Virology B2: Opportunistic Infections In Aids

Front 1

1) When did opportunistic diseases start being linked with AIDS?
2) Which organisms affected it?

Back 1

1) 1981
2) Pneumocystis carinii (homosexual men and community acquired)

Front 2

Which organs do the following diseases affect:

1) CMV
2) Candidiasis
3) Herpes simplex
4) Shingles
5) Toxoplasmosis
6) Cryptococcal meningitis
7) Pneumocystis carinii
8) Mycobacterium avium
9) Tuberculosis
10) Histoplasmosis
11) Cryptosporidiosis
12) Human papillomavirus

Back 2

1) Eyes, gut
2) Mouth, throat, genitals
3) Skin, genitals
4) Skin
5) Brain
6) Brain
7) Lungs (pnuemonia)
8) Lungs
9) Lungs
10) Lungs
11) Gut
12) Genitals

Front 3

Herpes simplex:

1) DNA or RNA virus?
2) What kind of cell is characteristic?
3) Shape?
4) What kind of infection?
5) What kind of transmission?
6) How is it spread?
7) What % of adults >25 test positive?
8) Where does HSV-1 usually cause infection? HSV-2?

Back 3

1) DNA
2) Tzank cell in nucleus
3) Enveloped icosahedral
4) Latent infection following primary
5) Person to person
6) Contact - virus is in saliva, tears, genital tract
7) 90%
8) Above waist, below waist

Front 4

Herpes continued:

9) Recurrences occur in __% of orally infected individuals, __% of patients with genital herpes
10) Where does herpes lie dormant?
11) What reactivates it?
12) Three main diseases caused?

Back 4

9) 45%, 60^
10) Craniospinal ganglia(HSV-2) trigeminal ganglia (HSV-1)
11) Stress, fever, infection, sunlight
12) Acute gingivostomatitis, herpes labialis, herpes genitalis

Front 5

What are the three types of oral-facial herpes?

Back 5

1) Acute gingivostomatitis - most common manifestation of primary herpetic infection

2) Herpes labialis (cold sores), reactive in 45% of infected individuals - preceded by prodrome

3) Herpes gladiatorum

Front 6

Molluscum contagiosum

1) What category of virus is it?
2) Main details?

Back 6

1) Poxvirus
2) Benign, ubiquitous, common in children, can cause severe disfiguring diseases in HIV/AIDS patients

Front 7

Papilloma virus

1) Envelope/nonenveloped?
2) Shape?
3) How many types are there and how are they identified?
4) What kind of problems do they cause?

Back 7

1) Naked
2) Icosahderal
3) >100, genetic sequence of outer capsid protein L1
4) Warts (verrucae), genital infection, genital cancer, epidermodysplasia verruciformis

Front 8

Which strains of human papillomaviruses are the high-risk types?

What do strains 16 and 18 cause?

What do strains 6, 11, 16, 18 cause?

Back 8

16, 18, 31, 45.

16/18 = 70% of cervical cancer, carcinoma in situ. Possess oncogenes

6, 11, 16, 18 - 90% of genital warts

Front 9

What % of sexually active women will contract HPV by age 50?

How many people ages 15-24 are infected with HPV?

Back 9

80%

1 in 4

Front 10

Cervical carcinoma:

1) What is it caused by?
2) What is the outcome?

Back 10

1) Human papillomavirus, usually strains 16/18
2) 90% spontaneously resolve, rest transform and probably virally integrate into DNA

Front 11

What is the human papillomavirus vaccine made out of? How does it work? Who are they recommended for?

Back 11

Quadrivalent, recombinant 6, 11, 16, 18 L1 antigens. L1 proteins assemble into non-oncogenic, non-infectious virus like particles

Recommended for girls 11-12, catch up in women 13-26, delay if you're preggo.

Front 12

Parvoviruses:

1) What is unique about them?
2) What does it target?
3) What diseases does it cause?

Back 12

1) ssDNA, smallest DNA virus, only b19 infects humans
2) Targets RBC precursors
3) Erythema infectiosum (Fifth disease), aplastic crisis in sickle cell anemia patients, crosses placenta to cause hydrops fetalis

Front 13

Herpesviruses:

1) Enveloped/noneveloped?
2) Shape?
3) Pattern of infection?
4) What type of transmission?

Back 13

1) Enveloped
2) Icosahedral DNA
3) Primary infection -> latent infection for life
4) Human to human transmission

Front 14

HSV-1 & HSV-2:

1) Where does each cause an infection?
2) What % of adults are serologically positive for HSV-1?
3) How is it spread?
4) Recurrence occurs in ____% of orally infected patients, __% of patients with genital herpes
5) How similar are these two strains and what does this mean?
6) How does the primary infection compare to the latent infection?
7) Clinical manifestations of HSV
8) What is the most common manifestation of HSV?

Back 14

1) HSV-1 - above waist. HSV-2 - below waist
2) 90% >25 yrs old
3) Contact - virus is shed in saliva, tears, genital and other secretions
4) 45%, 60%
5) 50-70% gene homology, there are several cross-reactive epitopes
6) Primary is usually trivial, subclinical
7) Acute gingivostomatitis, herpes labialis (cold sore), herpes geniatalis
8) Acute gingivostomatitis

Front 15

1) After initial infection, where does the herpesvirus lie dormant?
2) What triggers its reactivation?

