Infectious Disease Flashcards

1
Q

Which type of HIV is most common?

A

HIV-1. HIV-2 infection also results in AIDS, but HIV-2 infection has a considerably longer clinically latent period than HIV-1. HIV-2 originates from West Africa. Rare cases in North America have been traced back to there.

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2
Q

Vertical transmission rates to neonate a?

A

Vertical transmission from mother to child may occur in utero, during labor, or through breastfeeding. In the absence of antiretroviral treatment, HIV infects 25% to 30% of infants born to HIV-infected mothers. The rate of vertical transmission can be reduced to less than 2% by prenatal and perinatal treatment of the mother and postnatal

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3
Q

Opportunistic infections indicative of AIDS infection

A

Opportunistic Infections Indicative of a Defect in Cellular Immune Function Associated with AIDS

Protozoan Infection
Toxoplasma gondii encephalitis
Cryptosporidium parvum enteritis ( > 1 mo)
Isospora belli enteritis ( > 1 mo)

Fungal Infection 
Candida esophagitis 
Crypto occurs neoformans meningitis Disseminated histoplasmosis 
Disseminated coccidioidomycosis 
Pneumocystis jirovecii pneumonia (PCP)

Bacterial Infection
Disseminated Mycobacterium avium-intracellulare Active Mycobacterium tuberculosis infection Recurrent Salmonella septicemia
Recurrent bacterial pneumonia

Viral Infection
Chronic ( > 1 mo) mucocutaneous or esophageal herpes simplex virus infection
Cytomegalovirus retinitis, esophagitis, or colitis
Progressive multifocal leukoencephalopathy (JC virus)

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4
Q

Other non-infectious conditions associated with AIDS

A

Other Conditions Fulfilling Clinical Criteria for AIDS

Neoplasms
Kaposi sarcoma
High-grade, B-cell non-Hodgkin lymphoma Immunoblastic sarcoma Primary brain lymphoma Invasive carcinoma of the cervix

Systemic Illness
Human immunodeficiency virus (HIV) wasting syndrome (unintentional, unexplained loss of > 10% of body weight

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5
Q

Risk of HIV infection from needle injury?

A

HIV-contaminated hollow needle, the risk of infection is approximately 0.3%. Observational data suggest that this risk can be reduced at least 10-fold by prompt postexposure prophylaxis.

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6
Q

Acute retro viral syndrome signs and symptoms

A

Over 50% of HIV-infected persons experience a mono­ nucleosis-like syndrome (acute retroviral syndrome) 2 to 6 weeks after initial infection. Acute symptoms may include fever, sore throat, lymph node enlargement, rash, arthralgias, and headache and usually persist for several days to 3 weeks. A maculopapular rash is common, is short-lived, and usually affects the trunk or face.

Acute, self-limited aseptic meningitis, documented by cerebrospinal fluid (CSF) pleocytosis and isolation of HIV from CSF, is the most common clinical neurologic presentation and occurs in up to 10% of patients. The acute retroviral syndrome is sufficiently severe that a large proportion of patients seek medical attention. In the absence of a high index of suspicion, these symptoms are often mislabeled as an “acute viral syndrome.”

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7
Q

Presenting symptoms of acute retro viral syndrome by percentage?

A

Acute HIV Retroviral Syndrome: Common Signs and Symptoms

Sign or Symptom  Frequency (%)
Fever  98%
Lymph node enlargement  75
Sore throat 70
Myalgia or arthralgia 60
Rash 50
Headache 35
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8
Q

How many HIV+ will progress to AIDS after 10 years

A

Untreated HIV infection usually results in a slow, nonlinear progression to severe immunodeficiency. Approximately 50% of untreated individuals develop AIDS within 10 years after HIV infection

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9
Q

What does the early symptomatic phase of AIDS look like?

