Diseases :P Flashcards

1
Q

The Berlin patient

A

-first person cured of HIV (stem cell transplants)
-London patient, city of hope, and New York patient followed

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2
Q

stem cell transplants

A

-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

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3
Q

1920 (HIV)

A

-Democratic Republic of Congo
-HIV cross species from chimps to humans

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4
Q

HIV-1

A

-primary HIV
-worldwide
-99% cases genetically related to Simian Immunodeficiency Virus (SIV) carried by chimps

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5
Q

HIV-2

A

-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

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6
Q

HIV origin

A

-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

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7
Q

HIV classification and virus description

A

-family: Retroviridae
-genus: Lentivirus
-enveloped with ssRNA

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8
Q

HIV virions have

A

-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)

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9
Q

reverse transcriptase

A

-enzyme
-RNA template to synthesize DNA
-high error rate

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10
Q

HIV resistance

A

-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

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11
Q

HIV resistance theory

A

-host traits preventing HIV-1 entry into cells reduce chance of infection/slow or eliminate the development if infection occurs

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12
Q

HIV stages

A

-1: acute HIV infection
-2: chronic HIV infection
-3: acquired immunodeficiency syndrome (AIDS)

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13
Q

HIV stage 1 (acute HIV infection)

A

-large amount HIV in blood
-very contagious
-flu-like symptoms

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14
Q

HIV stage 2 (chronic HIV infection)

A

-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

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15
Q

HIV stage 3 (AIDS)

A

-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

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16
Q

HIV symptoms

A

-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

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17
Q

HIV early symptomatic stage other possible infections

A

-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

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18
Q

HIV AIDS other possible infections

A

-opportunistic infection: pneumocystis jirovecii or candidiasis of esophagus, trachea, bronchi, lungs
-unusual cancers: Kaposi’s sarcoma

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19
Q

HIV targets

A

-CD4+ T cells and replicates rapidly
-viral load: concentration of virus in the blood

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20
Q

HIV clinical progression four stages

A

-primary (including seroconversion)
-clinical latency (slow steady loss of T cells)
-early symptomatic disease
-AIDS (acquired immunodeficiency syndrome)

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21
Q

HIV transmission

A

-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)

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22
Q

HIV tests

A

-antibody test
-antigen/antibody test
-nucleic acid test (NAT)

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23
Q

HIV antibody test

A

-tests for antibodies to HIV in blood or oral fluid
-only HIV self-test approved by FDA

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24
Q

HIV antibody/antigen test

A

-looks for HIV antibodies and antigens
-recommended for testing in lab
-uses blood from finger

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25
Q

HIV nucleic acid test (NAT)

A

-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

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26
Q

HIV treatment

A

-antiretroviral drugs
-target important points in replication cycle

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26
Q

HIV treatment

A

-antiretroviral drugs
-target important points in replication cycle

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27
Q

HIV most common in

A

men (80%)

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28
Q

HIV decrease

A

-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

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29
Q

HIV and reemerging diseases

A

-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)

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30
Q

microbiome risks

A

-microbiota may escape from niche and cause disease
-opportunistic pathogens among microbiota cause disease in immunocompromised hosts

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31
Q

s agalactiae (streptococcus)

A

-vaginal flora
-infections: septicemia, meningitis, pneumonia, osteomyelitis
-common population: newborns (especially vaginal birth)

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32
Q

s pneumoniae (streptococcus)

A

-upper respiratory tract
-infections: meningitis, otitis media, pneumonia, sepsis
-common population: children, elderly, immunocompromised, asplenic

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33
Q

s pyogenes (streptococcus)

A

-skin, throat
-infections: pyogenic infections, toxin-mediated infections, autoimmune sequelae, necrotizing fasclitis
-common population: children

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34
Q

viridans group streptococci

A

-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

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35
Q

first infections of streptococcus

A

-described by Hippocrates
-description by Theodor Billroth, associated with wound infections and erysipelas (more surface layers of skin)

