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Other Opportunistic Infections Flashcards

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1
Q

What are the phases of infection of herpes viruses?

A

Primary infection
Latency
Reactivation

Immune compromised patients increased risk of worse primary infections and reactivation

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2
Q

What are the three groups of herpes viruses?

A

1 alpha - hsv, VZV. Primary targetcmucoepithelial with latency developing in nerve cells

  1. Beta - cmv, hhv 6 and 7
  2. Gamma - ebv, KSHV (hhv8)
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3
Q

What is the incidence of herpes zoster (shingles) in general population?

A

1.5-3 per 1000 persons per year
More frequently in those over 60 and who are immunocompromised

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4
Q

What is the relative risk of herpes zoster in HIV patients

A

15 or greater compared to age matched hiv zero negative individuals

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5
Q

At what CD4 count are herpes zoster outbreaks more frequent?

A

Cd4 <200-250

Recurrences common - up to 20-30% of cases

Effect of ARVs unclear

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6
Q

Risk of primary zoster infection in HIV positive population?

A

Uncommon due to childhood infections but can result in severe disease with visceral dissemination particularly pneumonitis

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7
Q

How might zoster present in HIV patients?

A

Usually vesicles along single deratome

In HIV can be bullous, haemorrhagic, necrotic and painful

Blisters and crusts usually last 2-3 weeks - necrotic lesions may last up to 6 weeks and heal with severe scarring

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8
Q

Can herpes zoster be part of IRIS?

A

Yes - 2-4 fold increase in risk in first few months of starting HAART. Same presentation as other HIV+ pts.

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9
Q

What is HZO?

A

Herpes zoster ophthalmicus involves ophthalmic division of trigeminal nerve

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10
Q

Symptoms of HZO?

A

Skin lesions
Involvement of conjunctiva, cornea and other eye structures can result in visual loss, keratitis, anterior uveitis, severe post heretic neuralgia, necrotising retinopathy

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11
Q

Presentation of disseminated herpes zoster?

A

Multi focal leukoencephalitis, vascularised with cerebral infarcts, myelitis, ventriculitis, optic neuritis, meningitis, focal brainstem lesions

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12
Q

Can herpes zoster CNS disease occur in absence of neurological lesions?

A

Yes
Should always be considered in patients presenting with neurological disease especially if advanced immune deficiency

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13
Q

How is VZV diagnosed?

A

Usually skin lesions diagnosed in clinical appearance

VZV antigen testing using fluoroscein-conjugated monoclonal antibodies to confirm presence of VZV antigens

Culture less sensitive but may allow for aciclovir resistance to be detected

PCR rapid and more sensitive than culture

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14
Q

What is found on CSF testing for VZV?

A

Pleocytosis
Mildly raised protein
Positive PCR for VZV DNA - absence of this does not exclude

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15
Q

What is the treatment of primary varicella?

A

IV aciclovir 5-10mg/kg TDS for 7-10 days
More prolonged treatment courses may be required until all lesions are healed

If no evidence of visceral involvement can switch to 800mg po 5x day when afebrile

In patients with high CD4 counts oral aciclovir may be considered if started within 24hrs

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16
Q

What is the treatment of herpes zoster?

A

Begin within 72hrs rash

Localised dermatomal illness 800mg 5x day

If severe cutaneous disease or disseminated infection admit to hospital for iv aciclovir 10mg/kg tds for 10-14 days
Start on ART or optimise to improve immune deficiency

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17
Q

How to tell if patient is resistant to aciclovir?

A

Failure to respond to treatment
Has been reported in patients with advanced hiv disease
IV foscarnet used instead

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18
Q

What is the relationship between HSV and HIV?

A

Genital HSV2 increases acquisition risk of HIV - doubles risk of becoming infected through sexual transmission

Coinfected individuals are more likely to transmit infection - ? High titres of HIV in genital secretions during HSV2 outbreak

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19
Q

What is the definition of primary genital herpes?

A

First infection of HSV 1 or 2 in an individual with no pre-existing antibodies to either type

Non primary first episode is forst infection of hsv 1 or 2 but person has antibodies to other type

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20
Q

What may be different about primary HSV in immunocompromised person?

A

May not resolve spontaneously but persist with development of progressive, eruptive and coalescing mucocutaneous anogenital lesions

Healing may be delayed beyond 2-3 weeks

Systemic symptoms such as fever and myalgia

Rare severe systemic complications - hepatitis, pneumonia, a sceptic meningitis, autonomic neuropathy

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21
Q

What is the typical frequency of genital HSV recurrences in HIV zero negative population?

