Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

5. HDS Neuro Psych > Opportunistic Infections > Flashcards

Opportunistic Infections Flashcards

1
Q

HIV Opportunistic Infections (OIs)

General Principles

A
  • Low CD4 count is the major risk factor for many OIs
  • Many pts w/ HIV dx w/ OIs
  • Many people living w/ HIV who are being diagnosed w/ were not aware of HIV or not engaged in care
  • Many OIs have similar or overlapping signs and sx
  • Multiple OIs may be present at the same time
  • Treatment does exist for most OIs w/ good prognosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Opportunistic Infections

Overview

A
  • Select infections:
  • Toxoplasmosis
  • Pneumocystis pneumonia
  • Cryptococcosis
  • Cytomegalovirus
  • All AIDS defining illnesses
  • Requires deficient CMI for fulminant disease
  • CD4+ T-cell count < 200 cells/μl
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Toxoplasmosis

A
  • Systemic disease caused by obligate intracellular Protozoan parasite T. gondii
  • #1 Food borne illness
  • Most infections are asymptomatic
  • Mild disease in the immunocompetent host
  • Devastating in immunodeficient hosts or if passed congenitally
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Toxoplasma gondii

Epidemiology

A
  • Ubiquitous worldwide
    • Prevalent in warm, humid, low altitude environments
    • France
    • Central America
  • 50% of adults seropositive for T. gondii
    • 1% will be dx w/ disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Toxoplasma gondii

Lifecycle

A

Complex life cycle:

  • Oocyst ⇒ formed during the sexual cycle in the cat & excreted in feces
  • Tachyzoite ⇒ replicating form which disseminates through blood to tissue
  • Bradyzoite ⇒ dormant form contained within cysts in tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Toxoplasma gondii

Transmission

A
  • Reservoir: house cat
  • Intermediate hosts: sheep, cattle
    • Ingest the oocysts → dormant tissue cysts containing bradyzoites
  • Methods of transmission:
    • Ingestion of undercooked meat from intermediate hosts
    • Oral contact with oocytes (cat feces)
    • Drinking unfiltered water
    • Transfusion and transplantation
    • Congenital
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Toxoplasma gondii

Pathogenesis

A
  • Ingestion → trophozoites released from oocysts → penetrate gut wall → hematogenous spread → can invade all nucleated cells
    • Prefers heart, lung, brain, lymphoid tissues, and eyes
    • Replication within MΦ
  • Self-limiting mononucleosis-like symptoms:
    • Cervical or generalized lymphadenopathy
    • Pharyngitis, low grade fever, fatigue
  • Activated MΦ can kill the organism
  • Within several weeks of infection, once host mounts CMI response → infection controlled
  • Immune pressure → formation of dormant cysts in body tissues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Toxoplasma gondii

Reactivation Disease

A
  • Immunocompromised individuals, esp. AIDS pts
  • Type II strains
  • Cysts rupture releasing tachyzoites
  • Uncontrolled tachyzoite replication ⇒ necrosis and intense inflammatory response
  • Disease manifestations include:
    • Encephalitis, cerebral mass lesions, pneumonitis, systemic toxoplasmosis and chorioretinitis
    • Hemiparesis, seizures, lethargy, confusion, visual impairment
  • Highly lethal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Toxoplasma gondii

Congenital Disease

A
  • Pregnant woman acquires a primary infection w/ T. gondii
    • 1st trimester ⇒ usually causes spontaneous abortion or stillbirth
  • > 70% of congenitally acquired toxoplasmosis manifests months to years after birth
    • Mental retardation
    • Visual impairment
    • Hearing loss
    • Learning disabilities
    • Hydrocephalus
    • Chorioretinitis
    • Hepatosplenomegaly
    • Thrombocytopenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Toxoplasma gondii

Diagnosis

A
  • Congenital Infection or Symptomatic Primary Infection
    • Dx by serology
    • ↑ IgG titers (4-fold) & specific lgM
  • Latent infection
    • Variable IgG titers, no IgM
    • Presumptive dx of encephalitis based on clinical and radiographic findings
      • Brain MRI ⇒ multiple ring enhancing lesions
    • Ocular toxoplasmosis ⇒ retinal changes
    • Biopsy specimens ⇒ visualize organisms in tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Toxoplasma gondii

