Infectious Diseases Flashcards

1
Q

What are the Baseline investigations for all patients newly diagnosed with HIV?

A
  • Confirmatory HIV test: HIV ELISA
  • Serum HIV rapid test/ HIV non invasive test
  • CD4 count
  • HIV viral load (serum RNA)
  • HIV resistance profile
  • Serum western blot
  • HLA B*5701 status
  • Serology for syphilis, hepatitis B (sAg, cAb, sAb), hepatitis C, hepatitis A
  • Toxoplasma IgG, measles IgG, varicella IgG, rubella IgG
  • Other bloods: FBC, U&Es, LFTs, bone profile, lipid profile
  • Schistosoma serology (if has spent >1 month in sub-Saharan Africa)
  • Women: pregnancy test, annual cervical cytology
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2
Q

How does HIV present?

A
  • Fever, night sweats > 1 month
  • Skin rashes and post inflammatory scars
  • Weight loss
  • Oral candidiasis
  • Diarrhoea > 1 month
  • TB
  • Karposi’s sarcoma
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3
Q

What additional testing may be required on samples of bodily fluids or tissues for suspected HIV patients?

A
  • TB and MAI culture
  • Fungal culture and PCR, fungal stains
  • Cryptococcal antigen (CRAG - commonly performed in CSF if serum CRAG positive)
  • Toxoplasma PCR
  • Viral PCR (e.g. EBV, CMV, HSV, VZV, JC virus)
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4
Q

What are the RFs for HIV?

A
  • Affected country
  • IVDU
  • Unprotected sex
  • Perc. needle prick
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5
Q

How is HIV treated?

A
  • No cure
  • ARVs - NRTI - tenofovir, abacavir, NNRTI, protease inhibitors of integrase inhibitor
  • Patients with low CD4 counts:
    • PCP prophylaxis (if CD4<200) - Co-trimoxazole 480mg PO OD
    • if CD4 <50 - Azithromycin 1250mg PO once weekly - protect against MAI
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6
Q

What measures should be taken for patients with low CD4 counts?

A
  • If CD4<200 - Co-trimoxazole 480mg PO OD - prophylaxis against PCP.
  • If the CD4 is <50 Azithromycin 1250mg PO once weekly - should also be given to protect against MAI
  • CD4 <50 should - Ophthalmology with dilated fundoscopy to look for evidence of intra-ocular infections such as CMV retinitis
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7
Q

What vaccinations should HIV patients be given?

A
  • Hepatitis B
  • Pneumococcal
  • Influenza yearly
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8
Q

What are some of the complications of HIV and what pharmacological agent can deal with this?

A
  • TB: t: RIPE
  • Karposi sarcoma;
  • CMV/ CMV retinitis: ganiclovir
  • Pneumocystic Jiroveci: co-trimoxazole
  • Oral/ oesophageal candidiasis: fluconazole
  • Meningoencephalitis
  • Chronic meningitis: cryptococcus neoformans: amphotericin
  • MAI: Mycobacterium avium infections
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9
Q

How is HIV transmitted?

A

Blood, sexual fluids, and breast milk

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10
Q

What is the pathophysiology of HIV?

A
  • HIV binds, via its gp120 envelope glycoprotein, to cd4 receptors on helper t cells, monocytes, and macrophages
  • These ‘CD4 cells’ migrate to lymphoid tissue where the virus replicates, producing billions of new virions.
  • These are released, and in turn infect new cd4 cells.
  • As infection progresses, depletion or impaired function of cd4 cells leads to ↓immune function.
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11
Q

What is used for PEP HIV?

A
  • 1st-line pep6 in uk - Truvada® (tenofovir/emtricitabine)
  • Raltegravir for 28 days
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12
Q

How does HIV present?

A
  • Fever
  • Lymphadenopathy
  • Rash
  • Cough/SOB
  • Diarrhoea
  • Abdominal pain
  • Dysphagia
  • ↑Liver enzymes
  • AKI
  • Headache/seizures/focal neurology
  • Eye disease
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13
Q

What are some of the opportunistic infections in HIV and how are they treated?