A

5 episodes per year for first 2 years and reduce in frequency after

Frequency and severity of outbreaks significantly greater in hiv infected persons with low CD4 counts

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22
Q

How can HSV affect the eye?

A

Keratoconjunctivitis
Acute retinal necrosis

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23
Q

Possible outcomes of

A

Pneumonia
Hepatitis
Oesophagitis
CNS disease

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24
Q

What can HSV infection of CNS cause?

A

Aseptic meningitis (usually a consequence of primary HSV2 infection)
Encephalitis
Myelitis
Radiculopathy

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25
How is HSV diagnosed?
Swabs taken from base of lesion PCR rapid and sensitive Culture less sensitive and requires cold chain 4 degrees
26
How is HSV diagnosed and typed in asymptomatic individuals?
Type specific serology tests detect HSV specific gylcoproteins g1 and g2 which are specific to types 1 and 2 hsv respectively
27
How is HSV encephalitis or meningitis diagnosed?
CSF - PCR of HSV DNA method of choice. Lymphocytosis and elevated protein, low glucose may occur. MRI supportive but not diagnostic Culture not recommended
28
Treatment for orolabial herpes
First or severe recurrences - aciclovir 200-400mg 5x day for 7-10 days (alternatives valaciclovir, famiciclovir) Severe oral mucocutaneous disease 5-10mg/kg every 8hrs IV aciclovir
29
Treatment for genital HSV ?
Aciclovir 400mg 5x day for 7-10 days Alternatively valaciclovir 1g po bd 5-10 days or famiciclovir 250-750 TDS for 10/7 Severe disease or systemic complications - aciclovir 5-10mg/kg iv every 8 hours
30
Dose of aciclovir for HSV suppression
For those with >6 recurrences/year 400-800mg orally two or 3 times a day, three a day in pregnancy Valaciclovir 500mg BD or famciclovir 500mg bd
31
When should suppressive aciclovir for recurrent HSV be stopped?
In hiv-ve discontinuation would happen at 12 months If hiv+ with low cd4 - may delay this, would give episodic tx course to take home to use in event of outbreak
32
Treatment of systemic HSV infection
IV aciclovir 5-10mg/kg every 8 hours for 10-21 days HSV meningitis 10mg/kg every 8 hours HSV encephalitis 10mg/kg every 8 hours for 14-21 days and quantative PCR in CSF may be helpful to monitor response to treatment Low threshold for ICU Involve neurologist
33
What to do if aciclovir resistance suspected?
In any immunocompromised patient developing clinical hsv lesions despite adequate doses of aciclovir should have sample taken for viral culture and antiviral sensitivity. Try increasing dose antivirals and if still new lesions after 5 days - switch - foscarnet or cidofovir
34
What is the most common cause of aciclovir resistance?
Mutation affecting gene encoding viral thymidine kinase (TK) - the enzyme that phosphorylates aciclovir in HSV affected cells Foscarnet and cidofovir do not require tk dependant phosphorylation
35
Via where does MAC infection occur?
Respiratory and GI tracts
36
Can MAC be passedmperson to person?
No
37
In whom does disseminated MAC typically occur
<50 cells/uL
38
Symptoms of DMAC
Fever, night sweats, fatigue, weight loss, anorexia and diarrhoea
39
Signs of DMAC
Hepatomegaly Lymphadenopathy Anaemia Leukopenia Elevated alk phos Hypoalbuminaemia
40
Radiological features of DMAC
Hepatosplenamegaly and infra-abdominal lymphadenopathy
41
How is DMAC diagnosed?
Culture in blood or bone marrow aspirate or fluid from a STERILE SITE In the absence of radiological evidence non sterile site positive eg stool or sputum doc or stool not enough to be diagnostic
42
Is culture from non sterile site without supporting radiology enough to warrant anti mycobacterial tx for DMAC?
No. Although may start tx cultures pending.
43
How many blood cultures needed to confirm MAC?
One will pick up 91%, two increases rate to 98% No more than two needed
44
How quickly can you get a mycobacteria result using radiometric detection system?
6-12 days blood 15-20 days solid media DNA probes can identify species within 2hrs PCR a rapid cost effective alternative Stains on biopsy specimens may demonstrate acid fast organisms or granulomata weeks before positive blood cultures
45
Preferred culture method for MAC
