Contact Infectious Disease Flashcards

1
Q

Describe this Contact Infectious Disease: Trachoma (Non-sexual disease)

(Causative Agent/Characteristic, Virulence Factors, Reservoir, Mode of Transmission, Predisposing Factors, SXS, Diagnosis, Treatment, Preventative Measures, Misc)

A

AKA/Causative Agent/Characteristc

  • AKA: x
  • CA: Chlamydia trachomatis strain (different serotype than Genital Chlamydia)
  • Characteristic: Gram-negative, coccobacillus, obligate intracellular parasite

Virulence Factors

  • Invades and Replicates in epithelial cells
  • 2 morphological forms
    -> Elementary bodies:
    –» Infectious, invade epithelial cells
    -> Reticulate bodies:
    –» Non-infectious, replicate intracellularly

Tissue/Organ Affected

  • x

Reservoir

  • Human

Mode of Transmission

  • Direct: Hand-to-eye contact
    -> Eye discharge
  • Indirect: Sharing objects
    -> Towels/handkerchiefs
  • Arthropod: Sand Flies
    -> Carrying eye discharge

Predisposing Factors

  • Unsanitary conditions
  • Over-crowding
  • Children

Incubation Period

  • x

SXS

  • Inflammation (conjunctivitis) of upper eyelid
    -> scarring/contraction of conjunctiva -> eyelashes turn inward -> eyelashes scratch cornea -> corneal cloudiness -> permanent blindness

Diagnosis

  • Clinical/SXS

Treatment

  • Surgery
  • ABX

Preventative Measures

  • No vaccine available
  • Vector control of sand flies
  • Washing hands

MISC

  • POE - mucous membrane (conjunctiva)
  • Leading preventable causes of blindness worldwide
  • Most cases of blinding trachoma occur in Africa
    -> HIGH infection rates < 5yr
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2
Q

Describe this Contact Infectious Disease: Gonorrhea

(Causative Agent/Characteristic, Virulence Factors, Reservoir, Mode of Transmission, SXS, Diagnosis, Treatment, Preventative Measures, Misc)

A

AKA/Causative Agent/Characteristic

  • AKA: x
  • CA: Neisseria gonorrhoeae
  • Characteristic: Gram-negative, encapsulated diplococcus (coffee-bean)

Virulence Factors

  • Capsule & Fimbriae
    -> attaches to epithelial mucosa
  • Op proteins in CW
    -> Bind to T cell receptors -> inhibit immune response

Tissue/Organ Affected

  • x

Reservoir

  • Human

Mode of Transmission

  • Direct: sexual contact

Predisposing Factors

  • x

Incubation Period

  • x

SXS

  • Gonococcal Urethritis (caused by N. gonorrhea)
  • Men: (More SXS)
    -> Painful urination
    -> Creamy, yellow discharge
    -> Epididymitis (testicular pain)
  • Women (Few/No SXS)
    -> Pelvic inflammatory disease (PID; inflammation of ovaries/fallopian tubes = major cause of sterility)

MAY BECOME SYSTEMIC IF UNTREATED:
-> Endocarditis (heart inflammation)
-> Meningitis (brain/spinal cord membrane inflammation)
-> Arthritis (joint inflammation)

Infants:
-> Ophthalmia neonatorum (neonatal conjunctivitis)
–> Infant blindness bc gonorrhea/genital chlamydia inf of eyes during vaginal birth

Diagnosis

  • Urine test or oral/urethral-rectal swab
  • PCR
  • Culture (look for gonococci)

Treatment

  • ABX
    -> Injection
    -> Oral meds

Preventative Measures

  • Education & safe sex practices

MISC

  • Highest infection rates in teens/young adults (bc sexually active)
  • Coinfection with Genital Chlamydia
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3
Q

Describe this Contact Infectious Disease: Genital Chlamydia

(AKA/Causative Agent/Characteristic, Virulence Factors, Reservoir, Mode of Transmission, SXS, Diagnosis, Treatment, Preventative Measures, Misc)

A

AKA/Causative Agent/Characteristic

  • AKA: Chlamydia
  • CA: Chlamydia trachomatis strain (different serotype than Trachoma)
  • Characteristic: Gram-negative, coccobacillus; obligate intracellular parasite

Virulence Factors

  • Invades and Replicates in epithelial cells
  • 2 morphological forms
    -> Elementary bodies:
    -» Infectious, invade epithelial cells
    -> Reticulate bodies:
    -> Non-infectious, replicate intracellularly

