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year 4 CDM 2 > Case 13: AID's, Syphilis and TB > Flashcards

Case 13: AID's, Syphilis and TB Flashcards

1
Q

Complications of HIV: CD4 count <50

A
  • CMV retinitis
  • Mycobacterium avium-intracellulare infection
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2
Q

How to distinguish oral hairy leukoplakia and oral candidiasis

A
  • oral hairy leukoplakia cannot be scraped away
  • oral hairy leukoplakia is painless
  • oral hairy leukoplakia is usually on the sides of the tongue
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3
Q

Stages of HIV

A
  • Stage 1: Asymptomatic, persistent generalised lymphadenopathy. CD4 >500
  • Stage 2 (minor symptoms): folliculitis, shingles, herpes. CD4 350-500
  • Stage 3 (moderate symptoms): oral candidiasis, TB, oral hairy Leukoplakia. CD4 200-350
  • Stage 4 (AID’s defining illness): Kaposi sarcoma, Cryptococcus, Toxoplasmosis. CD4 <200
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4
Q

Oral candidiasis

A
  • Other causes: recent antibiotics, steroid inhaler use
  • Treatment: oral fluconazole
  • In advanced stages can cause dysphagia and be picked up on upper GI endoscopy (oesophageal candidiasis)
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5
Q

AID’s defining illnesses

A
  • pneumocystis pneumonia
  • Kaposi’s sarcoma
  • progressive multifocal leukoencephalopathy
  • infections with non-tuberculosis mycobacteria e.g. avium complex
  • retinitis or colitis due to reactivated CMV
  • cerebral toxoplasmosis
  • primary CNS lymphomas
  • cryptococcal meningitis
  • TB meningitis
  • non-Hodgkin lymphoma
  • cervical cancer
  • persistent cryptosporidiosis diarrhoea
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6
Q

Pneumocystis pneumonia (PCP)

A
  • Causative agent: Pneumocystis jiroveci (fungus)
  • Presents: exertional SOB, dry cough, fever, weight loss
  • Treated with high dose co-trimoxazole and steroids. Prescribe HAART in 2 weeks
  • Prophylaxis for PCP: Co-trimoxazole
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7
Q

Investigations for PCP

A
  • Bedside: measure oxygen sats whilst patient is exerting, if quickly desaturates suggests PCP
  • Diagnosis: CXR, deep sputum sample (induced or bronchoalveolar lavage) for staining, PCR and fluoroscopic examination
  • CXR: bilateral hilar interstitial infiltrates with bat wing distribution (no dense consolidation)
  • BAL: PJP oocytes and PCP cysts
  • Investigations: HIV test, ECG, ABG, D-dimer
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8
Q

How does Kaposi sarcoma present

A
  • Skin lesions: purple/ brown raised lesions, usually on lower limbs or head and neck. May affect mucosal surfaces in oropharynx causing small lesions on hard palate
  • Visceral lesions: may involve bronchial walls causing dyspnoea and haemoptysis. may involve GI tract causing haematemesis, dysphagia, bowel obstruction and meleana
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9
Q

Kaposi sarcoma: diagnosis and treatment

A
  • Purple-brown lesions on lower limbs or head and neck
  • Bronchial wall lesions: haemoptysis and dyspnoea
  • GI tract: haematemesis, dysphagia, bowel obstruction and melaena
  • Diagnosis: skin biopsies, investigate visceral lesions with OGD/colonoscopy
  • Treatment: may regress with antiretroviral therapy. Visceral lesions or extensive skin disease may require chemotherapy
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10
Q

Cerebral Toxoplasmosis: presentation and imaging

A
  • Causative agent: Toxoplasma gondii (protozoan parasite)
  • Cats are hosts can get it from a litter box or faecal-oral
  • Imaging: causes space occupying lesions to form which are concentrated around the basal ganglia. Rim enhances with IV contrast
  • Presents with focal neurology (weakness, jerking) and chronic headache. Can cause ‘glandular fever like picture.’ Causes CNS infection and space occupying lesion
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11
Q

Cerebral Toxoplasmosis: diagnosis and treatment

A
  • contrast enhanced CT head: ring enhancing lesion with surrounding oedema
  • brain biopsy for definite diagnosis (high risk procedure so trial treatment first and see if this lesions decrease in size after two weeks)
  • Treatment: Sulphadiazone, Pyrimethamine and folinic acid and started on antiretroviral treatment
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12
Q

TB meningitis

A
  • CSF protein is massively elevated
  • Diagnosed: analysis of CSF including ZN stain
  • IGRA: test for latent TB and TB exposure
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13
Q