Back 15

1) Nerves near spine - craniospinal ganglia, trigeminal ganglia
2) Stress, fever, infection, period, immunosuppression

Front 16

Acute gingivostomatitis:

1) Where does it occur and what is it caused by?
2) Symptoms?
3) How long do these symptoms last?

Back 16

1) Oral-facial herpes, caused by HSV
2) Gingival pain/bleeding, 1-8 mm ulcers with necrotic bases, lymphadenopathy, fever
3) Self-limiting, last ~13 days

Front 17

Herpes labialis

1) What is it caused by?
2) Reactivation occurs in ___% of orally infected individuals
3) What do people usually feel before infection reoccurs?

Back 17

1) Caused by oral-facial herpes (HSV)
2) 45%
3) Prodrome - warmth, tingling, itching at site that it occurs ~12 hours before appearance of lesion

Front 18

What are the three types of oral-facial herpes?

Back 18

1) Acute gingivostomatitis
2) Herpes labialis
3) Herpes gladiotorum

Front 19

Herpes gladiatorum:

1) What is it caused by?
2) Who is it most common in?

Back 19

1) Oral-facial herpes (HSV)
2) Wrestlers, athletes who participate in close skin contact sports

Front 20

1) What is the most common cause of corneal blindness in the US?
2) What kind of infection is it usually?
3) There is a high risk of?
4) How does it usually get into the eye?

Back 20

1) Ocular HSV-1
2) Recurrent
3) Herpes keratitis -> blindness
4) Autoinoculation - disease starts in mouth, pt puts finger in mouth and then rubs eye

Front 21

HSV-2:

1) What % of people are undiagnosed asymptomatic HSV-2 patients?

2) What are some symptoms of HSV-2?

3) What are the three main complications of HSV-2 infection?

Back 21

1) 60%

2) Cervicitis, periurethral lesions in vestibule, cutaneous

3) Encephalitis, neonatal, infection, eczema herpeticum

Front 22

1) What is the tx for encephalitis caused by HSV-2? Why is this encephalitis unique?

2) What happens if a neonate is infected with HSV?

3) Where does eczema herpeticum occur, and how common is it?

Back 22

1) Acyclovir - this encephalitis has a high mortality rate, but it's one of the few forms that can be treated

2) Dissemination, encephalitis, high mortality

3) Site of eczema or dermatitis, it's rare

Front 23

How do you diagnosis HSV in laboratory diagnosis?

Back 23

1) EM
2) Immunofluorescence
3) Virus isolation (easy to grow 1 & 2 in culture in about 1-5 days)
4) Serology (antibodies appear after 1-2 weeks)
5) Tzank prep
6) ***PCR***

Front 24

What is a Tzank cell?

Back 24

Multinucleated cell with intranuclear inclusion and chromatin margination, common in HSV-1 and HSV-2

Front 25

What are the two main treatments for HSV, which infections are they used for, and how do they work?

Back 25

1) Acyclovir - used for severe infections, terminates viral DNA synthesis. Three forms - oral (must take forever or else recurrence), cream (HSV infection of skin and mucous membrane, useful for prodrome), ophthalmic ointment

2) Valacyclovir - DOC for genital herpes

Front 26

Acyclovir:

1) What is it used to treat?
2) How does it work?

Back 26

1) HSV
2) Halts DNA synthesis - inactive until phosphorylated, and HSV thymidine kinase adds the first phosphate. Host kinases add the rest, drug incorporates into viral DNA and halts synthesis.

Front 27

What two disease are caused by varicella zoster virus?

Back 27

1) Chicken pox
2) Shingles

Front 28

Chicken pox:

1) Caused by what virus?
2) How is it transmitted and how long is the incubation time?
3) Where does it replicate?
4) Where is it latent?

Back 28

1) Varicella zoster
2) Respiratory, 14 days
3) Nasopharynx, regional lymph nodes
4) Cerebral/posterior root ganglia

Front 29

Shingles:

1) What virus is it caused by?
2) What is the main symptom and how is it caused?
3) What predisposes you to getting shingles?

Back 29

1) Varicella zoster
2) Rash in distribution of dermatome due to reactivation that travels down sensory nerve to area of skin innervated by nerve
3) Age, immune suppression

Front 30

Chicken pox:

1) What is it caused by?
2) Most common complication?
3) More serious but rare complications?
4) What happens if it's congenital?

Back 30

1) Varicella zoster
2) Secondary bacterial infection
3) Pneumonia, encephalitis
4) Neonatal pnuemonia, low birth weight, scarring, eye/neurological abnormalities

Front 31

How can you tell the difference with smallpox vs. chicken pox?

Back 31

In smallpox, all lesions are in the same stage and are found on the palms and soles

Chicken pox, all stages are present (papules, vesicles, pustules)

Front 32

Shingles:

1) What is it caused by? What is another name for it?
2) Most patients are how old?
3) What is the usual symptom?
4) What body part can it affect?
5) Is patient infectious?
6) DOC?