A

Mucocutaneous lesions may be the first manifestations of immune dysfunction, especially polydermatomal varicella-zoster infection (shingles), recurrent genital herpes simplex virus (HSV) infections, oral or vaginal candidiasis, or oral hairy leukoplakia (OHL). Patients with only mod­ erate immunodeficiency (CD4 counts between 200 and 500 cells/mm 3 ) exhibit diminished antibody response to protein and polysaccharide antigens, as well as decreased cell-mediated immune function. These functional impairments are manifested clinically by a threefold to fourfold increase in incidence of bacteremic pneumonias caused by common pulmonary pathogens (especially Streptococcus pneumoniae and Haemophilus influenzae ), as well as a marked increase in incidence of active pulmonary tuberculosis in endemic areas.

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10
Q

What does the advanced symptomatic phase of AIDS look like?

A

With advanced immunodeficiency, indicated by CD4 counts below 200 cells/mm 3 patients are at high risk for developing OIs .

CD4 counts less than 50 cells/mm 3 indicate profound immunosuppression and, in the absence of effective ART, are associated with a high mortality within the subsequent 12 to 24 months. Cytomegalovirus (CMV) retinitis, which can lead rapidly to blindness, and disseminated Mycobacterium avium-intracellulare (MAI) infections occur frequently. They respond adequately to specific therapy only when it is accompanied by effective control of viral replication.

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11
Q

What are some sex specific manifestations of HIV infection?

A
  • recurrent candida vaginitis
  • recurrent HSV outbreaks
  • cervical dysplasia or neoplasm
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12
Q

Infections related to CD4 counts in HIV

A

Relation of CD4 Lymphocyte Counts to the Onset of Certain HIV-Associated Infections and Neoplasms in North America

CD4 Count (cells/mm 3 ) * OI or Neoplasm
> 500 Herpes zoster, polydermatomal
200-500 
Mycobacterium tuberculosis infection 
Oral hairy leukoplakia 
Candida pharyngitis (thrush) 
Kaposi sarcoma, mucocutaneous (Male)
Bacterial pneumonia, recurrent Cervical neoplasia (Female)

100-200
Pneumocystis jirovecii pneumonia
Histoplasmosis capsulatum infection, disseminated
Kaposi sarcoma, visceral (M)
Progressive multifocal leukoencephalopathy Lymphoma, non-Hodgkin

< 100
Candida esophagitis
Cytomegalovirus retinitis
Mycobacterium avium-intracellulare, disseminated Toxoplasma gondii encephalitis
Cryptosporidium parvum enteritis
Cryptococcus neoformans meningitis
Herpes simplex virus, chronic, ulcerative Cytomegalovirus esophagitis or colitis Lymphoma, central nervous system

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13
Q

Management of early HIV

A

Management of Early HIV

Disease Monitoring
Confirm positive HIV test result
Complete baseline history and physical examination: HIV-specific interval interview and examination every 3-4 mo

Laboratory Evaluation
Baseline plasma HIV RNA level and CD4 cell count with repeat every 3-4 mo Baseline purified protein derivative (PPD) Baseline Toxoplasma antibody, syphilis serology, hepatitis B and C antibodies, liver function tests, and chest radiograph*
Baseline genotypic resistance testing

Health Care Maintenance
Assessment for ongoing counseling needs and referral for significant psychiatric or social problems
Discussions regarding safer sex and avoidance of needle sharing
Pneumococcal vaccine, hepatitis A and B vaccine (if HAV, HBV seronegative)
Yearly influenza vaccine
*many only order cxr when clinically indicated

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14
Q

Principles of anti-retro viral therapy

A

Antiretroviral treatment is not curative but suppressive; because HIV infection cannot be eradicated, treatment may be lifelong with currently available drugs.
• All effective treatment regimens may be associated with toxicities, some of which can be life threatening.
• There is a risk for the development of resistance to therapy that increases with the degree of nonadherence to therapy.
• Although damage to the host immune system occurs throughout the course of HIV infection, loss of protective immune response to the most serious OIs occurs only with advanced HIV disease.

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15
Q

Treatment Guidelines

A

Guidelines for the Initiation Therapy in the Chronically HIV-Infected Patient

Symptomatic (eg AIDS, thrush), any valueCD4 + T-Cell Count and HIV RNA, treat

Asymptomatic, CD4350
Treatment may be considered in some cases, although benefit may be limited in this group of patients. Treat Asymptomatic with concomitant (a) pregnancy; Any value (b) hepatitis B with an indication for treatment; or (c) HIV-associated nephropathy

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16
Q

Starting drug regimen for HIV?