Tissue/Organ Affected

  • x

Reservoir

  • Human

Mode of Transmission

  • Direct: sexual contact (through epithelial mucosa)

Predisposing Factors

  • x

Incubation Period

  • x

SXS

  • Non-gonococcal urethritis (caused by N. gonorrhea)
  • Men: (More SXS)
    -> Painful urination
    -> Watery, clear discharge
  • Women (Few/No SXS)
    -> Pelvic inflammatory disease (PID; inflammation of ovaries/fallopian tubes = major cause of sterility)

May also cause (in infant):
-> Ophthalmia neonatorum (neonatal conjunctivitis)
–> Infant blindness bc gonorrhea/ genital chlamydia inf of eyes during vaginal birth

Diagnosis

  • Nucleic Acid Amplification Tests (NAAT)
    -> most sensitive test available
    -> PCR is a type of NAAT
    -> Performed on vaginal/urethral swabs or urine

Treatment

  • ABX

Preventative Measures

  • Education & safe sex practices

MISC

  • Most common bacterial STD in U.S = millions cases (in US)
  • Coinfection with Gonorrhea
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4
Q

Describe this Contact Infectious Disease: Syphilis

(Causative Agent/Characteristic, Virulence Factors, Reservoir, Mode of Transmission, SXS, Diagnosis, Treatment, Preventative Measures, Misc)

A

AKA/Causative Agent/Characteristic

  • AKA: x
  • CA: Treponema pallidum
  • Characteristic: Gram-negative, spirochete (endo flagella/axial filaments); motile

Virulence Factors

  • Lipid outer layer
    -> weak immune system

Tissue/Organ Affected

  • x

Reservoir

  • Human

Mode of Transmission

  • Direct: sexual contact

Predisposing Factors

  • x

Incubation Period

  • x

SXS

Primary Stage/Phase:
-> Chancre (painless core at site of infection)
–» Highly infectious

Secondary Stage/Phase:
-> Flat, skin & Mucosal rashes
–» Palms & soles
-> Latent period: decades

Tertiary Stage/Phase:
-> Appears decades later after latency
-> Formation of gummas (soft tumor-like lesions) on bone, brain, heart & skin
-> Arthritis
-> Cardiovascular dmg -> cardiovascular syphilis
-> Neurological dmg, dementia -> neurosyphilis

Diagnosis

  • Serology
    -> Direct DXS: look for T. Pallidum
    -> Indirect DXS: look for Ab

Treatment

  • ABX
    -> effective only in early stages

Preventative Measures

  • Education & safe sex practices

MISC

  • Congenital syphilis
    -> Development damage to fetus & stillbirths
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5
Q

Describe this Contact Infectious Disease: Trichomoniasis

(AKA/Causative Agent/Characteristic, Virulence Factors, Reservoir, Mode of Transmission, SXS, Diagnosis, Treatment, Preventative Measures, Misc)

A

AKA/Causative Agent/Characteristic

  • AKA: Trich
  • CA: Trichomonas vaginalis
  • Characteristic: Kingdom Protista, protozoan parasite; Motile: Flagella, undulating membrane; Pear-shaped

Virulence Factors

  • Axostyle: sharp point for anchoring to epithelial cells

Tissue/Organ Affected

  • x

Reservoir

  • Men

Mode of Transmission

  • Direct: sexual contact

Predisposing Factors

  • x

Incubation Period

  • x

SXS

  • Men:
    -> Asymptomatic carriers: found in urine & semen
    -> Some urethral discharge
    -> Painful urination
  • Women:
    -> Symptomatic
    -> Frothy, greenish-yellow, foul odor discharge
    -> Painful urination

Diagnosis

  • Microscopic observations of live, motile protozoa from swab of the infection site

Treatment

  • Antiparasitic/antiprotozoal drugs

Preventative Measures

  • Education & safe sex practices

MISC

  • Most common non-viral STD in U.S = millions+ new cases/year
  • Risk of low birth weight or premature births
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6
Q

Describe this Contact Infectious Disease: Genital Herpes

(Causative Agent, Virulence Factors, Reservoir, Mode of Transmission, SXS, Diagnosis, Treatment, Preventative Measures, Misc)

A

AKA/Causative Agent/Characteristic

  • AKA: x
  • CA: Herpes Simplex Virus Type 2 (HSV-2), HHV; Herpesviridae family; DNA
  • Characteristic: x