Cryptococcal meningitis

A
  • Diagnosed: analysis of CSF including India ink stain (shows encapsulated yeast), PCR and culture
  • CSF: protein slightly low and glucose slightly elevated but not as much as bacterial meningitis, its largely lymphocytic
  • Presentation: headache is not always accompanied by fever or neurology
  • Treatment: Amphotericin B and flucytosine followed by fluconazole
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14
Q

Restarting HAART

A
  • Antiretroviral therapy be commenced 5 weeks after cryptococcal meningitis
  • ART should be started for most opportunistic infections within 2 weeks
  • If ART is started too quickly in Cryptococcal meningitis there is a risk of IRIS (immune reconstitution inflammatory syndrome) which occurs as a failing immune system recovers and starts to mount more exaggerating inflammatory responses. Manage with NSAID’s
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15
Q

HIV: Cryptosporadiun

A
  • Diagnosis: stool culture
  • Persistent Cryptosporidium infection is an AID’s defining illness
  • Type of organism: Protozoan parasite
  • Infection by drinking contaminated water
  • Treatment: Antiretroviral therapy
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16
Q

When to test for HIV

A
  • Universal testing: TOP/ GUM/ ante-natal/ drug dependency/ TB/ hepatitis/ lymphoma services
  • AIDS defining illness: TB, PCP, Cerebral Toxoplasmosis, Cryptococcal meningitis, PML, Kaposi sarcoma, NHL, Cervical cancer, CMV retinitis
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17
Q

Syphilis

A
  • A sexually transmitted disease caused by Treponema pallidum which is a Spirochaete
  • Transmitted through minor abrasions at genital skin or mucous membranes: sexual contact (only in early syphilis), sharing of needles, vertical
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18
Q

Syphilis: contact tracing/Partner notification

A
  • done for all STI’s, is voluntary. Can be done by patient or clinic (provider referral).
  • Syphilis: Primary (last 3 months), Secondary/Early latent (past 2 years or 3 months before last negative test)
  • Management of syphilis contacts: test and empirical antibiotics or test now and at end of 12 week window period

Risk factors: MSM, HIV infection, IV drug use

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19
Q

Syphilis stages

A
  • Primary syphilis: chancre (ulcer), resolves after 3-6 weeks. Polymorphonuclear leukocytes infiltrate the lesion
  • Secondary syphilis: due to haematogenous spread of bacteria causing endarteritis obliterans (inflammation of the tunica intima). Causes rash and systemic symptoms. 15-40% of untreated secondary syphilis progress to late. Resolves due to Macrophages
  • Late syphilis: Neurosyphilis, Gummatous syphilis, cardiovascular syphilis
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20
Q

Types of late syphilis

A
  • Neurosyphilis: chronic inflammation of the meninges. Spinal cord involvement causes tabes dorsalis. Causes paraesthesia, personality change, loss of bladder control
  • Gummatous syphilis: presence of granulomas, consistent with a cellular hypersensitivity reaction
  • Cardiovascular syphilis: due to vasculitis of the vasa vasorum. Can cause necrosis of the tunica media leading to aortic aneurysms. Narrowing of the coronary ostia causes aortic regurgitation
  • Progressive dementia (general paresis)
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21
Q

Primary syphilis

A
  • Painless chancre: highly infectious, hard anogenital ulcer with local lymphadenopathy, usually painless. Occurs at site of infection i.e. mouth, anus or vagina
  • Develops 3 weeks post exposure and resolves within 3-6 weeks
22
Q

Secondary syphilis

A
  • 6 weeks - 6 months post infection with systemic involvement.
  • 2-6 weeks after primary infection
  • Symmetrical maculopapular rash: on trunk, face, palms or soles, might be scaly not itchy
  • Condylomata lata: moist, warty lesions near genitals
  • Constitutional symptoms: fever, malaise, myalgia, fatigue and arthralgia
  • Other symptoms: Lymphadenopathy, Tonsilitis, Splenomegaly, Hepatitis, alopecia
23
Q

Latent syphilis

A
  • Asymptomatic infection following untreated primary or secondary syphilis
  • Early latent syphilis: confirmed infection in the absence of any current clinical effects, <2 years of infection. Can transmit infection sexually and vertically. Can have recurrence of secondary syphilis. Can be treated with single dose on penicillin
  • Late latent syphilis: >2 years of infection. Only vertical transmission. Requires longer treatment courses
24
Q

Ocular syphilis

A
  • Uveitis: painful red eye
  • visual disturbance (floaters/ flashing lights)
  • may cause blindness
  • Can occur at any stage
25
Q

Tertiary or late syphilis

A
  • > 2 years post infection (typically 15-40)
  • 15-30% of untreated patients will go on to develop the complications of tertiary syphilis.
  • Tertiary latent syphilis: serological confirmation of infection in the absence of clinical features
  • Gummatous, neurosyphilis
  • Cardiovascular: Aortitis → Aneurysm, aortic regurgitation
26
Q