Back 32

1) Varicella zoster. Herpes zoster.
2) >50
3) Unilateral vesicular rash on single dermatome, with INTENSE pain
4) Eye
5) Very infectious
6) Acyclovir or valacyclovir, + analgesia

Front 33

Herpes zoster:
1) What is this also known as?
2) Who is it more serious in?
3) Complications?
4) Vaccine?

Back 33

1) Shingles
2) Immunocompromised patients
3) Rare, encephalitis, disseminated herpes zoster
4) Live attenuated varicella vaccine, MMRVaricella vaccine, **herpes zoster vaccine** (zostavax) for people >60. Post vaccine shingles rarely occur

Front 34

Epstein Barr virus:

1) Which cells does it attack?
2) How is it transmitted?
3) What diseases is it associated with?

Back 34

1) B lymphocytes - remains latent there
2) Saliva
3) Infective mono, Burkitt's, Nasopharyngeal carcinoma, Lymphoproliferative disease/lymphoma in immunosuppressed, Hairy leukoplakia in AIDS patients

Front 35

Infective mono

1) What main virus is associated with it?
2) How does it affect children vs. adults?
3) What are the main symptoms?
4) What unique things are present in the blood?
5) How do you diagnose it?
6) Therapy?
7) What symptom is often seen in the mouth? What is a dead giveaway for mono in the mouth?

Back 35

1) Epstein Barr
2) Children - subclinical. Adults - symptomatic in 50%
3) Fever, pharyngitis (sore, worse than strep), lymphadenopathy, splenomegaly, jaundice
4) Atypical lymphocytes
5) EBV IgM (old test monospot, heterophile antibodies)
6) Supportive
7) Membranous pharyngitis. Dead giveaway - Palatal petechiae

Front 36

Burkitt's lymphoma

1) What is it caused by?
2) Where is it endemic?
3) Where is it restricted to?
4) Who does cases occur in here?

Back 36

1) Epstein Barr
2) Children in Africa
3) Places with endemic malaria (may be cofactor)
4) HIV patients, sporadic here

Front 37

Nasopharyngeal carcinoma

1) What is it caused by?
2) What is it?
3) Where is it common?

Back 37

1) Epstein Barr
2) Malignant tumor of squamous epithelium in nasopharynx
3) Southern China - most common tumor in men and second most common in women

Front 38

B cell lymphoma:

1) What is it caused by?
2) Who is it normally seen in?

Back 38

1) Epstein Barr virus
2) Patients with HIV/AIDS, immunosuppressed transplant patients

Front 39

Cytomegalovirus:

1) What kind of virus is this?
2) How is it transmitted?
3) Where does it replicate?
4) Where does it become latent?
5) Where are inclusion bodies seen?
6) Where is the virus shed?
7) What is its characteristic appearance?
8) How do you diagnose it?
9) Symptoms?
10) What are the three main types of patients it affects and what are the symptoms?
11) How do you diagnose it?
12) DOC?

Back 39

1) Herpesvirus
2) Vertically and horizontally
3) PMN (basophils, eosinophils, neutrophils)
4) Myeloid cells (young cell of granulocytes), macrophages, endothelial cells
5) Cytoplasm and nucleus
6) Urine and saliva
7) Owl eyes
8) Urine test
9) Usually asymptomatic
10) Babies - congenital infection = mental handicap

Transplant recipients, AIDS patients = pnuemonitis, retinitis, colitis, encephalopathy

11) Inclusion bodies, PCR, CMV IgG, viral culture (urine)

12) Gancyclovir

Front 40

Kaposi's Sarcoma Herpes Virus:

1) What was it named before?
2) What other virus is it closely related to?
3) What cells is it latent in?
4) What disease is it strongly associated with?
5) Most patients with KS often have antibodies against?

Back 40

1) HHV-8
2) Epstein Barr
3) B lymphocytes
4) Kaposi's sarcoma
5) KSHV

Front 41

HepB:

1) Enveloped/noneveloped?
2) Shape?
3) What are the three markers and why are they important?
4) How can you tell if a patient is highly infectious?
5) Describe hepB replication, starting with viral entry
6) Where does hepB replicate?

Back 41

1) Enveloped
2) Icosahedral
3) a) HBsAg: this is the hep B surface antigen. Marker of infection produced in excess during replication. Most important.

b) HBcAg: core antigen, not found in the serum

c) HBeAg: product of HBcAg, marker of HIGH INFECTIVITY and viral replication

4) High HBsAg and HBeAg

5) HBsAg used to get small, partially dsDNA in. ds viral DNA completed and transferred to nucleus where it's transcribed to mRNA. mRNA moved to cytoplasm, translated by ribosomes into viral proteins, SYNTHESIZES - DNA BY VIRAL REVERSE TRANSCRIPTASE, + DNA is synthesized, RNA degraded
6) Only the liver, because it doesn't infect any other tissue

Front 42

Hepatitis B modes of transmission:

1) Carrier state (chronicity) is more likely to occur following what?

2) What are the 4 main modes of transmissionl, and their chronicity rates?

3) Children infected between what ages have a ___30% risk of chronicity

4) How long can HBV survive in the environment?

5) What was the MAIN risk factor in hepB acquisition?