A
  • Pneumocystis jirovecii - progressive sob on exertion, malaise, dry cough. Haemoptysis and pleuritic pain rare. co-trimoxazole + prednisalone
  • Tuberculosis - RIPE - rifampacin, isoniazid 300mg/ day
  • Oral Candidiasis
  • CMV Retinitis
  • CMV
  • Cryptosporidium: acute or sub-acute non-bloody, watery diarrhoea. Also cholangitis, pancreatitis
  • Kaposi’s sarcoma: cutaneous or mucosal lesions: patch, plaque, or nodular. Visceral disease less common
  • Lymphoma
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14
Q

What things should be considered when assessing patients with infection?

A
  1. Evidence
  2. Severity
  3. Patient factors
  4. Micro organisms
  5. Antimicrobial therapy
  6. Route of administration
  7. Any other treatment
  8. Risk of transmission to others
  9. Planning follow up and discharge
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15
Q

What questions should be asked for those with a fever in a returned traveller?

A
  • Geographic region of travel
  • Travel and duration
  • Careful documentation
  • Types of accomodation + rural vs urban stays
  • Recreational activities + exposures
  • Food and water consumed
  • Sexual history, sexual exposure while abroad.
  • PMH and predisposition to infection
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16
Q

What infectious diseases do you expect in the following time frames?

  • 0-10 days
  • 10-21 days
  • >21 days
A
  • 0-10 days: Dengue, rickettsia, viral
  • 10-21 days: Malaria, typhoid, primary HIV infections
  • >21 days: Malaria, chronic bacterial infections, TB, parasitis infections (helminths, protozoa)
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17
Q

What pre-travel immunizations and chemoprophylaxis should be given/ noted in a history?

A
  • Vaccination: Hep A, B, typhoid, tetanus, childhood vaccinations (e.g. MMR) + yellow fever and rabies
  • Malaria chemoprophylaxis (as directed).
  • Personal protective measures e.g. insect repellent and bed-net use
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18
Q

What should be examined in clinical examination?

A
  • Vital signs: HR
  • Skin:
    • A maculopapular rash
    • Rose spots
    • Necrotic ulcer
    • Petechiae, ecchymoses, haemorrhagic lesions
  • Eyes
  • Splenomegaly
  • Neurological system
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19
Q

What do each of the things examined in clinical examination indicate?

A
  • Vital signs: HR
  • Skin:
    • A maculopapular rash: dengue fever, leptospirosis, rickettsia, infectious mononucleosis (EBV, CMV), childhood viruses (rubella, parvovirus B19), primary HIV infection
    • Rose spots: pink macules, 2 to 3 mm in diameter) on chest or abdomen (typhoid fever)
    • Necrotic ulcer: rickettsia (tick exposure)
    • Petechiae, ecchymoses, haemorrhagic lesions
  • Eyes: conjunctival suffusion - leptospirosis.
  • Splenomegaly: mononucleosis, malaria, visceral leishmaniasis, typhoid fever, brucellosis.
  • Neurological system: fever and altered mental status: meningo-encephalitis
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20
Q

What suggested investigations should be performed in patients with fever from unknown traveller?

A
  • FBC, LFTs, U+E, electrolytes
  • Malaria smears ± antigen detection dipstick: at least 3 times over 24-48 hours
  • Blood cultures x2 (must have biohazard labels/travel documented)
  • Urinalysis (± urine culture)
  • Stool culture +/- stool for ova, cysts and parasites (OCP)
  • CXR
  • HIV, Hep B, Hep C and Syphillis (treponema) serology (white top)
  • Acute serology tube to be saved in lab (white top)
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21
Q

What is malaria?

A
  • Blood protozoa/parasite (plasmodium species) that is transmitted by night-biting Anopheles mosquitoes.
  • P. falciparum results in the most serious illness.
  • Approximately 90 percent of malaria cases originate in Africa.
  • Other common species: P. vivax, P. ovale (mostly SE Asia)
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22
Q

How does malaria present?