Treatment

A
  • Active disease
    • 1° disease in immunocompetent host usually self-limiting ⇒ requires no treatment
    • Congenitally acquired infection, damage is done in utero ⇒ tx after birth ineffective
    • AIDS pts w/ toxoplasmosis tx ⇒ Pyrimethamine + Sulfadiazine (synergistic)
      • High dose therapy for 4-6 weeks
      • Low dose maintenance therapy due to high relapse rate
  • Chemoprophylaxis for toxo-seropositive HIV pts (< 100 CD4 count)
    • Trimethoprim/sulfamethoxazole
      • Active vs tachyzoites form
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Toxoplasma gondii

Prevention

A
  • Cook meat to 165°F
  • Wash hands after gardening
  • Wash all fruits and vegetables
  • Avoid cat litter – or change daily
  • Screen women for anti-toxoplasma Ab during early pregnancy
    • Women who are seropositive (indicating previous infection) have no risk of producing a congenitally infected child
    • Seronegative women can be given preventative advice
    • Seroconvert during pregnancy can be further counseled and treated
    • Risk of drug toxicities to the fetus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cryptococcus neoformans

Characteristics

A
  • Causes Cryptococcosis
  • Oval budding yeast at both 25° and 37° (not-dimorphic)
  • Large acidic mucopolysaccharide capsule ⇒ ⊗ phagocytosis
  • Asexual
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Cryptococcus neoformans

Epidemiology and Transmission

A
  • Nitrogen rich environments ⇒ pigeon droppings
  • Found worldwide
  • Acquired by inhalation of aerosolized fungal elements
  • Person to person transmission does not occur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Cryptococcus neoformans

Clinical Diseases

A
  • Immunocompetent ⇒ usually asymptomatic
  • 1° infection in the lung ⇒ Pulmonary Cryptococcosis
    • Mild to fulminant PNA
    • CXR may show a solitary nodule or focal infiltrate
    • Hematogenous spread from lungs → meninges
  • Cryptococcal meningitis (most common clinical manifestation)
    • Causes meningitis, meningo-encephalitis, space occupying lesions
    • Behavioral changes, fever, HA, seizure, AMS
    • Leading cause of fungal meningitis
    • Highest mortality occurring in AIDS pts and transplant recipients
    • Meningitis due to mild disease w/ C. neoformans also seen in pts w/o underlying disease
  • Brain abscesses
  • Skin and bone lesions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Cryptococcus neoformans

Diagnosis

A
  • Examination of CSF for budding yeast cells w/ capsules using India Ink staining ⇒ ⊕ in 50% of cryptococcal cases
    • Clear halo around organisms d/t dye exclusion by the capsule
  • Latex agglutination and EIA tests for cryptococcal Ag ⇒ rapid, sensitive, and specific tests
    • False ⊕ reactions may be caused by rheumatoid factor
  • Dx confirmed by culture on SDA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cryptococcus neoformans

Treatment

A
  • Pulmonary cryptococcosis
    • Frequently self-limiting
    • When symptomatic, can usually be cured by excision of the nodule
  • Cryptococcal meningitis
    • Long term, combination antifungal agents
      • Amphotericin B + Flucytosine (induction therapy)
      • Then 8 wks of fluconazole
    • AIDS pts may need lifelong maintenance therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Pneumocystis jiroveci

Characteristics

A

Previously P. carinii

  • Primitive fungus
  • Lack ergosterol in cell membrane
  • Poorly defined cell wall
  • Extracellular trophozoite ⇒ divides by binary fission
  • Cyst form ⇒ contains intracystic bodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Pneumocystis jiroveci

Epidemiology

A
  • Ubiquitous
  • 75% seropositive by age 4
  • Infants infected after maternal Ab wanes
    • Almost always asymptomatic
20
Q

Pneumocystis jiroveci

Transmission

A
  • Person to person by respiratory secretions
  • Droplet inhalation
  • Inhalation from the environment
  • Infants colonized
  • Exogenous reinfection
21
Q

Pneumocystis jiroveci

Risk Factors

A
  • Symptomatic disease in immunosuppressed
    • AIDS pts: CD4 count < 200 cell/ml
    • Cancer chemotherapy
    • Organ recipients
    • Malnourished children who live in overcrowded conditions
  • Usually manifest after a debilitating illness → ? reactivation or carrier state
22
Q

Pneumocystis jiroveci

Pathogenesis

A
  • Inhaled as sporozoites
  • In the host, sporozoites → trophozoites
    • Binds Type I cells in alveolus
    • Remains extracellular
    • Eventually transform back into cysts (probably d/t sexual mating)
    • Each cyst can release 2 to 8 sporozoite forms (spore like)
  • CMI (Alveolar MΦ and CD4+ T cells) kill organisms
  • Alveolar damage through host and pathogen mediated mechs.
23
Q