Syphilis Investigations

A
  • Skin, genital, eye and neurological exam
  • Referral to a GUM specialist for a full sexual health screen (including HIV)
  • Primary syphilis (direct detection): Dark field microscopy (Spirochete), PCR
  • Treponemal tests: show exposure to syphilis, positive for life so cant see response to treatment or re-infection. For example EIA, TPA, IgM
  • Non-treponemal tests: Determine disease activity and show response to treatment. For example, RPR and VDRL
  • Contact testing
27
Q

Syphilis Management

A
  • Referral to GUM or other specialist sexual health services
  • Avoid all sexual contact until successful treatment has been confirmed
  • Benzathine benzylpenicillin IM
  • Alternative: Doxycycline 14 days for early syphilis, 28 days for late syphilis
  • In pregnancy: Erythromycin 500mg/6h PO
  • Follow up: at 3, 6, and 12 months in specialist GUM clinic
  • Monitoring efficacy: 4 fold decrease in non-treponemal test titre
28
Q

Duration of Syphilis treatment

A
  • Early syphilis (primary, secondary, early latent)- single dose
  • Lat syphilis (late latent, unknown, tertiary)- 3x weekly dose
  • Ocular and neurosyphilis- daily for 10-14 days
29
Q

Jarsich-Herxheimer reaction

A
  • Triggered by penicillin treatment: good sign as shows infection is being treated
  • Acute onset fever, muscle ache, flushing, rash and palpitation
  • Manage conservatively: steroids started prior to treatment for prevention in neurosyphilis
30
Q

How neurosyphilis will present (6%of untreated patients)

A
  • Meningovascular: cranial nerve palsies e.g. decreased vision, stroke
  • General paresis of insane: dementia, psychosis
  • Tabes dorsalis: loss of proprioception, vibration sense, incontinence and ataxia
  • Meningitis, altered behaviour, stroke secondary to vasculitits
  • Asymptomatic: anormal CSF findings
  • Can occur at any stage
31
Q

Congenital syphilis

A
  • Adverse pregnancy outcomes: miscarriage, stillbirth, pre-maturity
  • Early congenital syphilis: Hepatosplenomegaly, Lymphadenopathy, desquamating rash, severe anaemia, jaundice. Significant mortality
  • Late congenital: Hutchinson’s triad (pegged teeth, keratitis, sensorineural deafness), saddle nose, bone and joint deformity, developmental delay
  • All pregnant women have antenatal screening for syphilis
32
Q

Late syphilis Gummatous

A

Granulomas in skin, mucosa, bone, joints and viscera such as lung and testis. These are rubbery lesions with a necrotic centre and may gradually replace normal tissue.

33
Q

TB

A
  • A disease caused by members of the Myobacterium tuberculosis complex.
  • Typically affects the lungs and is transmitted via airborne droplets. Bacilli (rod like shape). Tends to spread in overcrowded living and prisons
  • Organisms: M.tuberculosis (most common), M.bovis, M.africanum (central/west Africa)
  • Called Acid Fast Bacilli (AFB)
34
Q

TB: facts and figures

A
  • 10% develop the active infection. The remaining 90% contain the disease and will develop latent TB
  • 20-30% of household contacts of infectious people become infected with TB
  • Lifetime risk of reactivation of latent TB: 10% (higher if HIV, immunosuppressed or comorbidities)
35
Q

Ziehl Neelson stain: TB

A
  • Special stain has to be used as TB cell wall contains mycolic acid (a high molecular weight lipid)
  • Appears as a red colour against a light blue background
  • Fluorescent staining: appear bright green against a dark background making it easy to spot
36
Q

Risk factors for TB

A
  • Immunosuppression: HIV, Immunosuppressant drugs, TNFα inhibitors.
  • Diabetes mellitus, end-stage renal disease.
  • Previous lung disease (silicosis).
  • Smoking.
  • Drug abuse, alcoholism.
  • Malnutrition, poverty.
  • Certain living conditions (prisons, homeless shelters).
  • Occupational (hospitals).
37
Q

Pathophysiology of TB

A

Inhalation of Mycobacterium tuberculosis via droplet → deposition in the lungs (alveoli) → engulfed by alveolar macrophages → proliferates in macrophages → release → immune response.