Virulence Factors

  • Hide in NS = latent viral infection

Tissue/Organ Affected

  • x

Reservoir

  • Human

Mode of Transmission

  • Direct: sexual contact

Predisposing Factors

  • x

Incubation Period

  • x

SXS

  • Painful, fluid-filled/raised vesicles on the genitals
    -> Heals within 2 weeks (not cured)
    -> Outbreaks of vesicles; primary episode -> recurrent outbreaks
  • Painful urination

Diagnosis

  • Culture
  • PCR

Treatment

  • Antivirals (management/suppress SXS)

Preventative Measures

  • Education & safe sex practices

MISC

  • 25% adults >30yr infected in U.S
  • Neonatal Herpes:
    -> Herpes crosses the placental barrier -> infects the fetus
    -» Damage CNS = developmental delays, blindness, hearing loss
    -> Low Survival rate (40%)
    -> Newborns infected during delivery
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7
Q

Describe this Contact Infectious Disease: Hepatitis B

(Causative Agent, Mode of Transmission, SXS, Diagnosis, Treatment, Preventative Measures, Misc)

A

AKA/Causative Agent/Characteristic

  • AKA: x
  • CA: Hepatitis B Virus: DNA
  • Characteristic: x

Virulence Factors

  • x

Tissue/Organ Affected

  • x

Reservoir

  • x

Mode of Transmission

  • Direct: sexual contact (body fluids)
  • Accidental needle sticks (healthcare workers)

Predisposing Factors

  • x

Incubation Period

  • x

SXS

Mild to Severe SXS:

Acute Infection:
-> Most adults fully recover
-> Jaundice
-> Loss of appetite
-> Fever
-> Nausea
-> Vomiting

Chronic Infection:
-> Liver failure
-> Cirrhosis
-> Liver cancer

Diagnosis

  • Serology (Abs)
  • Liver Ultrasound
  • Liver Biopsy

Treatment

  • NO CURE (management)

To manage chronic disease:
- Antivirals
- Interferon Injection
- Liver transplant

Preventative Measures

  • Vaccine
  • Education & safe sex practices

MISC

  • Small % of infected patients -> chronic Hepatitis B
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8
Q

Describe this Contact Infectious Disease: Hepatitis C (NOT STD)

(Causative Agent, Mode of Transmission, SXS, Diagnosis, Treatment, Preventative Measures, Misc)

A

AKA/Causative Agent/Characteristic

  • AKA: x
  • CA: Hepatitis C Virus: RNA
  • Characteristic: x

Virulence Factors

  • x

Tissue/Organ Affected

  • x

Reservoir

  • x

Mode of Transmission

  • Contaminated blood
    -> blood transfusions
    -> tattoos
    -> IV drug use

Predisposing Factors

  • x

Incubation Period

  • x

SXS

Acute Infection:
-> Most PT will develop chronic hepatitis
-> Usually asymptomatic
-> Jaundice
-> Loss of appetite
-> Fever
-> Nausea
-> Vomiting

Developed Chronic Infection:
-> Liver failure (~25%)
-> Cirrhosis (~25%)
-> Liver cancer

Diagnosis

  • Serology (Abs)
  • Liver Ultrasound
  • Liver Biopsy

Treatment

  • NO CURE (management)
  • Daily Antiviral: 2-6mnth
    -> Can help 95% of people
    -> Notoriously expensive ($1000/pill)
    -> Virus is undetectable in blood
  • Liver transplant

Preventative Measures

  • NO VACCINE
  • Universally safe precautions/blood handling

MISC

  • Large % of infected patients -> chronic Hepatitis C
  • Large % of PT with Hepatitis C were born ~mid 1900’s
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9
Q

Describe this Contact Infectious Disease: HIV/AIDS

(Causative Agent/Characteristic, Virulence Factor, Mode of Transmission, Predisposing Factors, SXS, Diagnosis, Treatment, Preventative Measures)

A

AKA/Causative Agent/Characteristic

  • AKA: x
  • CA: HIV (human immunodeficiency virus), Retroviridae Family, Retrovirus, RNA
    Two strains: HIV-1 (more deadly) & HIV-2
  • Characteristic: Enveloped, spikes (gp120; attach to host cell), enzymes (reverse transcriptase, integrase)

Virulence Factors

  • High gene mutation
    -> Rapid antigenic variation
  • Targets human host cells: CD4+ T cells (surface marker on T helper cells) = destroy Cell-Mediated Immunity