A
  • Abrupt onset of rigors
  • High fevers, malaise, severe headache and myalgia, vague abdominal pain, nausea, vomiting.
  • Diarrhea: 25 percent of patients
  • Jaundice and hepatosplenomegaly
  • Bloods: anaemia, thrombocytopenia, leukopenia, and abnormal LFTs
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23
Q

What are the complications of malaria?

A
  • Hypoglycemia
  • Renal failure
  • Pulmonary edema
  • Neurologic deterioration
  • Leading to death
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24
Q

What investigations should be performed for malaria?

A
  • Microscopy of thick and thin blood smear.
  • Rapid diagnostic test (rdt) detection of parasite antigen. If malaria is suspected but blood film is negative: repeat at 12–24h and after further 24h
  • Other: FBC (anaemia, thrombocytopenia), creatinine and urine output (aki), clotting (dic), glucose (hypoglycaemia), ABG/lactate (acidosis), urinalysis (haemoglobinuria).
25
Q

What is typhoid fever?

A
  • Typhoid infection is a faecal-oral transmissible disease caused by the bacterium Salmonella enterica, serotype S typhi.
  • Common in many developing nations in South East Asia, Southern and Central America.
26
Q

What are the symptoms of typhoid fever?

A
  • Most important for diagnosis: dry cough, constipation, fever (stepwise, rising each day with progressive peaks)
  • Other: Fatigue, headache, anorexia
  • Abdominal pain, relative bradycardia (Faget’s sign)
  • Symptoms arise up to 21 days after return
  • Rose spots
  • Diarrhoea (‘pea-soup’)
  • Hepatosplenomegaly
27
Q

What is found on physical examination of typhoid fever?

A
  • Pulse-temperature dissociation
  • Hepatosplenomegaly
  • Rose spots
28
Q

What are the laboratory findings for typhoid?

A
  • Leucopenia
  • Lymphopenia
  • CRP
29
Q

How is typhoid diagnosed?

A
  • Stool, urine, bone marrow, blood cultures
  • Bloods:
30
Q

How is typhoid treated?

A
  • IV Ceftriaxone 2g OD: give to patients who have grown s.typhi from stools
  • Once sensitivities known, can switch to PO Ciprofloxacin 500mg BD, or PO Azithromycin 500mg OD.
31
Q

What is the classical definition of patients with fever unknown origin?

A
  • Temperature > 38 degrees on multiple occasions
  • Illness of >3 weeks duration
  • No diagnosis despite >1 week’s worth of inpatient
32
Q

What are the common causes of pyrexia of unknown origin?

A
  • Infective – tuberculosis, abscesses, infective endocarditis, brucellosis
  • Autoimmune/connective tissue – adult onset Still’s disease, temporal arteritis, Wegener’s granulomatosis
  • Neoplastic – leukaemias, lymphomas, renal cell carcinoma
  • Other – drugs, thromboembolism, hyperthyroidism, adrenal insufficiency
33
Q

What questions should be asked to a patient with pyrexia of unknown origin?

A
  • Chronology of symptoms?
  • Pets/animal exposure?
  • Travel?
  • Occupation?
  • Medications?
  • Family history?
  • Vaccination history?
  • Sexual contacts?
34
Q

What else should be examined in PUO?

A
  • Lymph nodes
  • Stigmata of endocarditis
  • Evidence of weight loss
  • Joint abnormalities
35
Q

What investigations should be performed for PUO?