Back 42

1) Mild disease

2) Sexual - 2-6% chronicity, Parenteral (IV drugs, needle stick), Other contact with blood, perinatal - 90% risk of chronicity

3) 1-5, 30%

4) At least 7 days

5) Heterosexual sex

Front 43

What body fluids is HBV found in a:

1) High concentration
2) Moderate concentration
3) Detectable concentration

Back 43

1) Blood, serum, wound exudates
2) Saliva, semen, vaginal fluid
3) Urine, feces, sweat, tears, breast milk

Front 44

Acute viral hepatitis:

1) What liver enzymes are elevated as a result of infection
2) How do you know if the liver is involved?
3) How long is the incubation period?
4) What two types of diseases are present?
5) What is a good way to tell between the type of hep diseases?
6) How long do the symptoms persist?

Back 44

1) ALT, AST, alakaline phosphatase, bilirubin
2) Jaundice
3) 2 months - 6 months
4) Anicteric - non-specific symptoms, without jaundice, anorexia, dark urine

Icteric - jaundice, malaise, anorexia, dark urine

5) Different heps have different types of diseases

6) Weeks to months

Front 45

1) What is the most important cause of neonatal hepatitis?

2) How is it acquired?

3) How do you prevent it?

Back 45

1) HepB
2) Contact with infectious secretions in birth canal - doesn't usually cross anything else
3) Recombinant vaccine given to women at risk - women with + HBsAg should have their neonates given HBIG given within 12 hours of birth. All neonates should be given vaccine.

Front 46

What are the hepB outcomes related to age?

Back 46

Chronic carrier - Neonates 90%, children 20%, adults 5%

Recover - Neonates 10%, Children 80%, Adults >95%

Neonates a lot more at risk for becoming chronic carrier, less recovery rate

Front 47

Describe the spectrum of chronic hepB (4 stages)

Back 47

1) Chronic persistent hep - asymptomatic

2) Chronic active hep - symptomatic exacerbations of hep

3) Cirrhosis of liver

4) Hepatocellular carcinoma

Front 48

Hepatocellular carcinoma:

Risk is greater in who?

How often should persistent carriers be screened for this? What do the screenings look for specifically?

Back 48

1) Persistently infected patients (100x the risk!)
2) HBeAg positive patients

Twice a year. Alpha fetoprotein, hepatic U/S

Front 49

Describe the levels of antibodies in an ACUTE hepatitis infection:

If the patient is over infection, what can you find?

Why do antibodies to HBc appear before HBs?

Back 49

1) HBsAg will rise, peak at 12 weeks
2) May or may not have HBeAg
3) After HBsAg, IgM anti-HbC peaks, anti-HBs appears much later

Anti-HBe, anti-HBc

HBs is tied up in immune complexes earlier

Front 50

Describe the levels of antibodies in a CHRONIC hepatitis infection.

What is carrier state defined by?

Back 50

HBsAg peaks at 12 weeks, remains high. Anti-HBc remains high. IgM anti-HBc peaks later and goes down. Anti-HBe can suddenly disappear.

HBsAg positivity for at least 6 months.

Front 51

Describe the hep B serology with HBsAg, total-antiHBc, IgM anti-HBc, Anti-HBs, if you're:

1) Never infected
2) Early acute infection
3) Acute infection
4) Recovered, immune
5) Chronic infection
6) Immunized

Back 51

1) HBsAg -, total antiHBc -, IgM anti-Hbc -, antiHBs -

2) HBsAg +, total anti-HBc -, IgM anti-Hbc -, antiHBs -

3) HBsAg +, total anti-HBc +, IgM anti-Hbc +, antiHBs -

4) HBsAg -, total anti-HBc +, IgM anti-Hbc -, antiHBs +

5) HBsAg +, total anti-HBc +, IgM anti-Hbc -, antiHBs -

6) Everything negative except antiHBs (+)

Front 52

What are the three methods of treatment for HepB? Who are they administered to and how do they work?

Back 52

1) PEG-Interferon - HBeAg+ carriers with chronic active hep, not well tolerated

2) Lamivudine - nucleoside analog, inhibits HBV-DNA synthesis (well tolerated, but rapid emergence of drug resistance

3) Adefovir - blocks DNA polymerase - disappearance of HBsAg and HBV-DNA

Front 53

What are the three ways to prevent HepB?

Back 53

1) Immunization (recombinant vaccine) - healthcare workers, neonates, boosters only for dialysis and immunoincompetent patients

2) HepB Immunoglobulin - protect those exposed to hep B

3) Other measures - screen blood donors, blood/body fluid precautions

Front 54

Herpes simplex in AIDS:

1) Primary or recurrent infection?
2) How does it affect AIDS patients differently?
3) DOC?
4) What can it cause in the brain?
5) Does it have unique chronic ulcers?

Back 54

1) Recurrent
2) Increased severity, disseminates to esophagus/causes encephalitis, chronicity
3) Acyclovir
4) Edema, hemorrhages, necrosis
5) No, you usually can't tell it's herpes immediately

Front 55

How can HSV-2 increase susceptibility to HIV?

Who has an increased probability of HIV acquisition?