38
Q

TB: stages of disease

A
  • When infected an immune response occurs and the Primary complex forms. You then get clinical symptoms or containment
  • Primary disease: active disease 1-2 years after infection
  • Latent infection: Can either get resolution, persistent latent infection or reactivation with Post-primary tuberculosis
  • If you have resolution and re-infection that will be Post primary TB
  • Reactivation: occurs when the immune system is suppressed
  • Miliary tuberculosis: disseminated and severe disease
39
Q

TB transmissibility facts

A
  • Only 20-30% of household contacts are infected
  • Immunosuppression i.e. HIV increases risk
  • Primary TB: (only 5-10% of people): more likely in infancy, adolescence or old age
40
Q

Symptoms or primary or re-activated TB

A
  • Constitutional: Fever (gradual and low grade), Night sweats, Weight loss, anorexia and malaise
  • Pulmonary tuberculosis: most common: cough (dry then productive- yellow +/- blood)
  • Pleural TB: pleurisy
  • Weeks to months for symptoms to occur
  • Extrapulmonary tuberculosis: less common
41
Q

Pulmonary TB

A
  • Dyspnoea,cough (+/-haemoptysis), chest pain.
  • Cough: over 2 to 3 weeks; initially dry, later productive. (yellow sputum)
  • Chest examination: crackles, bronchial breath sounds, or maybe normal.
42
Q

Clinical signs of TB O/E

A
  • often normal but there may be
  • effusion
  • crackles
  • lymphadenopathy
  • clubbing (rare)
  • hepatomegaly
  • CNS signs in TB meningitis
  • abdo masses
  • skin manifestations (erythema nodosum)
43
Q

Extrapulmonary TB

A
  • Pleura, bones/joints, lymphatic system, liver, central nervous system, urogenital tract, gastrointestinal tract, and the skin.
  • Symptoms based on the organ-involvement (enlarged lymph node, pleuritic chest pain, skeletal pain, urinary symptoms, abdominal swelling, abdominal pain, headache).
  • Spinal pain in spinal tuberculosis (Pott’s disease of the skin)
  • CNS i.e. TB meningitis
  • Miliary TB: where TB ruptures and spreads
44
Q

Latent TB

A
  • Lifetime risk of reactivating TB is about 10% and is highest in first two years
  • TH1 response forms caseating granulomas which causes containment.
  • Risk factors: immunosuppression, age and frailty and co-morbidities
45
Q

Latent TB investigations

A
  • Tuberculin skin test (TST) or interferon-gamma release assays (IGRAs): for latent TB
  • IGRA is preferred with history of BCG vaccine. For example, Quantiferon test
  • Dont use tests alone to exclude diagnosis
  • TST: tuberculin is injected into arm measure diameter after 48-72hr. (Mantoux test)
  • IGRA: blood test to measure levels on interferon-y
46
Q

TB investigations- active pulmonary infection

A
  • Chest x-ray, threesputum samples obtained for microscopy, culture, sensitivity and NAAT.
  • If unable to produce sputum spontaneously induce with nebulised saline (airway irritant) or bronchoalveolar lavage
  • Acid-fast stain (Ziehl-Neelsen stain) identifies the bacilli: AFB smear +
  • Sputum culture (gold standard): takes 4-8 weeks
  • Sputum: NAAT: Can detect drug resistance and allows rapid diagnosis
  • CT and bronchoalveolar lavage (BAL): if CXR shows nothing
47
Q

MoA of TB drugs

A
  • Ethambutol: does not kill bacterial but prevents drug resistance and replication
  • Isoniazid: kills rapidly dividing organisms
  • Rifampicin: kills rapidly dividing organisms and persisters
  • Pyrazinamide: kills intracellular organisms taken over by macrophages and lymphocytes
48
Q

Non diagnostic tests for TB

A
  • Aspirate or biopsy lymph nodes, pleural fluid, ascites, organs, pus, urine or CSF for microscopy, culture and sensitivities. Especially if unable to produce sputum
  • Lumbar puncture: for TB meningitis
  • Pleural fluid: lymphocytes predominant on cytology, exudate on lights criteria
  • Pleural biopsy or lung biopsy: if other testing is not diagnostic
  • Whole genome sequencing: to see if sensitive to TB drugs
  • Endobronchial US and fine needle aspiration/biopsy of lymph node
  • Routine bloods, HIV screen
49
Q

Stains and cultures for TB diagnosis

A
  • Solid or liquid culture: to confirm species. Medium for TB solid culture- Lowenstein Jenson (LJ)
  • TB identification: whole genome sequencing (can identify outbreaks in community- by matching genomic profiles) and PCR (quicker can identify resistance). Identifies the bacteria and tests for antibiotic susceptibility
50
Q

TB: CXR

A
  • Primary: hilarlymphadenopathy effusion, pulmonary infiltrates, calcification.
  • Reactivation: upper lobe cavitary lesion with mediastinal adenopathy
  • thick walled cavities/ cavitating consolidation
  • nodular tree in bud pattern
  • Necrotic adenopathy
  • Disseminatedmiliary tuberculosisgives an appearance ofmillet seedsuniformly distributed across the lung fields.

year 4 CDM 2 (39 decks)

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