regurgitation with possible stenosis over time
acute poststreptococcal glomerulonephritis (sequelae)
edema, hypertensions, urinary sediment abnormalities, complement deficiency
bacteremia (invasive)
high fever, nausea, vomiting
puerperal sepsis (invasive)
fever, chills, abdominal pain in pregnant women
cellulitis (invasive)
acute, tender, erythematous, swollen area of skin
necrotizing fasciitis (invasive)
fever, exquisitely tender skin lesions, vomiting, diarrhea, toxemia, tissue destruction
streptococcal toxic shock syndrome
high fever, rapid onset hypotension, accelerated multisystem failure
who can get gonorrhea
anyone sexually active
gonorrhea drug resistance
develops resistance to antibiotics
gonorrhea infectious agent
-nisesseria gonorrhoeae
gonorrhea bacteria infects
-mucous membranes in genitals, rectum. throat, and eyes
nisesseria gonorrhoeae description
-gram -
-diplococcus
-colonizes mucosal areas
pili fimbriae, and opa proteins
facilitate adhesion of gonococcus to epithelial cells
lipoligosaccharide (LOS) in gonorrhea
-lipopolusaccharide endotoxin
-part of outer membrane structure
-enhance pathogenicity
antigenic variation of surface proteins
-help avoid immune detection
-antigenic variation of type IV pili to avoid immune defense
gonorrhea commonality
-second most commonly reported disease in the US
gonorrhea virulence factors
-pilus (contribute to antigenic diversity)
-por proteins
-opa proteins
-LOS
-rmp proteins
-igA protease
-capsule
por proteins (gonorrhea)
-form pores through outer membrane
-antigenic
-specific serotypes associated with virulence
rmp proteins (gonorrhea)
inhibit cidal activity of serum
IgA protease (gonorrhea)
-core has enzyme, released by cell to destroy IgA1
capsule
-resist phagocytosis unless antibody is present
gonorrhea peak age and infection window
-15-24 year olds
-2-7 days after infection (can take 30 days)
men and gonorrhea
85-90% have symptoms:
-painful pee
-yellow/white discharge from penis
-swelling of testes and penis
women and gonorrhea
80% do not have symptoms:
-painful burning pee
-yellow/white or bloody discharge (1-3 weeks after infection)
-can infect fallopian tubes and tissue
-cause sterility and ectopic pregnancies
gonorrhea untreated in women
-pelvic inflammatory disease (PID)
-scar tissue blocks fallopian tubes
-ectopic pregnancy (outside womb)
-infertility
-long term pelvic ab pain
gonorrhea untreated in men
-rare but infertility (painful condition in tubes attached to testes)
rare but if gonorrhea is left untreated
-can spread to blood or joints (life threatening)
-can increase chances of getting/giving HIV
ophthalmia neonatorum
-conjunctivitis of newborn
-newborn eyes infected as pass through infected birth canal
-prevent with antimicrobial eyedrops
gonorrhea diagnosis
-culture and gram stain/cell and colony morphology: need co2, survives poorly outside the body, special transport media to keep it viable (still short term)
-nucleic acid amplification
-serological test
gonorrhea treatment
-ceftriaxone injection
-tell partners so they can get treated
gonorrhea highest during
1981, 20-24 years old
gonorrhea prevention
-avoid sexual contact with infected
-long-term monogamous relationship with a tested uninfected partner
-condoms
-currently no vaccine and treatments are becoming less effective