Back 55

1) Disrupts normal barrier with ulcers
2) Recruits inflammatory cells (CD4+) to sites of viral activity, increases viral targets
3) Directly promotes growth of HIV

People having sex with HIV + partner WITH HSV-2

Front 56

CMV disease and AIDS:

1) Present in __% of AIDS patients
2) What are the most common manifestations of the disease in AIDS patients?
3) What is a unique symptom of CMV in end stage AIDS patients?
4) Oral lesions in AIDS are mostly?
5) DOC?

Back 56

1) 30%
2) Sight threatening **retinitis, pneumonia**, colitis, encephalopathy
3) Sialadenitis (inflammation of salivary gland)
4) Chronic ulcers
5) Gancyclovir

Front 57

Epstein Barr virus and AIDS:

1) What is the primary manifestation of EB in AIDS? How is this unique? What is it strongly associated with? When does it usually manifest? CD4+ count? What reduces incidence?

2) EB is associated with most what in AIDS?

Back 57

1) Primary CNS lymphoma - most common CNS neoplasm in HIV/AIDS, strong association with EB virus. Late stage. CD4+ <50-100 ml. HAART reduces incidence

2) Most systemic lymphomas

Front 58

1) Besides primary CNS lymphoma, what else does Epstein Barr cause in AIDS patients?

2) Specific location it affects?
3) What is it?
4) What kind of superinfection can occur?
5) What can it indicate?
6) Tx?
7) Symptoms?

Back 58

1) ****Oral hairy leukoplakia.
2) Lateral borders of tongue, often bilateral
3) Vertical white-yellow hyperkeratinized lesions that can't be detached
4) Candida
5) Poor prognosis
6) Acyclovir, AZT therapy of AIDS
7) Asymptomatic

Front 59

Herpes Zoster and AIDS:

1) How does it affect HIV/AIDS patients differently?
2) Recurrence?
3) What other symptoms can occur?
4) Tx
5) If you see it around the tongue, what's affected?

Back 59

1) More severe - may affect more than one dermatome
2) More frequent
3) Chronic viremia, disseminate to cause encephalitis, ocular blindness
4) ****Acyclovir + analgesia
5) Third branch of trigeminal nerve

Front 60

Candida:

1) Where are they found?
2) How do they reproduce?
3) Shape?
4) What do you culture it on, and how do they appear?
5) Treatment

Back 60

1) Common flora of the oral cavity, skin, genital tract, gut

2) Budding yeast w/ pseudohyphae, chlamydospores (spores formed on the pseudomycelium under certain culture conditions)
3) Polymorphic
4) Sabouraud's medium, creamy white colonies
5) Nystatin, azoles for superficial infection. Amphotericin B for severe sytemic

Front 61

Thrush:

1) AKA
2) Caused by?
3) 5 types

Back 61

1) Oral candidiasis
2) Candida spp.
3) oral candidiasis Can't PACE

Chronic hyperplastic - confluent white plaques that can't be removed (rare)

Pseudomembranous - white lesions easily wiped off with gauze

Angular stomatitis (chelitis, perleche)

Chronic atrophic - 60% of denture stomatitis in elderly

Erythematous - painful, deep, red, papillated

Front 62

Denture stomatitis:

1) Caused by?
2) Treatment?

Back 62

1) Candida spp. +/- oral bacteria. (Chronic atrophic ~60%) Dentures worn day and night, exacerbated by unclean dentures or insufficient oral hygiene

2) Leave dentures out

Front 63

Kaposi's Sarcoma Herpes Virus and AIDS:

1) What was it previously named?
2) What is it strongly associated with?
3) Where is it latent?
4) Most patients with KS have antibodies against?

Back 63

1) HHV-8
2) Karposi's Sarcoma
3) B lymphocytes
4) KSHV

Front 64

JC virus:

1) What kind of virus?
2) When are most people infected?
3) Symptoms? Where does it persist?
4) Who does it react in?
5) Main symptom in AIDS patient?
6) What do you see in a brain scan?

Back 64

1) DNA papovavirus
2) Childhood - everyone's had it
3) Asymptomatic, not latent but persists in kidney
4) Immunodeficient people (like AIDS)
5) Progressive multifocal leukoencephalopathy (PML) - leads to severe loss of function/dementia
6) Demyelination, lack of symmetry between cerebellar hemispheres

Front 65

HPV and AIDS patients:

1) Main manifestations?
2) What is considered AIDS defining in a HIV patient?
3) What causes cancer? What type?

Back 65

1) Oral warts (condylomata acuminata, cauliflower lesions)
2) Cervical cancer in HIV patient
3) Types 16 and 18 cause ~70% of cervical cancer, carcinoma in situ

Front 66

Molluscum contagiousum:

1) How does it affect people normally?
2) AIDS patient?
3) Who does it mostly affect?

Back 66

1) Nothing - dots on fingers, donuts with depressed center.
2) Mollusk like growth all over face
3) Children

Front 67

1) Why are Hep C and HIV infection so closely related?
2) How does HIV affect Hep C people?
3) What is associated with faster progression to end-stage liver disease?
4) Does HCV accelerate HIV progression?