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36
Q

streptococcus epidemiology

A

-carrier state: nasopharynx
-s. pyogenes or s. agalactiae: 5-15%
-s. pneumoniae: 20-40%

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37
Q

s. pyogenes respiratory disease peak

A

-6 years old and 13 years old
-most common late winter and early spring

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38
Q

streptococcus infectious agent description

A

-streptococcus spp.
-non motile
-gram +
-chains/pairs

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39
Q

Streptococcus has

A

-varied pathogenic potential
-may infect respiratory or skin

40
Q

streptococcus transmission

A

-s pyogenes: respiratory droplets, contact with fomites
-skin infections may have irritation
-may be traced to rectal carriers, food borne

41
Q

lipoteichoic acid (streptococcus)

A

-cell wall component
-facilitates adherence to host

42
Q

streptolysins

A

lyse blood cells

43
Q

streptococcal enzymes that degrade

A

-DNA (DNAses)
-fibrin (streptokinase)
-connective tissue (hyaluronidase)

44
Q

m protein streptococcus

A

-antiphagocytic function
-critical to survival in human tissues and fluids

45
Q

SPEs (streptococcal pyogenic exotoxins)

A

-formerly erythrogenic toxins
-scarlet fever, streptococcal toxic shock syndrome, and necrotizing fasciitis

46
Q

s sequelae (streptococcus)

A

-pathological conditions result after a primary disease has run its course
-antibodies cross-react with host cells in autoimmune reaction -> serious sequelae

47
Q

s pyogenes cytoplasmic membrane

A

-antigens similar to human cardiac, skeletal, and smooth muscle, heart valve fibroblasts, neuronal tissues -> molecular mimicry

48
Q

post streptococcal sequelae

A

-acute rheumatic fever (ARF)
-young kids (4-9)
-high fever
-damage to heart, joints, skin, nervous system
-cross reactive antibodies
-glomerulonephritis (kidney disease)

49
Q

streptococcal pharyngitis

A

-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

50
Q

scarlet fever

A

-SPEs cause
-rash and fever starting on head and neck, spread to trunk and then limbs
-may also have bumpy red tongue (strawberry tongue)

51
Q

erysipelas (streptococcus skin infection)

A

-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

52
Q

cellulitis (streptococcal skin infection)

A

-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

53
Q

cellulitis diagnosis

A

-base on symptoms
-remove aspirates from advancing edge of cellulitis
-site of trauma
-skin biopsies
-blood

54
Q

impetigo (streptococcus skin infection)

A

-highly contagious
-can be from s pyogenes or staphylococcus aureus

55
Q

necrotizing fasciitis (streptococcus skin infection)

A

-flesh eating
-polymicrobial
-usually s pyogenes and sometimes s aureus
-fatal
-therapy antibiotics

56
Q

streptococcus spp. diagnosis

A

-serology: detection of antibodies (antibodies against streptococcal m protein, ELISA, fluorescent antibody, direct bacterial agglutination)
-bacterial culturing
-throat or skin cultures

57
Q

ARF long term complications

A

-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

58
Q

ARF diagnosis JONES criteria

A

-joints (migratory polyarthritis)
-O (carditis)
-nodules on extensor surfaces
-erythema marginatum rash
-sydenham chorea (neurological symptoms)

59
Q

rheumatic heart disease (RHD) (streptococcus long term complication)

A

-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

60
Q

pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) (streptococcus long term complication)

A

-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)

61
Q

streptococcus prevention

A

-vaccines: PCV13 (pneumococcal conjugate) and PPSV23 (pneumococcal polysaccharide vaccine

62
Q

pharyngitis (superficial)

A

-sore throat
-malaise
-fever

63
Q

scarlet fever (superficial)

A

-deep red rash
-strawberry tongue
-exudative pharyngitis

64
Q

impetigo (superficial)