Tissue/Organ Affected

  • x

Reservoir

  • x

Mode of Transmission

  • Primary method: sexual contact
    -> Exchange body fluids
  • Secondary method: non-sexual contact
    -> Blood (contaminated) transfusions/organ transplant
    -> Breast milk
    -> Transplacental
    -> Sharing contaminated IV needles (HIV-contaminated blood)

Predisposing Factors

In chronological order from most to least:

  • Men having sex with men (MSM)
  • Heterosexuals
  • IV drug users
  • MSM and IV drug users

Incubation Period

  • x

SXS

Viremia (Sys inf):

Phase 1:

  • Asymptomatic
    -Hardened, swollen lymph nodes = lymphadenopathy

Phase 2:

  • Serious disease SXS
    -> Persistent Candida albicans (fungal) infections
    -> Persistent diarrhea
    -> Fever

Phase 3:

  • Clinical AIDS indicator Conditions unusual opportunistic infection (bc weak immune system)
    -> Atypical (fungal) Pneumonia
    -> Kaposi’s Sarcoma (cancer of the skin and BV; HHV-8)
    -> Miliary TB (Sys TB infection)

Diagnosis

  • ELISA
    -> Detects pathogen or Ab
  • Plasma Viral Load
    -> Detects & quantifies the amount of HIV circulating in the blood
  • Rapid tests & self-testing Kits
    -> Detects HIV ab in saliva
    -> Results available in 20 minutes

Treatment

  • NO CURE
  • Anti-Retroviral drugs/therapy (ART) - management
    -> HAART
    -> Fusion/Cell Entry Inhibitors
    -> Reverse Transcriptase Inhibitor (2 types)
    -> Integrase Inhibitors
    -> Protease Inhibitor

Preventative Measures

  • NO VACCINE
  • Education & safe sex practices
  • PrEP (Pre-exposure prophylaxis)
    -> Sold under the name Truvada

MISC

  • x
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10
Q

What does HIV stand for? What does AIDS stand for?

A

HIV = human immunodeficiency virus
AIDS = acquired immunodeficiency syndrome

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11
Q

Generally describe how HIV/AIDS became known as. Include specific dates

A

1981: cluster of Pneomocytis (atypical) pneumonia, Kaposi sarcoma (cancer), and loss of immune function were discovered in young, homosexual men. AIDS EPIDEMIC BEGINS

1982: term Acquired Immunodeficiency Syndrome is used for first time

1983: discovery of virus causing the loss of immune function -> eventually named Human Immunodeficicy Virus (HIV)

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12
Q

HIV/AIDS spread from “__________” ________ (africa) to human populations

A

old world
monkeys

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13
Q

What does SIV stand for? Where does it come from?

A

SIV = Simian Immunodeficiency Virus
-> comes from monkeys

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14
Q

Name the different strains of human HIV
Which is the most deadly? Name some important info about them

A

HIV-1 = MOST PATHOGENIC/DEADLY
- Related to SIV in gorillas and chimpanzes
- 99% of cases WW

HIV-2
- endemic to West Africa
- Lower mortality rate than HIV-1

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15
Q

Where is HIV/AIDs most prevalent in the world?

A

Africa

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16
Q

____________ is the most common mode of HIV transmission worldwide

A

Heterosexual transmission

17
Q

Name, in chronological order from highest to smallest, the common predisposing grous for new HIV infections in the US

A
  1. Men having sex with men (MSM)
  2. Heterosexuals
  3. IV drug users
  4. MSM and IV drug users
18
Q

Describe the pathogenesis of HIV to CD4+ T cells

A
  1. Viremia -> HIV (in blood) travels to lymphoid tissue, where CD4+ T helper cells are present
  2. HIV uses its gp120 (glycoporotein spike) to attach to the human host CD4+ T helper cell receptors and coreceptors (Attachment)
  3. Virus enters via fusion and is inside host CD4+ T helper cell (Entry)
  4. HIV gets uncoated to expose the viral RNA inside the host CD4+ T cell (Uncoating)
  5. Viral RNA is reversely transcribed into DNA (via reverse transcriptase)
  6. Viral DNA integrates (via integrase) into host CD4+ T helper cells chromosomal DNA = PROVIRUS = enters lytic OR lysogenic cycle
    -> Active infection: new virions (progeny HIV) bud from host cell (lytic; underwent biosynthesis, maturation, release)
    -> Latent infection: DNA is hidden in the chromosome as provirus (lysogenic cycle)
19
Q