Back 67

1) They have similar risk factors - drug abusers with needles are the primary gainers of the disease.
2) Speeds progression of HCV to end-stage liver disease
3) Low CD4 counts
4) Not known

Front 68

Hep B and HIV infection:

1) Why are they usually found together?
2) __% of HIV people have previous markers of infection for HepB, What % have chronic hepB?
3) How does HIV infection relate to chronic hep B
4) What two things do HIV/HBV coinfected patients have a chance of getting?

Back 68

1) Similar risk factors
2) 90%. 10% have chronic HepB
3) **HIV infection increases risk of CHRONIC hep after hepB exposure**
4) Greater HbE antigenemia (highly infectious), increased risk of liver disease and liver related mortality

Front 69

HIV associated aphthous ulcers:

1) What type are they? What determines how big they are?
2) Increasing severity with?
3) Etiology?

Back 69

1) Major type - less CD4 cells = bigger and more painful
2) Increasing immunodeficiency
3) Unclear - HSV, CMV, or fungi

Front 70

Pneumocystis jirovecii:

1) What is it?
2) Why is it unusual?
3) Two forms?
4) Transmission?
5) How do you identify it?
6) Presents as?
7) DOC?

Back 70

1) Fungus
2) Lacks ergosterol
3) Trophozoite form, cyst form
4) Airborne
5) Silver stain (difficult to culture/stain), bronchiolar lavage
6) Pneumonia
7) Trimethoprim sulfamethoxazole

Front 71

Cryptococcus neoformans:

1) What is it?
2) Where is it found? What form?
3) What is its main virulence factor?
4) What infections does it cause?
5) Diagnosis?
6) DOC?

Back 71

1) Fungi - budding yeast with no pseudohyphae
2) Spore in pigeon, chicken feces
3) Anti-phagocytic capsule
4) Pulmonary - most common. MENINGITIS - 2nd most common, ESPECIALLY IN AIDS
5) India ink, cryptococcal latex test
6) Amphotericin B

Front 72

Rhizopus arrhizus:

1) What is it?
2) What does it cause?
3) Where is it found?
4) Structural makeup?
5) DOC?
6) Unique qualities?

Back 72

1) Fungus
2) Zygomycosis (mucormycosis), rhinofacial/rhinocerebral disease
3) Molds in fruits/vegetables
4) Non-septate hyphae
5) Amphotericin B, surgery, treat underlying condition
6) Very fast growing lid pusher

Front 73

Rhinocerebral/rhinofacial zygomycosis:

1) Caused by?
2) What does it typically occur in?
3) What happens?
4) Who does this occur in?

Back 73

1) Rhizopus arrhizus
2) Diabetics with ketoacidosis, patients on steroids or cytotoxic therapy
3) Pt ingest contaminated food, spores invade through soft palate, sinuses, cribriform plate, into brain and behind eyes. Fatal within days.

Front 74

Histoplasma capsulatum:

1) What is it?
2) Where is it found?
3) Most common manifestation?
4) DOC?

Back 74

1) Dimorphic fungi
2) Ohio, Missouri, Mississippi River Valley, blackbird, starling, bat, chicken poop
3) Pulmonary infection resembling TB, may disseminate
4) Amphotericin B

Front 75

1) What is the most common prodromal manifestation of AIDS?

2) DOC - a) topical b) oral c) esophageal d) parenteral

3) What is a danger of this prodrome?

Back 75

1) Candida albicans' candidiasis

2) a) topical - nystatin b) oral - ketaconazole, fluconazole c) - esophageal - micafungin d) parenteral - amphotericin B

3) If it disseminates into the bloodstream, it can get anywhere (systemic - brain, lungs)

Front 76

1) How is esophageal candidiasis different from herpes?

2) What does esophageal candidiasis look like?

Back 76

1) Can scrape off esophageal candidiasis, can't scrape off herpes

2) Budding yeasts and pseudohyphae

Front 77

1) What is the most common oral manifestation of HIV?
2) What % of AIDS patients develop this in their lifetime?
3) Predictive for development of full blown AIDS if not treated in _ years
4) Clinical types seen? What is the most common seen in an AIDS patient?

Back 77

1) Oral candidiasis
2) 90%
3) 2 years
4) Pseudomembranous, erythematous, hyperplastic, angular cheilitis

Front 78

Erythematous candidiasis:

1) What does it look like?
2) What happens?
3) What is a lesion known as?

Back 78

1) Pizza burn, trauma, radiation, xerostomia
2) Papillae disappear, it's painful
3) Kissing lesion - see tongue on palate

Front 79

Hyperplastic candidiasis:

1) Characterized by?
2) What sensation is associated with it?
3) What other condition is it confused with?
4) 9-40% cases of hyperplastic candidiasis are associated with?

Back 79

1) Chronic, nonremovable white plaques. Hard, rough to touch.
2) Burning
3) Hairy leukoplakia
4) Oral cancer

Front 80

Pneumocystic jirovecii and HIV:

1) What kind of organism is it?
2) Why is it unique?
3) Where is it found?
4) Stain?
5) IMPORTANT in AIDS because?
6) 95% occurs in who?
7) Incidence increasing or declining?
8) How does frequency of occurence affect survival?