A

-skin pustules mature into honey colored scabs

65
Q

acute rheumatic fever (sequelae)

A

-polyarthritis, carditis, rapid and jerky movements, rash, subcutaneous nodules

66
Q

rheumatic heart disease (sequelae)

A

mitral and or aortic regurgitation with possible stenosis over time

67
Q

acute poststreptococcal glomerulonephritis (sequelae)

A

edema, hypertensions, urinary sediment abnormalities, complement deficiency

68
Q

bacteremia (invasive)

A

high fever, nausea, vomiting

69
Q

puerperal sepsis (invasive)

A

fever, chills, abdominal pain in pregnant women

70
Q

cellulitis (invasive)

A

acute, tender, erythematous, swollen area of skin

71
Q

necrotizing fasciitis (invasive)

A

fever, exquisitely tender skin lesions, vomiting, diarrhea, toxemia, tissue destruction

72
Q

streptococcal toxic shock syndrome

A

high fever, rapid onset hypotension, accelerated multisystem failure

73
Q

who can get gonorrhea

A

anyone sexually active

74
Q

gonorrhea drug resistance

A

develops resistance to antibiotics

75
Q

gonorrhea infectious agent

A

-nisesseria gonorrhoeae

76
Q

gonorrhea bacteria infects

A

-mucous membranes in genitals, rectum. throat, and eyes

77
Q

nisesseria gonorrhoeae description

A

-gram -
-diplococcus
-colonizes mucosal areas

78
Q

pili fimbriae, and opa proteins

A

facilitate adhesion of gonococcus to epithelial cells

79
Q

lipoligosaccharide (LOS) in gonorrhea

A

-lipopolusaccharide endotoxin
-part of outer membrane structure
-enhance pathogenicity

80
Q

antigenic variation of surface proteins

A

-help avoid immune detection
-antigenic variation of type IV pili to avoid immune defense

81
Q

gonorrhea commonality

A

-second most commonly reported disease in the US

82
Q

gonorrhea virulence factors

A

-pilus (contribute to antigenic diversity)
-por proteins
-opa proteins
-LOS
-rmp proteins
-igA protease
-capsule

83
Q

por proteins (gonorrhea)

A

-form pores through outer membrane
-antigenic
-specific serotypes associated with virulence

84
Q

rmp proteins (gonorrhea)

A

inhibit cidal activity of serum

85
Q

IgA protease (gonorrhea)

A

-core has enzyme, released by cell to destroy IgA1

86
Q

capsule

A

-resist phagocytosis unless antibody is present

87
Q

gonorrhea peak age and infection window

A

-15-24 year olds
-2-7 days after infection (can take 30 days)

88
Q

men and gonorrhea

A

85-90% have symptoms:
-painful pee
-yellow/white discharge from penis
-swelling of testes and penis

89
Q

women and gonorrhea

A

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

90
Q

gonorrhea untreated in women

A

-pelvic inflammatory disease (PID)
-scar tissue blocks fallopian tubes
-ectopic pregnancy (outside womb)
-infertility
-long term pelvic ab pain

91
Q

gonorrhea untreated in men

A

-rare but infertility (painful condition in tubes attached to testes)

92
Q

rare but if gonorrhea is left untreated

A

-can spread to blood or joints (life threatening)
-can increase chances of getting/giving HIV

93
Q

ophthalmia neonatorum

A

-conjunctivitis of newborn
-newborn eyes infected as pass through infected birth canal
-prevent with antimicrobial eyedrops

94
Q

gonorrhea diagnosis

A

-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

95
Q

gonorrhea treatment

A

-ceftriaxone injection
-tell partners so they can get treated

96
Q

gonorrhea highest during

A

1981, 20-24 years old

97
Q

gonorrhea prevention

A

-avoid sexual contact with infected
-long-term monogamous relationship with a tested uninfected partner
-condoms
-currently no vaccine and treatments are becoming less effective