A
  • Blood: FBC/U+Es/LFTs/bone profile/CRP/clotting, TFTs, multiple sets of blood cultures, LDH, ferritin, B12, folate, immunoglobulins*, autoimmune screen* (RF, ANA, dsDNA, pANCA, cANCA, C3, C4)
  • Micro/virology: HIV, Hepatitis B+C, syphilis, MSU, sputum cultures, malaria films*, atypical pneumonia screen*, viral swabs, CMV+EBV serology, Brucella serology*, Coxiella serology*, ASO titre*, fungal serology/PCR*
  • Imaging: CXR, CT thorax/abdomen/pelvis, transthoracic echo, MR head*, MR spine*, radiolabelled white cell scans*, PET scan*
  • Biopsies*:MC+S, TB culture, histology on all samples. Sites: Bone marrow, lymph nodes, abscesses, liver
36
Q

What is the pathophysiology of TB?

A
  • Caused by infection with Mycobacterium tuberculosis.
  • Transmitted by aerosol inhalation and causes pulmonary infection, then spreads via haematogenous spread to anysite in the body
  • Initial infection can be asymptomatic. Can lie dormant for many years without causing symptoms (latent TB), then reactivate later in life to form active infection.
  • Common for people immigrating to the UK from endemic areas to experience reactivation after their arrival. ? Vitamin D
37
Q

What is active TB?

A
  • Occurs when containment by the immune system (t-cells/macrophages) is inadequate.
  • It can arise from primary infection, or re-activation of previously latent disease.
  • Transmission via inhalation of aerosol droplets containing bacterium. This means only pulmonary disease is communicable.
38
Q

What is Latent TB?

A
  • Infection without disease due to persistent immune system containment
  • Assymptomatic
  • Screening: CXR and measurement of interferon gamma (quantiFERON or T-spot)
39
Q

How is latent TB treated?

A
  • 3 months rifampicin and isoniazid or 6 months rifampicin alone
  • Treatment reduces risk of reactivation needs to be balanced against the risk of hepatotoxicity.
  • Pts > 35 - increased risk of hepatotoxicity. Guidelines advise against treating latent TB in these patients unless they have other risk factors (HIV or work as a healthcare worker)
40
Q

What is quanti-feron and how does it aid diagnosis of Tuberculosis?

A
  • Assesses the amount of interferon gamma released by T cells when they are exposed to proteins found on mycobacteria. Pre-exposed cells release more interferon
  • It does not differentiate between active and latent TB.
  • It is not used to diagnose active TB and can also be negative during infection.
  • Patients with immunosuppression may not release interferon gamma causing false negatives
41
Q

Who is routinely screened for TB?

A
  • Immigrants from high prevalence countries
  • Healthcare workers
  • HIV positive patients
  • Patient starting on immunosuppression
42
Q

What are the common symtoms of active TB?

A
  • Non-resolving cough
  • Unexplained persistent fever (low or high grade)
  • Drenching night sweats
  • Weight loss
43
Q

What are some of the signs of active TB?

A
  • Clubbing
  • Cachexia
  • Lymphadenopathy
  • Hepato/splenomegaly
  • Erythema nodosum.
  • Crepitations or bronchial breathing if there is pulmonary changes/pleural effusion.
  • Pericardial rub if there is pericardial involvement (see below)
44
Q

What are some of the investigations for active TB?

A
  • Imaging: CXR, CT, MRI
  • Biopsy
    • GOLD STANDARD: Culturing bacteria: Can take 6 weeks so ATT is usually started after samples taken
    • Sputum acid fast bacilli smear
    • Pulmonary TB: sputum samples: X3 induced sputum (sputum taken after a nebuliser of 7% hypertonic saline)
      • If a sputum sample is ‘smear negative’ then we usually proceed to bronchoscopy +/- EBUS (endobronchial ultrasound guided biopsy) of pulmonary lymph nodes
  • Immunological evidence? Tuberculin skin test, quantiferon TB gold, T-Spot TB gold ?
45
Q

How are Meningeal, lymph node, pericardial, GI TB diagnosed?

A
  • Meningeal TB – lumbar puncture for TB culture and TB PCR
  • Lymph node TB - core biopsy of lymph node (FNA is not adequate)
  • Pericardial TB – ideally pericardiocentesis – often not practical
  • Gastrointestinal – colonoscopy and bowel biopsy/ Ultrasound guided omentum biopsy
46
Q

What does histology show for TB?