Back 80

1) Fungus
2) Lacks ergosterol
3) Ubiquitious, most kids have antibodies
4) Silver stain - difficult to culture
5) Most common AIDS-defining opportunistic pathogen, most common cause of pneumonia in AIDS
6) AIDS patients with CD4 count <200/ul
7) Declining because of HAART therapy
8) Decreases chance of recovery

Front 81

What is the most common AIDS defining opportunistic pathogen?

Back 81

Pneumocystis jirovecii

Front 82

What is the most common cause of pneumonia in patients with AIDS?

Back 82

Pneumocystis jirovecii

Front 83

Pneumocystic jirovecii:

1) What does it present as?
2) How do you diagnose it?
3) DOC?
4) 20-40% die when CD4 count is ___, even with treatment
5) What will you see in a radiograph of the lungs? Regular picture?
6) **95% occurs in patients with CD4 count of?

Back 83

1) **Pneumonia (PCP), fever, nonproductive cough, dyspnea
2) Silver stain, broncheolar lavage
3) ***Trimethoprim sulfamethoxazole
4) <100/uL
5) Diffuse interstitial infiltrates. Honeycomb.
6) <200***

Front 84

Cryptococcus neoformans and AIDS:

1) What is it?
2) Where is it found?
3) What is its most common manifestation in AIDS patients? When does it occur?
4) Incidence increasing or declining?
5) DOC?

Back 84

1) Encapsulated yeast
2) Pigeon poop
3) ***Meningitis (85%), in patients with CD4 count <200 ul****
4) Decreasing due to HAART therapy
5) ***Amphotericin B

Front 85

If an AIDS patient has meningitis, what disease will you think of first?

Back 85

Cryptococcus neoformans

Front 86

Histoplasma capsulatum:

1) What is it and where is it found?
2) What does it cause in AIDS patients? Which patients is it most common in?
3) Main symptoms?
4) DOC?
5) Where does it usually start?

Back 86

1) Dimorphic fungus, Ohio, Miss valley, blackbird and guano poop
2 **progressive disseminated Histoplasmosis - pts with CD4+ <100 ul***
3) Fever, wasting, cough, **oral lesions, indurated ulcers**
4) Amphotericin B
5) Lungs, but it **disseminates**

Front 87

Rhizopus and AIDS:

1) What does it cause, and which AIDS patients are susceptible to it?
2) Common in patients with what other disease?

Back 87

1) Mucormycosis, particularly when neutrophil count is low
2) Diabetes

Front 88

If person has AIDS AND low neutrophil count, what disease should you think?

Back 88

Rhizopus - mucormycosis

Front 89

Which enteric bacteria are more common in HIV/AIDS patients?

Back 89

Salmonella, Campylobacter, Shigella

Front 90

1) How does HIV affect treponema pallidum?

2) _% of males with syphilis have AIDS

Back 90

1) Alters diagnosis, natural history, outcome of syphilis

2) 15%

Front 91

How is staph associated with AIDS?

Back 91

Rates of MRSA in AIDS patients increasing

Front 92

1) What are the most frequent causes of bacterial pneumonia in AIDS patients?

2) Bacterial respiratory infection severity increases as what?

Back 92

1) S. pnuemoniae and H. influenzae

2) CD4+ cell count declines

Front 93

S. pnuemoniae:

1) How many times more common in the HIV infected patient?
2) Recurrence rate?

Back 93

1) 150x
2) 8-25% within 6 months

Front 94

What is the most common cause of death from pneumonia in HIV/AIDS?

Back 94

Bacterial pneumonia from S. pnuemoniae or H. influenzae (more than P. jirovecii, fungus)

Front 95

Pseudomonas aeruginosa:

1) Who is susceptible?
2) Most common presentation in AIDS patients? When does this happen the most?
3) Mortality rate
4) What do you see in a radiograph of a lung?
5) What type of bacteria?
6) Virulence factors?

Back 95

1) Burn patients, cystic fibrosis, AIDS patients
2) **Pneumonia, bacteremia** Pts <100/ul
3) 50%
4) Pulmonary abscess
5) Gram -
6) Alginate capsule, pigment producer, endotoxin, exotoxin

Front 96

What is THE major opportunistic infection of AIDS patients worldwide?

Back 96

Mycobacterium tuberculosis.

Front 97

Primary TB in AIDS patients:

1) Caused by?
2) Comprises ___ of cases in HIV patients
3) What is the ANNUAL risk in HIV patients?
4) Who does it especially occur in?
5) What symptom of TB is increased?

Back 97

1) Mycobacterium tuberculosis
2) 1/3
3) 4-10% annually (really high risk!)
4) Advanced HIV patients (<200/ul, more extrapulmonary/disseminated disease)
5) **TB meningitis**

Front 98

Reactivation of latent TB in AIDS patients:

1) Annual risk in HIV patients?
2) vs. what risk in uninfected patients?

Back 98

1) 7-10% ANNUAL risk
2) vs. 5-10% LIFETIME risk

Front 99

How does TB affect HIV patients?

Back 99

Makes the progression of HIV faster (weeks/months)

Front 100

What is the most common cause of death among HIV patients worldwide? Stats?

Back 100

TB. 1 in 8 people with AIDS worldwide dies of TB.