Pneumocystis jiroveci

Diagnosis

A
  • ID organism in a tissue specimen or lavage fluids
    • Gomeri stain ⇒ thick-walled cystic forms
    • Giemsa staining ⇒ trophozoite forms
  • Serology is not useful
    • Wide prevalence of seropositive individuals
    • Titers rise several weeks after the onset of symptoms
24
Q

Pneumocystis Pneumonia

(PCP)

A

AIDS defining illness

  • Sx: dry cough, fever, rapid breathing, SOB, progressive respiratory insufficiency
  • Develops over weeks-months in AIDS pts
  • Bilateral diffuse interstitial pneumonitis w/ plasma cell infiltrates
    • Stays in air spaces
    • CXR ⇒ ground glass appearance
  • Usually responds to treatment but recurring bouts common
  • Rarely disseminates ⇒ extrapulmonary disease in pts w/ AIDS
25
Q

Pneumocystis jiroveci

Treatment/Prevention

A
  • P. carinii is resistant to antifungal drugs
  • Sensitive to a number of antibacterial and anti-protozoal drugs
  • Organism is ubiquitous ⇒ avoiding exposure is not possible
26
Q

Cytomegalovirus

Characteristics

A

Herpesviruses family / beta-herpesvirus subfamily

  • Large linear dsDNA viruses, enveloped
  • Transcription and translation highly regulated and consist of three phases:
    • Immediate early proteins ⇒ DNA binding proteins that regulate transcription
    • Early proteins ⇒ including the DNA polymerase
    • Late proteins ⇒ structural proteins
  • Replication and assembly occur in the nucleus
  • Virus buds from the nuclear membrane
  • Release from the cell occurs by exocytosis and cell lysis
  • Tendency to establish latent and recurrent infections
  • Manifestations of disease vary w/ age and immunocompetency
27
Q

Cytomegalovirus

Epidemiology & Transmission

A
  • Ubiquitous
  • No seasonal incidence
  • Transmission:
    • Direct person to person contact w/ virus containing secretions
    • Sexually
    • Blood transfusions
    • Tissue transplants
    • Vertically from mother to infant before, during and after birth
  • Virus can be isolated from tears, saliva, pharynx, semen, cervical secretions, peripheral blood leukocytes, amniotic fluid and urine
28
Q

Cytomegalovirus

Pathogenesis

A
  • 4-8 wk incubation
  • Initial infection usu. asymptomatic
    • Virus replicates in epithelial cells of respiratory and GI tract
    • Viremia
    • Infection of all organs and lymphoid tissue
    • Shed from most body fluids: pharynx, urine, genital tract
  • Latent infection in lymphocytes and MΦ and organs like the kidney and heart
  • Reactivation d/t profound immunosuppression ⇒ AIDS, prolonged corticosteroid use, chemotherapy
29
Q

Cytomegalovirus

Immune Response & Evasion

A
  • CMI critical to control infections
  • CMV blocks Ag presentation via MHC class I and II
    • ⊗ Transport to cell surface
30
Q

Cytomegalovirus

Infection in Children and Adults

A
  • Usually asymptomatic
  • May show a mononucleosis like syndrome w/ atypical lymphocytes
  • No heterophile antibody
31
Q

Cytomegalovirus

Infection in the Immunocompromised Host

A
  • May be due to reactivation or acquisition of primary infection
  • Interstitial pneumonia (15%), retinitis, esophagitis, chronic colitis (10%), and weight loss
    • CMV retinitis: white, fluffy retinal infiltrate or granular white area w/ hemorrhage, leads to blindness in 3-4 months
  • CMV is also frequently reactivated in transplant recipients ⇒ cause of transplant loss
    • Avoid seropositive → seronegative transplants
32
Q

CMV Retinitis

A

White, fluffy retinal infiltrate or granular white area w/ hemorrhage

Leads to blindness in 3-4 months

33
Q

Cytomegalovirus

Congenital or Perinatal Infection

A
  • 1% of live births are infected in utero
    • Usu. d/t 1° infection of the mother during pregnancy
    • 10-20% are diagnosed w/ mental retardation or deafness
  • Transmission from passage through the birth canal and postnatally by ingesting virus containing breast milk
  • Most term infants who acquire infection during or after birth have asymptomatic infections
  • Preterm infants at higher risk for interstitial pneumonia or hepatitis
34
Q

Cytomegalovirus

Diagnosis

A
  • In immunocompetent individuals, serology is a sensitive dx method
  • Seroconversion and IgM usually indicates a primary infection
    • Lymphocytosis w/ > 10% atypical lymphocytes
  • Immunodeficient individuals ⇒ Viral culture d/t presence of high titers of virus
  • Histological identification in tissues of the “owl’s eye”, basophilic intranuclear inclusion body is a hallmark of CMV infection
35
Q

