HIV related infections and complications Flashcards
cryptococcal meningoencephalitis
invasive fungal infection caused by Cryptococcus neoformans seen in HIV pts
originates from lungs but can get to CNS and present with traditional meningitis symptoms
Treatment of cryptococcal meningoencephalitis in HIV pts
Needs yeast eradication and given in several phases: induction, consolidation and maintenance
Induction therapy: consists of 2 weeks of amphotericin B +/- flucytosine.
Consolidation: After CSF is clear can be switched to 8 weeks of fluconazole
Maintenance: Then 1 year of fluconazole therapy
When do you discontinue fluconazole or maintenance therapy in HIV pts who had cryptococcal meningoencephalitis?
after consolidation therapy are on fluconazole for 1 yr post infection. However can be discontinued once CD4 >100 with antiretroviral therapy
When to do serial LP in HIV pts w/ cryptococcal menigoencephalitis ?
when there is increased ICP (CSF>200 mmHg) and (seen in 50% of pts) AND headache, AMS, visual hearing loss and cranial nerve deficits
Goal to reduce ICP <200 or by 50% and decreases mortality
If do not respond, need to get ventriculostomy drain.
Is there any role for acetazolamide to lower ICP in cryptococcal
No.
If newly diagnosis HIV pt without ART who has cryptococcal meningoencephalitis, when do you start antiviral therapy?
wait 2-10 weeks after starting antifungal therapy to treat HIV because thought is that if started right away the ART can cause IRIS (immune reconstitution inflammation syndrome)
Drugs that interfere with folic acid metabolism
methotrexate
phenytoin
pyrimethamine
trimethoprim
treatment of systemic CNS toxoplasmosis
sulfadiazine and pyrimethamine
if unable to tolerate sulfadiazine can take clindamycin (preferred) over atovaquone or azithromycin.
longterm side effect of pyrimethamine
inhibits dihydrofolate reductase (similar to methotrexate and trimethoprim)
Blocks dividing cells and can first manifest as bone marrow suppression.
How to treat folic acid deficiency while on pyrimethamine
leucovorin - reduced folic acid that bypasses the blocked enzyme and has equivalent activity to folic acid.
Should be given concurrently with pyrimethamine to prevent leukopenia, megaloblastic anemia, and thrombocytopenia
do we give anti seizure medications to pts who have toxoplasmosis of CNS?
no unless they have seizure history.
Also try to avoid phenytoin with pts who are on pyrimethamine
PCP prophylaxis
bactrim or TMP SMX but if already treated with sulfadiazine and pyrimethamine for CNS toxoplasmosis - no need for additional coverage
toxoplasma encephalitis clinical presentation
fever, headache, confusion, focal neurological deficits/seizures
primary CNS lymphoma presentation
fever, night sweats, weight loss (80% of pts) , confusion, memory deficits, aphasia, and motor deficits, and focal neurological deficits, seizures
progressive multifocal leukoencephalopathy PML presentation
rapidly progressive neurological deficits (confusion, motor deficits, ataxia, aphasia, visual symptoms, and cognitive impairment)
lab findings with toxoplasma encephalitis
CD4 count<100
toxoplasma IgG antibodies
lab findings with primary CNS lymphoma
CD4 count<50
positive CSF cytology or Epstein Barr virus polymerase chain reaction positivity
lab findings for PML (progressive multifocal leukoencephalopathy)
CD 4 count <200
imaging studies for toxoplasma encephalitis
multiple ring enhancing lesions with mass effect and edema
commonly seen involving the basal ganglia
imaging studies for primary CNS lymphoma
solitary enhancing lesions with mass effect and edema
larger lesions >4cm compared to toxoplasma encephalitis. generally can involve the corpus callosum, periventricular or periependymal areas.
PML imaging findings:
bilateral usually asymmetrical white matter lesions
no mass effect, enhancement or edema
brain abscess etiology
direct extension of a dental sinus or ear infection and hematolgenous dissemination tends to be drom IVDA and endocarditis that leads tomultiple findings.
bacteria that can cause a brain abscess are:
streptocuccus and staph aureas but HIV pts can have listeria, nocardia, fungal and parasitic (toxoplasmosis)
unilateral headache, focal neurological deficits, seizures, papilledema and see single or multiple ring enhancing lesions at the grey white matter junction and significant vasogenic edema and mass effect
brain abscess- may not see systemic fever or sepsis in brain abscess
treatment of brain abscess
antibiotics and surgical drainage.
HIV associated encephalopathy
affects whole brain and see progressive dementia and brain atrophy on CT. No ring enhancing lesions
what causes PML?
JC virus reactivation and this happens with CD4 counts <200 and we see multifocal areas of white matter demyelination without mass effect, edema or enhancement.
Prophylaxis for PCP in HIV
bactrim
alternate therapies:
dapsone
atovaquone
pentamidine
when is HIV pt at risk for PCP infection
CD4 count <200
OR oropharyngeal candidasis is present
or history of PCP infection
when is HIV pt at risk for toxoplasma gondii infection?