A

Caseating/necrotising granulomatous inflammation

47
Q

When are steroids given for TB treatment?

A

If TB is affecting sites where additional swelling cannot be tolerated (e.g. meningeal/spinal/pericardial TB)

48
Q

How is TB meningitis/CNS TB diagnosed?

A
  • 1% of patients with TB have meningeal involvement.
  • Lumbar puncture to exclude TB meningitis - high glucose, low glucose, lymphocytosis
  • MRI - leptomeningeal enhancement
49
Q

What are some of the complications of Pericardial TB?

A
  • Complications: Pericardial effusion, Tamponade
  • Pericardial rub/ kussmails sign
  • 6 months treatment. Steroids given at the beginning
50
Q

How does Miliary TB appear?

A
  • CXR/CT
  • It is widespread throughout the patient and is often found in multiple sites including CNS/bone marrow/pericardium.
51
Q

What is used to diagnose disseminated/ Miliary TB?

A
  • Neuroimaging (CT/MRI head)
  • +/- lumbar puncture to exclude CNS
  • Do not delay treatment whilst awaiting biopsies
  • ATT is usually started as soon as it is determined whether or not there is CNS involvement
52
Q

How is Multi-drug-resistant tuberculosis (MDR-TB) infection controlled?

A
  • Negative pressure room
  • Staff should wear masks/ PPE
53
Q

How is TB treated?

A
  • Standard ATT (Anti-TB Therapy): for all sites of TB except for CNS TB.
  • Standard ATT: 2 months (intensive phase) Rifampicin +Isoniazid + Ethambutol + Pyrazinamide (available as a combined tablet called RIFATER) plus pyridoxine (vitamin b)
  • 3 months (continuation phase): Rifampicin and isoniazid (combined tablet RIFINAH) plus pyridoxine
54
Q

What are the side effects of anti TB therapy?

A
  • Rifampicin: causes urine/tears to turn orange; drug induced hepatitis
  • Isoniazid: Peripheral neuropathy (reduced by giving pyridoxine); Colour blindness; drug induced hepatitis
  • Ethambutol: Optic neuropathy/ reduced visual acuity
  • Pyrazinamide: Drug induced hepatitis +++
55
Q

How is TB medication monitored?

A
  • Before treatment: measure LFT and visual acuity (if using ethambutol)
  • During treatment: monitor LFTS - if deranged treatment can either be stopped and the drugs gradually reintroduced once they have normalised, or a “liver friendly” regimen can be given (e.g. amikacin, levofloxacin and ethambutol) but the treatment duration is longer (up to 24 months)
56
Q

What are the current infection controls for TB?

A
  • Patients with non-resistant pulmonary TB should be nursed in a side room.
  • After 2 weeks of treatment patients considered non-infectious to immunocompetent individuals.
  • If the ward also manages immunocompromised patients, including HIV (i.e our ward!) then patients with respiratory TB need to be nursed in a side room until discharge regardless of whether they are smear +ve/-ve
  • Smear +ve patients can still be discharged home but would need to quarantine themselves at home until they have completed 2 weeks of treatment.
  • NICE guidance: staff do NOT need to wear masks/aprons unless MDR TB is suspected / they performing aerosol generating procedure e.g.nebuliser.
  • Patients with smear +ve TB DO need to wear a mask when leaving their room until they have completed 2 weeks of treatment.
57
Q

How is contract tracing performed for TB?

A
  • Pt referred to TB nurses
  • Contact test family: CXR + Quantiferon testing
  • Treat any latent TB
58
Q

How is HIV managed?

A
  • Conservative: psychological support, safe sex, inform partner
  • Pharmacological:
    • CD4<200 - co-trimoxazole 480mg PO OD
    • CD4<50 - Azithryomycin
    • Antiretroviral therapy regimen: bictegravir/emtricitabine/tenofovir alafenamide
    • Dolutegravir: should be used with caution in women of childbearing potential and those who are trying to conceive