Front 101

Mycobacterium tuberculosis:

1) Virulence factor
2) What kind of organisms
3) Transmission by?
4) Symptoms?
5) Diagnosis?
6) Tx?

Back 101

1) Cording factor, derived from mycolic acid, inhibits PMN migration and induces granuloma formation. Serpentine cord formation.

Sulfatides - glycolipids that inhibit phagosome formation.

2) Facultative intracellular
3) Respiratory - airborne droplets - most exposed people NOT infected
4) Cough, hemoptysis, fever, night sweats, weight loss, lethargy
5) PPD skin test, nucleic acid probe hybridization
6) TWO drugs simultaneously. Primary - isoniazid, streptomycin, rifampin. Secondary - amikacin, kanamycin

Front 102

1) TB primary infection symptoms
2) Three outcomes of primary infection?

Back 102

1) Primary - pulmonary, single focus TB, granuloma formation, T cell mediated immunity starts, GHON complex (lung focus that might granulate)

2) Asymptomatic, latent, progressive primary infection

Front 103

TB progressive primary infection symptoms

What can this lead to?

Back 103

Granuloma formation, CD4+ T cell mediated **(Th1)**, **epithelioid and giant cells**, necrosis and caveation of lung granuloma

Leads to systemic (hematogenous) spread, miliary TB (overwhelming spread)

Front 104

How is TB in AIDS patients different from TB in uninfected patients?

Back 104

TB in AIDS patients = poorly formed granuloma (no CD4 cells to make it). HIV - have well formed granulomas.

Front 105

How has the incidence of HIV coinfection with TB been since 1995?

Back 105

Declining

Front 106

Mycobacterium avium-intracellularle and AIDS:

1) What does it cause?
2) 95% of cases occur when?
3) Symptoms?

Back 106

1) Disseminated infection in AIDS - isolated pulmonary disease uncommon

2) CD4 count <50/ul

3) Multiple subcutaneous and lympho-node abscesses

Front 107

What does staph aureus cause in AIDS?

Back 107

1) Risk of MRSA

Front 108

Cryptosporidium parvus and AIDS:

1) What is it?
2) Reservoir?
3) How is it transmitted?
4) What happens in normal people vs. AIDS?
5) How do you resolve it?
6) Tx?

Back 108

1) Protozoan
2) Animal
3) Ingestion of cysts in contaminate dwater
4) Self limiting vs. profuse watery diarrhea in AIDS patients
5) ART with immune restoration (to CD4 > 100/ul) results in complete resolution
6) ***Paromomycin***, antidiarrheals

Front 109

Isospora:

1) What is it?
2) What does it respond to?

Back 109

1) Protozoa, rare opportunist
2) Sulfonamides

Front 110

Microsporidia:

1) What are they?
2) Style of living?
3) Overall prevalance in AIDS patients?
4) Risk greatest with?
5) Clinical presentation?
6) Diagnosis?

Back 110

1) Protists **related to fungi**
2) Obligate intracellular parasite
3) **15%**
4) CD4 <100cell/uL
5) **Diarrhea most common, pulmonary** (aspiration from GI), hepatitis,
6) Bronchiolar lavage, gram stain

Front 111

Toxoplasma gondii

1) Hosts?
2) Transmission?
3) How much of the population has it?
4) Who is at risk?
5) Conditions caused in AIDS patients?
6) DOC?

Back 111

1) Cats
2) Ingestion, transplacental
3) Ubiquitous, most of population has it
4) **Immunodeficient and fetus** at risk - stillbirth, microcephaly
5) Dissemination of cysts in visceral organs, lungs, ***eye (retinitis), CNS*** - often fatal
6) ***Trimethoprimsulfamethoxazole

Front 112

What accounts for 50% of brain lesions in all AIDS patients?

Symptoms?

Back 112

Toxoplasma gondii

Headache, confusion, fever, focal weakness, seizures, necrotizing abscess

Front 113

1) What is the trend in opportunistic infections now? Why?

2) Which ones reduced?

3) Which ones increased?

4) Which ones no change?

Back 113

1) Declining nicely due to HAART

2) Candidiasis, hairy leukoplakia, NUP, kaposi's sarcoma

3) Salivary gland disease, oral warts, dental caries

4) Oral ulcers

Front 114

Oral manifestations:

1) Present in _% of HIV patients
2) What are they?

Back 114

1) 80%
2) ** Infections - bacterial (perio disease, caries), viral (oral ulcerative), fungal

**Neoplasms, xerostomia, pigmentation

Front 115

What are the three highest oral lesions that have the most frequency in AIDS patients?

Back 115

1) Any oral lesions
2) Oral candidiasis
3) Hairy leukoplakia

Front 116

What is the most common primary CNS neoplasm in HIV?

Back 116

Epstein Barr

Front 117

Hep B acute infection:

1) What % what type?
2) Progression to chronic hepatitis is more common in what types of people?

Back 117

4) 90% resolve, 1% fatal, 9% HBsAg for more than 6 months.

Of the 9% HBsAg for more than 6 months, 50% resolve, 30% = chronic active hepatitis -> cirrhosis, hepatic cell carcinoma, extrahepatic disease
2) HbE+ subjects

Front 118

What indicates active replication of Hep B?

Back 118

HBV-DNA and HBeAg