CD4 count <100 and positive IgG antibody
prophylaxis against toxoplasma gondii in HIV pt
bactrim
alternate therapies:
dapsone + pyrimethamine + leucovorin (folinic acid)
atorvaquone + pyrimethamine + leucovorin
remember need leucovorin to prevent toxic effects of methotrexate or pyrimethamine.
when is a HIV pt at risk for histoplasma capsulatum
CD4 count <150 and in endemic area
prophylaxis against histoplasma capsulatum in HIV pt
itraconazole
when is a HIV pt at risk for varicella zoster virus infection?
close contact with person with chicken pox or shingles and no history of prior dx or negative antibody to VSV
prophylaxis against VZV in HIV pt?
variZIG (varicellar immunoglobulin) or IVIG administered within 4 days of exposure.
when do we do prophylaxis against PCP
CD4 <200 or if pt has oropharyngeal candidasis.
when can HIV prophylaxis be stopped
when ART improves CD4 count >200 for 3 months
reduces risk for drug toxicity and interactions or developing drug resistant organisms.
Do we provide MAC prophylaxis still for HIV pts CD4<50?
no we do not given low risk for MAC.
among pts taking ART and lack of differences in MAC dx outcomes in ppl who took prophylaxis and those who didn’t
previously azithromycin was used.
prophylaxis for coccidiomycosis
generally not recommended except in those that live or travel to endemic regions - can be screened twice annually with serological testing.
If seropositive and CD4<250 can give fluconazole prophylaxis if there is no dx manifestations
most common lymphomas related to HIV
See Hodgkin lymphoma and diffuse large B cell (non hodgkin lymphoma)
Seen with CD4 count is <100
poorly controlled HIV, marked body cavity lymphadenopathy and bone lucency
non hodgkin lymphoma
4% of HIV pts have lymphoma at time of diagnosis ..
risk factors for lymphoma with HIV
direct effects of HIV, immunosuppressive state, co infection with EBV virus
what helps to decrease incidence of lymphoma in HIV
HAART prevents severe immunosuppression.
CMV encephalitis happens when CD4 count is …?
CD4 count is <50 cells.
CMV encephalitis presentation
see dementia, delirium and focal neurological deficits
MRI of CMV encephalitis shows
see diffuse micronodular encephalitis or periventricular inflammation (ventriculoencephalitis)
skin concerns that can be 1st manifestation of a HIV infection?
sudden onset severe psoriasis
recurrent herpes zoster
disseminated molluscum contagiosum
severe seborrheic dermatitis.
AIDS nephropathy (kidney dx) also is associated with
associated with significant proteinuria
common causes of esophagitis in HIV pts?
candida lesions
CMV lesions
HSV lesions
clinical features of candida species causing esophagitis in an HIV pt
EGD findings are:
Biopsy results are :
involves the entire esophagus pain with solids more than liquids often associated with oral thrush EGD: white exudate (cottage cheese esophagus) Biopsy: pseudohyphae in mucosa
clinical features of CMV causing esophagitis in an HIV pt
EGD findings are:
Biopsy results are :
odynophagia and substernal chest pain
EGD: sharply demarcated, LINEAR UCLERS in distal 1/3 of esophagus
Biopsy: intranuclear inclusions (OWL eyes)
clinical features of HSV causing esophagitis in an HIV pt
EGD findings are:
Biopsy results are :
usually has oral lesions with abrupt onset
odynophagia and substernal chest pain
EGD: well circumscribed SHALLOW ulcers
can see other HSV infections elsewhere (herpes labialis)
Biopsy: stains positive for HSV and viral culture
Treatment of candida esophagitis in an HIV pt?
antifungal therapy (fluconazole)
Treatment of CMV esophagitis in an HIV pt?
IV ganciclovir
Treatment of HSV esophagitis in a HIV pt?
acyclovir
ulcerative esophagitis in HIV pt is seen with these pathogens
Typical presentation
Next step of management.
Seen due to viral infections like: CMV and HSV
retrosternal pain and fevers can occur, severe odynophagia, no typical findings of candida - oral thrush
needs endoscopy with culture and biopsy instead of empiric tx for candida
Complications of HSV ulcerative esophagitis
can lead to bleeding and tracheoesophageal fistula formation
CMV esophagitis often happens with (this other presentation)
concurrent retinitis which can lead to blindness.
PCP pneumonia presentation
subacute course of dyspnea, dry cough and fever is classic.
Can have chest pain, malaise, weight loss, headache, night sweats, chills and fatigue
advanced HIV/AIDS pts 6-7% can be asymptomatic
Does lack of fever exclude PCP pneumonia?
No. It just means it’s less likely a bacterial or mycobacterial source
what is seen on labs with 90% of HIV pts who have PCP pneumonia?