Describe the phases/stages of HIV infection

A

Phase 1: 0-3 years

  • # of CD4+ T helper cells declines because # HIV goes up
  • # of CD4+ T helper cells begin to go back up and # HIV declines quickly (but never reaches 0; stabalizes)
  • # of CD4+ T helper cells slowly decreases
  • Asymptomatic; hardened/swollen lymph nodes (lyphadenopathy)
  • Seroconverions occurs: makes Abs; detectable at end of 3 months

Phase 2: 3-8 years

  • # of CD4+ T helper cells decline steadily
  • Only a few infected cells release HIV
  • Few serious disease SXS occur:
    -> Persistant Candida albicans (fungal) infections
    -> Persistant diarrhea
    -> Fever

Phase 3: 8-10 years

  • # of CD4+ T helper cell count falls below 200 CD4+ T helper cells/μl of blood
  • Clinical AIDS Indiacator Conditions: unusual oppotunistic infections
    -> Atypical (fungal) pneumonia
    -> Kapsoi Sarcoma (cancer of skin and BV due to HHV8)
    -> Miliary TB (mycobacterial that has spread; sys inf).
20
Q

*TRUE or FALSE: Although AIDS indicator conditions are not present until Phase 3, you are still considered to have AIDS when you are in Phase 1 or 2

A

False, only at Phase 3 do you truly have HIV/AIDs

21
Q

How do our 3rd line of host defenses (adaptive immunity) respond to HIV exposure?

A

Humoral Immune Response
- HIV-specific antibodies are produced in the seroconversion stages
-> Takes 3 months (part of Phase 1)
-> PT can still transmit HIV before seroconversion

Cell-Mediated Immune Response
- CD8 + T helper cell suppresses viral replication

22
Q

TRUE or FALSE: HIV virus target CD4+ T helper cells and CD8+ T helper cells

A

False, the target is ONLY the CD4+ T helper cells

23
Q

Name and describe each diagnositic method for HIV/AIDS (what does it detect?)

A

ELISA (enzyme-linked immunosorbent assay) test
- detects pathogen (HIV) or Ab (IgM; anti-HIV Abs)

Plasma Viral Load (PVL)
- detects and quantifies concentration of HIV circulating in the blood
-> useful before seroconversion ends

Rapid Tests and Self-Testing Kits
- detects HIV antibodies in saliva (results avaliable in 20 minutes)

24
Q

Doctor Miguel wants to detect and quantify the amount of HIV circulating in the blood of a current patient, Abdullah. He notes that it has been 5 months since his patient was infected with HIV.

Nurse Josh wants to run a PVL (Plasma Viral Load) on the PT.
Nurse Abby says he cannot do this because the diagnostic tool would not be very useful.

Explain why running a PVL would not be very useful.

A

PVL are only useful before seroconversion ends, which is before 3 months. It has been 5 months since the patient was infected.

PVL are useful between months 1-3 of HIV infection.

25
Q

Define: Seroconversion

A

period of time between infection and detectable presence of HIV antibodies
(body is still making Abs, but they are not detectable until end of 3 months)

26
Q

Other than preventing HIV/AIDS through education and safe sex practices, PrEP (Pre-Exposure prophylaxis) is another way to prevent HIV/AIDS. Briefly describe this is

A
  • HIV medicine taken daily to decrease changes of HIV infection
    -> Lowers risk dramatically (protect >90% from sex; >70% from IV drug use)
  • Sold as: Truvada
  • HAS TO BE TAKEN BY HIV-NEGATIVE PERSON ONLY!
27
Q

One way to manage HIV/AIDs is through Anti-Retroviral drugs/therapy (ART). What is the goal of ART?

A

goal = decrease plasma viral load (concentration of HIV virus) to undetectable amounts (however, you are still HIV-positive)

28
Q

Name 5 categories of Anti-Retroviral drugs used for management of HIV/AIDS

A

Highly Active Antiretroviral Therapy (HAART)
- uses combination (cocktail) of multiple drugs to combat resistant HIV strains

Fusion/Cell Entry Inhibitors
- prevent fusion of HIV virus with host CD4+ T helper cells

Reserse Transcriptase Inhibitors
- Two types
- prevent conversion of viral RNA into viral DNA (= cannot integrate -= no hybrid DNA/provirus)

Integrase Inhibitors
- prevent integration of viral DNA into host cell (CD4+ T helper cell) DNA (= no hybrid DNA/provirus)

Protease Inhibitors
- inhibit protease that cleave viral precuror proteins into structural and functional proteins (ex: protein spikes)

29
Q

What type of infections are commonly associated with AIDS?

A

Fungal infections
Bacterial infections
Viral infections
Cancers