Lysis of peripheral blood leukocytes to release intracellular mycobacteria followed by inoculation on to solid media (eg Löwenstein-Jensen, middlebrook 7h11 agar) or into radiometric broth.
46
Treatment for DMAC
Macrolide and ethambutol with or without rifabutin
47
Which macrolide to use in treatment for DMAC
Clarithromycin better studied and more rapid clearance of MAC from blood 500mg BD Azithromycin fewer drug drug interactions and better tolerated
48
How is macrolide resistance in MAC treatment detected?
Return of clinical symptoms Increased bacterial counts Hence addition of at least one additional class recommended
49
When should rifabutin be added to DMAC treatment?
Patients with advanced immunosuppression (CD4<25), marked symptoms or inability to construct effective ARV regimen
50
Dose of rifabutin for DMAC treatment?
Max dose 300mg/day Or 450mg/day if given with EFV Or 150mg 3x week if given with ritonavir Due to risk of uveitis
51
What should be given if cannot tolerate first line regime?
Fluoroquinolones, amikacin Clofazimine should not be used - excessive toxicity and higher mortality rates
52
When should ARVs be started in DMAC,?
Simultaneously or within 1-2 weeks Continue if already on
53
When should DMAC therapy be stopped?
At least 3 months therapy Asymptomatic with negative blood cultures 6 weeks after incubation VL <50 on two consecutive occasions CD4 >100 at least 3 months apart If these are never met continue life long
54
What constitutes treatment failure for DMAC?
No clinical response and mycobacteria isolated from cultures after 4-8 weeks of treatment to which patient has been adherent
55
Treatment options if treatment failure for DMAC?
A new combo At least 2 drugs which the isolate is susceptible to Often keep ethambutol as facilitates penetration of other agents Eg rifabutin if not used previously, cipro, levo, linezolid, amikacin
56
Primary prophylaxis DMAC
Azithro 1250mg weekly for those with CD4 <50
57
When can primary prophylaxis for DMAC be stopped?
Viral load <50 CD4 >50 for at least 3/12 (Pierce study - almost all MAC cases occurred at cd4 <50)
58
How does MAC IRIS present?
Regional lymphadenopathy, liver lesions, bone lesions, hypercalcaemia Self limiting but can be severe
59
Treatment options for MAC IRIS
Oral pred 20-40mg /day for 4-8 weeks IL2 and GMCSF used in small number of patients Leukotriene inhibitors used in tb associated IRIS refractory/intolerant of steroids FNA of pus
60
Presentation of m.kansasii
Pulmonary - fever, cough, pulmonary cavities or infiltrates, focal pulm signs on exam
61
Diagnosis m.kansasii
Repeated isolation and compatible clinical and radiological picture (Can be a commensal)
62
Treatment of m.kansasii
Rifamycin plus ethambutol plus isoniazid for 12/12 Same for disseminated and pulmonary disease
63
Causes of PUO
Infection or lymphoma HIV rarely a cause of fever
64
Investigation of PUO
Travel hx important - lifetime - new and reactivated tropical infections not uncommon Consider non-HIV related illnesses if good counts IRIS
65
Specific features of bartonellosis
Bacillary angiomatosis - cutaneous lesions that can be friable, red, vascular and exophytic proliferating e lesions, non descript applies or subcut nodules Difficult to distinguish from KS PCR of blood or biopsy Erythromycin or doxycycline
66
Common diagnoses following the investigation of HIV associated PUO
Infection DMAC Mycobacterium tuberculosis Bacterial infections Leishmania Pneumocystic Jirovecii pneumonia Histoplasmosis CMV end organ disease Viral (hepatitis B, C, herpes virus, adenovirus) Neoplastic/Lymphoproliferative Lymphoma Kaposi's sarcoma Castleman's disease
67
Why are PLWH more at risk of Candida infection?
Immunological response against Candida at gastrointestinal mucosa or skin surface is dependant on T helper 17 cells - this T cell subset is disproportionally depleted during early stages of HIV associated T cell decline Vulvovaginal candidiasis less influenced by Th17 cell function and more by dye iOS is and alterations in vaginal pH
68
Why might PLWH on cART still be susceptible to Candida?
Impaired T cell responses to Candida can continue even after 2 years of therapy
69
Clinical risk factors for candidiasis other than immunosuppression in PLWH?
IVDU, TB

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