LDH levels >50 above baseline.
LDH>450 is predictive of PCP rather than a pulmonary process.
what is seen on the arterial blood gas of PCP pneumonia pt?
hypoxemia and increased alveolar arterial oxygen gradient and respiratory alkalosis
what is seen on CXR with PCP pneumonia?
see thinned walled cavitary lesions. Spontaneous pneumothorax develops in 5% of pts.
Pneumothorax likely due to rupture of cystic lesions that may present in active dx
what are side effects of bactrim?
skin - Steven Johnson syndrome, TEN (toxic epidermal necrolysis) exfoliative dermatitis
Hematological: megaloblastic pancytopenia (folate deficiency), can see G6PD deficiency - getting hemolytic episode.
Renal: hyperkalemia, impairs tubular secretion of Cr without affecting GFR
see crystalluria
interstitial nephritis
who is more sensitive to side effects of bactrim?
HIV positive pts 15% of pts with HIV can see SJS, TENs, and exfoliative dermatitis.
candida esophagitis in HIV pts will have these symptoms:
involves entire esophagus, pain with solids more than liquids
often seen with oral thrush
EGD: white exudate or cottage cheese esophagus
biopsy:pseudohyphae in mucosa
Treatment of candida esophagitis?
How long is treatment?
Do we use nystatin for treatment?
antifungal with fluconazole for 14-21 days
Systemic therapy is required.
Topical treatment with nystatin swish and swallow is only meant for people who don’t have HIV and there are high rates of failure.
CMV esophagitis will have these symptoms:
odynophagia and substernal chest pain
EGD: shows sharply demarcated linear lesions in distal 1/3 of esophagus
biopsy: see cells with intranuclear OWL eye inclusions
Herpes simplex HIV esophagitis will have these symptoms:
usually oral lesions with abrupt onset
odynophagia and substernal pain
EGD: well circumscribed shallow ulcers
Biopsy: stains positive for HSV and viral culture
treatment of HSV esophagitis:
acyclovir
Treatment of CMV esophagitis:
IV ganciclovir
if HIV pt with white plaques and angular cheillitis has signs of oral thrush you should also think that:
he has candidal esophagitis and treat with fluconazole
if there’s no oral thrush on exam, does that mean that HIV pt with odynophagia doesn’t have candidal esophagitis?
no. 18% don’t have oral thrush and still have candidal esophagitis.
if empiric treatment for candidal esophagitis fail to improve symptoms what must be done next?
get EGD and biopsy.
pt has new diagnosis of HIV and CD4 level is 730. He is a RN and from Ecuador. He has three birds and one cat. What is he at greatest risk for in terms of disease? histoplasmosis, Crytpococcus, PCP, toxoplasma gondi or TB
TB- because his CD4 count is 730 so not at risk for cryptococcus neoformans, histoplasmosis, PCP, or Toxoplasma gondii
He is a RN and from Ecuador.
TB co infection with HIV can happen at ANY CD4 level and hsould be considered. Needs testing for latent TB
How do HIV pts get cryptococcus neoformans infection?
when are they susceptible to infection?
What kind of infection do they get?
yeast transmitted from inhalation of bird feces. (remember the pigeons and doves ceremony for HIV pts)
Only susceptible when CD4 count is <200 and typically see disseminated cryptococcal dx or meningoencephalitis
Where do HIV pts get histoplasma capsulatum?
At what CD4 count are they susceptible to infection?
dimorphic fungus that can develop into disseminated dx in AIDS. Seen with bird or bat feces. endemic to ohio river valley
Seen when CD4<150
How do HIV pts get PCP or pneumocystis carinii (jirovecii)?
At what CD4 count are they susceptible to infection?
environmental fungus that is inhaled. Can get primary infection as a child but remain asymptomatic.
Seen when CD4<200
how to HIV pts get toxoplasma gondii?
At what CD4 count are they susceptible to infection?
parasite found in cat stools
oocytes remain dormant but can reactivate and cause neurological dx
seen when CD4 <100
what must be checked prior to starting dapsone as second line prophylaxis for PCP?
CD4< 200 need PCP prophylaxis
if using 2nd line dapsone need to check for G6PD deficiency prior to starting.
poorly controlled HIV
hypoxemic and CXR with bilateral infiltrates
normal ventricular function and valvular function
Think PCP or PJP
diagnosis of PCP
bronchoscopy
if pt has PCP and has hypoxemia <70 mmHg what do you give him?
steroids
bactrim, clindamycin and primaquine or dapsone for 21 days
Bacillary angiomatosis
cat scratch dx
seen in untreated HIV pts
fever, weight loss, classic exophytic papules that bleed when traumatized
see hemorrhagic angiomas of liver.
cats are vector and transmission happens with scratches, bites, infected feces.
diagnosis is with biopsies.
what virus causes Kaposi’s sarcoma in HIV pts?
HHV 8