A

Currently recommended initial regimens that predictably provide profound and durable suppression of viral replication include a potent NNRTI plus two NRTIs or a potent PI plus two NRTIs (often in addition to a low dose of the PI ritonavir, which tends to inhibit the hepatic metabolism of other drugs in this group).

17
Q

HIV medications and classes

A

Antiretroviral Drugs Approved for Use in Highly Active Antiretroviral Therapy Regimens for Treatment of HIV Infection

Nucleoside or Nucleotide Reverse Transcriptase Inhibitors (RTIs)
Abacavir Didanosine Emtricitabine Lamivudine Stavudine Zidovudine Zalcitabine Tenofovir*

Non-nucleoside Reverse Transcriptase Inhibitors (non-RTIs)
Efavirenz Nevirapine Etravirine

Viral Fusion Inhibitor
Enfuvirtide

Protease Inhibitors (PIs)
 Atazanavir Amprenavir Indinavir Lopinavir Nelfinavir Ritonavir Saquinavir Tipranavir Fosamprenavir Darunavir

Chemokine Receptor Inhibitor
Maraviroc

Integrase Inhibitor
Raltegravir

18
Q

Prophylaxis for OIs in HIV

A

Prophylaxis Against Opportunistic Infections (OIs) in HIV-Infected Adults *

Pathogen/ indication/ first choice/ alternative

Pneumocystis jirovecii/ CD4 count < 200, or history of thrush/ TMP-SMX 1 tab qd/ Dapsone, 100 mg qd Atovaquone, 1500 mg qd Pentamidine, aerosolized, 300 mg q mo

Mycobacterium tuberculosis

Isoniazid-sensitive/ TST reaction > 5 mm, or prior positive TST result without treatment, or contact with active case/ Isoniazid, 300 mg PO, plus pyridoxine, 50 mg qd × 9 mo/ Rifampin, 600 mg qd × 4 mo

Isoniazid-resistant/ same as above/ Rifampin, 600 mg qd × 4 mo/ Rifabutin 300mg qd x 4 mo

Toxoplasma gondii/ IgG antibody to Toxoplasma and CD4 count < 100/ TMP-SMZ, 1 double-strength tablet qd/ Dapsone, 50 mg PO qd, plus pyrimethimine, 50 mg PO q weekly

Mycobacterium avium-intracellulare/ CD4<50/ Azithromycin 1200mg q weekly/ Clarithromycin, 500 mg PO bid

May withdraw prophylaxis as CD4 counts rise with antiviral therapy

19
Q

Clinical difference between thrush and oral hairy leukaemia

A

OHL is a white, lichenified, plaquelike lesion most commonly seen on the lateral surfaces of the tongue that is likely caused by Epstein-Barr virus (EBV). Unlike thrush, the lesions of OHL cannot be scraped off with a tongue depressor. OHL may also be an early manifestation of moderately severe immunodeficiency. OHL is painless, may remit and relapse spontaneously, and almost always responds to effective ART.

20
Q

Clinical picture of aids dementia complex?

A

AIDS dementia complex (ADC) often begins insidiously and usually progresses over months to years (Table 108-11). ADC is characterized by poor concentration, diminished memory, slowing of thought processes, motor dysfunction, and occasionally behavioral abnormalities characterized by social withdrawal and apathy.

Symptoms of clinical depression overlap with many of the characteristics of early ADC and must be considered carefully in differential diagnosis and therapy

21
Q

What is PML?

A

PML is a demyelinating disease caused by a papovavirus (JC virus). Presenting signs and symptoms may include progressive dementia, visual impairment, seizures, and/or hemiparesis. MRI usually shows multiple lesions predominantly involving the white matter. These lesions are usually less visible on CT than on MRI and are not ring enhancing, which helps to distinguish PML from other mass lesions of the CNS. There is no effective specific treatment for PML; the disease often, but not always, regresses in response to effective ART.