Cytomegalovirus

Treatment

A

Anti-CMV agents

Ganciclovir, Cidofovir and Foscarnet

⊗ Viral DNA pol

36
Q

Cytomegalovirus

Prevention

A
  • Transplant organs between seronegative pts
  • Deplete leukocytes from transplanted organs
  • HAART for AIDS pts (CD4 counts < 50)
    • At risk for retinitis and esophagitis
37
Q

Mtb and MAC

A
  • Tb can occur w/ only mild immune impairment
    • Pulmonary Tb
    • May disseminate widely
    • Lymphadenitis, meningitis, hepatitis
  • MAC more commonly causes disseminated disease
    • Frequently of the GI tract & lymphoreticular organs
38
Q

Other Infections of Immunocompromised

A
  • Systemic candidiasis
  • Nocardia
  • Aspergillus
  • Histoplasma
  • Coccidiodes
39
Q

Kaposi’s Sarcoma (KS)

A

Caused by human herpes virus – 8 (HHV8)

  • More common w/ CD4 < 200 cells/mm3
    • May occur at any CD4 count
  • Clinical Appearance:
    • Non-tender, purple-reddish maculopapular skin lesions
    • Indistinguishable from Bacillary angiomatosis caused by Bartonella henselae
    • Can have similar lesion in the oropharynx
    • May also involve lymph nodes, lungs, digestive tract
  • Diagnosis:
    • Biopsy
  • Treatment:
    • Antiretroviral therapy (ART) for mild-moderate KS
    • ART plus chemo for disseminated KS
40
Q

Primary CNS Lymphoma

A

A diffuse, large-cell non-Hodgkin lymphoma of B-cell origin which is caused by Epstein-Barr virus

  • Clinical presentation:
    • Generally w/ CD4 < 100 cells/mm3
    • Symptoms include lethargy, headache, personality changes, memory loss, confusion
    • Often have focal neurologic symptoms: weakness, seizures, cranial nerve involvement
  • Diagnosis:
    • EBV PCR in CSF w/ compatible lesion on imaging
    • CT or MRI generally shows a single lesion which is enhancing w/ contrast, but can be multiple lesions
    • Brain biopsy for definitive dx
  • Treatment:
    • Chemo and radiation therapy + ART
41
Q

Progressive Multifocal Leukoencephalopathy (PML)

Overview

A

Central nervous system infection caused by the polyoma JC virus

  • Belongs to papovavirus family
  • Naked circular dsDNA genome
  • Replicated and assembled in the nucleus
42
Q

Progressive Multifocal Leukoencephalopathy (PML)

Epidemiology

A
  • ~65% of the population is seropositive
    • 20-30% of adults w/ a normal immune system have JC DNA in urine
  • Most individuals acquire asymptomatic infection during childhood
  • Disease remains latent in kidney afterwards
  • Profound immunosuppression permits renewed viral replication, dissemination of virus to CNS, and progressive disease
43
Q

Progressive Multifocal Leukoencephalopathy (PML)

Clinical Presentation

A
  • Characterized by focal demyelination
  • Present w/ focal neurologic deficits w/ insidious onset and steady progression
  • Starts as a partial deficit that worsens over time as lesions expand
  • Symptoms progress over several weeks
44
Q

Progressive Multifocal Leukoencephalopathy (PML)

Diagnosis and Treatment

A
  • Diagnosis:
    • MRI for white matter lesions
    • Confirm w/ CSF testing for JC virus PCR
  • Treatment:
    • No specific treatment
    • Initiation of ART may help
    • Generally poor prognosis
45
Q

Immune Reconstitution Inflammatory Syndrome (IRIS)

A
  • IRIS usually occurs within weeks to a few months after starting ART
    • Antiretroviral therapy initiated ⇒ ↓ HIV viral load ⇒ ↑ CD4 count ⇒ improved immune function
  • Can have a dramatic immune response if an opportunistic infection is present
  • Most common w/ mycobacterial infections (Tuberculosis or M. avium complex) or disseminated fungal infections
  • Most common sx: fever, lymphadenopathy, worsening respiratory sx
  • Treatment is supportive and symptoms resolve w/ time
    • Continue ART
    • May need to start steroids for inflammation if symptoms are severe enough
46
Q

Toxoplasmosis

vs

Primary CNS Lymphoma

vs

PML

5. HDS Neuro Psych (46 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions