Opportunistic Infections Flashcards
(55 cards)
1
Q
Describe the relationship between HIV and opportunistic infections?
A
- HIV attacks CD4+ cells
- As CD4 count drops OIs proliferate in individuals
- These diseases are rare in immunocompetent individuals
- CD4 Count less that 200 poses greatest risk to OIs
2
Q
What is the pathophysiology of OIs?
A
- Virion binds to CD4+ and chemokine receptor
- Fusion follows
- The pathogenic feature of HIV is progressive reduction in CD4+ cells leading to destruction of cell mediated immunity and antibody mediated immunity
- OI are manifested depending on the CD4 count suppression
3
Q
Which opportunistic infection can occur at all CD4+ counts?
A
tuberculosis
4
Q
Describe the opportunistic infection of TB in HIV?
A
- Bacilli persist for years referred to as LTBI
- About 3 to 16% of untreated infection have annual risk of reactivation with TB
- risk for HIV negative persons is 5%
- Meningitis, UTI and Disseminated Blood stream infections may occur
5
Q
How do you diagnose TB in HIV positive patients?
A
- TST - tuberculin skin test
- IGRA (interferon gamma release assays) sputum for AAFBs (acid fast bacillus)
- abnormal chest X ray findings e.g., fibrotic lesions, effusion
6
Q
What OI is present at a CD4+ count <250 cell/mm3?
A
Coccidiomycosis
7
Q
What pathogens cause coccidiomycosis and where are these pathogens found?
A
Coccidioides immitis andCoccidioidesposadasii
- found in soil
8
Q
What are the 4 different syndromes associated with coccidiomycosis?
A
- focal pneumonia presenting with fever, cough and pleuritic chest pain
- diffuse pneumonia with fever, dyspnea, hypoxemia
- meningitis with headache, lethargy
- positive serology tests without evidence of localized infection
9
Q
How do you diagnose coccidiomycosis?
A
Blood/fluid culture
- CSF IgG
10
Q
Treatment for coccidiomycosis?
A
Fluconazole or itraconazole
- options in the treatment of mild disease as well as meningitis
11
Q
What OIs are present at the CD4+ count <200 cells/mm3?
A
Pneumocystis jirovecii pneumonia (PCP)
Mucocutaneous candidiasis
12
Q
What is the clinical presentation of PCP?
A
- Usually present with Dyspnea, non productive cough and hypoxemia
- CXR shows diffuse bilateral symmetrical interstitial infiltrates with a ground glass pattern
13
Q
How do you diagnose PCP?
A
- Giemsa, Diff-Quik, and Wright stains for trophoizite
- Gomori methenamine silver, toluidine blue, and cresyl violet are used to stain the cyst wall
- Beta D glucan
- PCR
14
Q
Describe the management of PCP?
A
All HIV positive patients, including pregnant women, must be started on TMP-SMX for chemoprophylaxis when their CD4+ countis less than 200 cells/mm
- Alternative prophylactic medications include
i. dapsone
ii. dapsone plus pyrimethamine plus leucovorin
iii. atovaquone
iv. aerosolized pentamidine
15
Q
What is the treatment for PCP?
A
PCP is treated with TMP-SMX Other drugs include: i. dapsone ii. TMP iii. clindamycin plus primaquine or IV pentamidine iv. atovaquone suspension
16
Q
What cause mucocutaneous candidiasis?
A
candida albicans
17
Q
Describe the clinical presentation of mucocutaneous candidiasis?
A
- Oropharyngeal infection presents as painless, creamy white plaque like lesions
- Angular chelosis may occur
- Esophageal candida presents with odynophagia and retrsosternal burning
18
Q
Diagnosis of mucocutaneous candidiasis?
A
- potassium hydroxide
2. endoscopy
19
Q
Treatment for mucocutaneous candidiasis?
A
Oral fluconazole
20
Q
What OI is present at CD4+<150 cells/mm3?
A
Histoplasma capsulatum
21
Q
Describe the clinical presentation of acute pulmonary histoplasmosis?
A
fever, myalgia, chills, headaches, and a non-productive cough.
- severe cases : lymphadenopathy, hepatosplenomegaly, mucocutaneous ulcers of the nose, mouth, tongue
22
Q
Describe the clinical presentation of chronic pulmonary histoplasmosis?
A
reactivation process in HIV patients
23
Q
Diagnosis of histoplasmosis?
A
detecting Histoplasma antigen in blood or urine for disseminated infections
- Culture is slow; bone marrow, blood, respiratory secretions
24
Q
Management of histoplasmosis?
A
- IV liposomal amphotericin B isused in severe disseminated histoplasmosis
- Duration of treatment is 2weeks followed by 3 days of oral itraconazole 200 mg 3 times daily and finally 200 mg daily for at least 12 months
25
What OI is present at CD4+ count <100 cells/mm3?
Cryptococcus neoformans
| Cryptosporidiosis
26
Clinical presentation of cryptococcosis?
- Can manifest as subacute meningitis or meningoencephalitis
- Fever, malaise, headache are the common presenting symptoms
- Pulmonary cryptococcosis can present with fever, chest pain, cough, dyspnea, positive blood cultures
27
Diagnosis of cryptococcosis?
antigen in CSF and Serum
Culture
Indian ink stain
28
Management of cryptococcosis?
Combination therapy of flucytosine and amphotericin B
- fluconazole and flucytosine
Duration of combination therapy is 2 weeks,
fluconazole 400 mg daily for 8 weeks (condolidation phase)
Following this, the dose is reduced to 200 mg daily for 1 year
29
Cause of cryptosporidiosis?
the protozoa, Cryptosporidium
30
Clinical presentation of cryptosporidiosis?
Chronic diarrhea
| Watery diarrhea with abdominal pain, nausea and vomiting are common.
31
Diagnosis of cryptosporidiosis?
oocytes in stool or tissue by direct immunofluorescence or enzyme-linked immunosorbent assay
32
Treatment of cryptosporidiosis?
ART must be initiated in patients with a goal to restore CD4+ cells count greater than 100 cells/mm^3 as this leads to the resolution of clinical cryptosporidiosis
33
Clinical presentation of herpes simplex virus?
oropharyngeal disease, keratoconjunctivitis, genital herpes, eczema herpeticum, encephalitis, and neonatal herpes
34
Diagnosis of HSV?
HSV DNA PCR
viral culture
HSV antigen detection
35
Causes of microsporidiosis?
They are ubiquitous organisms, predominantly zoonotic or waterborne
35
Causes of microsporidiosis?
They are ubiquitous organisms, predominantly zoonotic or waterborne
36
Diagnosis of microsporidiosis?
calcofluor white and Uvitex 2B
37
Treatment for microsporidiosis?
ART must be initiated in patients with a goal to restore CD4+ cells count over 100 cells/mm^3 as this leads to the resolution of clinical microsporidiosis
38
Clinical presentation of JC virus infection?
progressive multifocal leukoencephalopathy (PML)
characterized by focal demyelination
weakness in one extremity to hemiparesis, aphasia.
Optic nerves are never involved, and it rarely affects the spinal cord
mass effect from the PML lesions
Fever and headaches are not typical and may suggest a concomitant opportunistic infection
39
Treatment for JC virus?
no definitive treatment available for JCV. Initiation of ART is mainstay treatment
40
Diagnosis of JC virus?
clinical and neuroradiologic clue
MRI findings of white matter lesions which are hyperintense (bright) on T2-weighted images and hypointense (dark) on T1-weighted sequences,
PCR can be utilized to detect JCV DNA in CSF.
41
OI present at CD+ < 50 cells/mm3?
cytomegalovirus
42
Clinical presentation of cytomegalovirus?
The most common manifestation is retinitis
Often unilateral, but ultimately leads to bilateral involvement
colitis, esophagitis, ventriculoencephalitis present.
CMV pneumonitis is not common
43
Diagnosis of cytomegalovirus?
CMV viremia by PCR occurs in both end-organ disease and without an end-organ state
negative IgG level helps to look for an alternate etiology for symptoms.
ophthalmoscopic examination
CMV colitis is diagnosed by the demonstration of mucosal ulcerations on endoscopy or colonoscopy
44
Management of cytomegalovirus?
Oral or IV ganciclovir, IV foscarnet
45
Clinical presentation of Mycobacterium avium complex (MAC)?
can involve any organ and leads to persistent bacteremia and extensive infiltration of the tissues resulting in organ dysfunction
in the lung, nodules and cavitary lesions are common
Other manifestations include pericarditis, soft tissue abscesses, skin lesions, lymph node enlargement, central nervous system lesions, and bone infection
cultures of blood, lymph node, or any other sterile tissues or body fluids
46
Treatment for MAC?
Clarithromycin is the preferred drug of choice and the first agent along with ethambutol
47
Clinical presentation of toxoplasma gondii encephalitis?
Symptoms of fever, confusion, headaches, or motor weakness should be promptly worked up
48
Diagnosis of taxoplasma gondii encephalitis?
Detection of anti-toxoplasma immunoglobulins G
CT or MRI of mass lesions, AND
demonstration of the organisms on brain biopsy is necessary for a definitive diagnosis.
49
Treatment of toxoplasma gondii encephalitis?
prophylactic SXT or “dapsone-pyrimethamine and leucovorin
Acute infections can be treated with a combination of pyrimethamine and sulfadiazine and leucovorin
Alternative drugs include spiramycin, clindamycin, trimethoprim-sulfamethoxazole
50
What causes Bartonellosis?
Bartonella henselae and Bartonella quintana
51
Clinical presentation of Bartonellosis?
Bacillary angiomatosis (BA), and bacillary peliosis hepatitis only present in immunocompromised patients
BA is hematogenously spread, and hence lesions are seen in most organ systems
skin manifestations are the easiest to diagnose
Fever, weight loss, night sweats are common
B. quintana is associated with osteomyelitis and culture-negative endocarditis
52
Treatment of Bartonellosis?
Doxycycline and erythromycin have been used to treat BA, bacteremia, peliosis hepatis, bone infections successfully
Duration of the therapy is usually long and requires treatment for at least 3 months.
CNS infections receive treatment with doxycycline with or without RIF
53
Pathogens that undergo coinfection with HIV?
Syphilis
Hepatitis B
Hepatitis C
Human papillomavirus
54
Prognosis and complications of coinfections?
Prognosis Remains poor
| Management should be multi disciplinary
