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medicine block (y3) > Week 2: Infectious disease (3)(ID summaries) > Flashcards

Week 2: Infectious disease (3)(ID summaries) Flashcards

1
Q

malaria: demographic affected: Malaria

A
  • Commonest imported infection in the UK
  • 75% falciparum (90% of cases from Africa)
  • 25% Ovale (90% of cases from India)
    • Initially ALWAYS REAT AS FACIPARUM
      o Mortality rate 10-20%
      o More common in travellers
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2
Q

pathogen: malaria

A
  • 5 main species of Plasmodium
     Falciparum
     Vivax
     Ovale
     Malaria
     Knowlesii
  • Vector= female anopheles mosquito
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3
Q

course of illness: malaria

A

o Incubation period
 Minimum 7 days
• Falciparum- 4 weeks
• Vivax/ ovale up to a year (lay dormant in the liver)

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4
Q

Signs and symptoms: Malaria

A
  • Fever/ chills and sweats
  • Cycle every 3rd or 4th day
  • Severe headache, malaise, myalgia, vague abdominal pain, nausea, vomiting
  • Examination- few signs except fever +- splenomegaly
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5
Q

Diagnosis/investigations: Malaria

A

o X3 blood films to diagnose

o Bloods (FBC, U&E, LFTs, glucose, coagulation)

  • Anaemia
  • Thrombocytopenia
  • Leukopenia
  • Abnormal Liver test

o Rapid antigen test

o Head CT if CNS symptoms
o CXR

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6
Q

management: Malaria

A

Non-falciparum

  • oral artemisinin combination therapy (ACT)

Falciparum

Admit all patients with falciparum

  • uncomplicated
    • artemisinin combination therapy (ACT).
    • or quinine with doxycyline
  • complicated
    • IV artesunate
    • or intravenous quinine (need to monitor for hypoglycaemia)
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7
Q

Prevention: Malaria

A

Nets, antimalarials (DEET), repellent

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8
Q

When diagnosing infectious disease via blood screens can use PCR or serology

A
  • IgM= recent infection
  • IgG= cant tell how recent
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9
Q

Life cycle of Plasmodium species

A
  • Mosquito feeds on human and malaria sporozoites enter in blood and infect liver cells
  • Parasite develops into mature schizonts creating many merozoites which burst out of the cell and enter blood cell and infect blood cells
  • Causing RBC to burst and releasing more merozoites
  • These go and infect other blood cells and can cause anaemia and microvascular occlusion of organs (very sticky cells)- end organ damage e.g. kidney
  • Some merozoites develop into gametocytes which can be ingested by other mosquitos

Complex life-cycle makes malaria hard to create a vaccine

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10
Q

Malaria treatment depends on

A

species

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11
Q

P. falciparum (‘malignant’) treatment

A 
o Artemisinin ( IV artesunate/PO Riamet)
o Quinine plus doxycycline (7 days)
o Plus supportive therapy/ ITU
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12
Q

P. vivax, ovale, malaria (‘benign’)

A

o Chloroquine (3-4 days)
o +primaquine (14 days)
 Hypnozoites- liver stage
 Can recur months-years later

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13
Q

Severe falciparum malaria

A

Untreated P.Falciparum infection can cause hypoglycaemia, renal failure, pulmonary oedema and neurologic deterioration leading to death.

  • Impaired consciousness or seizures
  • Renal impairment (oliguria <0.4ml/kg bodyweight per hour or creatinine >256umol/l)
  • Acidosis <7.3)
  • Hypoglycaemia <2.2mmol/l)
  • Pulmonary oedema or ARDS
  • Haemoglobin <80 g/l
  • Spontaneous bleeding- IDC
  • Shock (algid malaria <90/60 mmHg)
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14
Q

demographic affected: dengue fever

A

o Found throughout the world: Africa, Asia, India, S and C America
o ‘re-infection’ mainly affects those living in Dengue endemic areas
 Children
 Rare in travellers

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15
Q

Pathogen: dengue virus

A 
o Arbovirus (arthropod born virus)
 4 serotypes
o Vector= mosquito
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16
Q

Course of illness: Dengue fever

A

o First infection ranges from asymptomatic to non-specific febrile illness (classic dengue)
 Lasts 1-5 days
 Improves 3-4 days after rash
 Supportive treatment only
o Re-infection with different serotype is very dangerous
 Antibody dependent enhancement (immune system overdrive)
• Dengue haemorrhagic fever (children)
• Dengue shock syndrome

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17
Q

signs and symptoms: dengue fever

A
  • a high temperature, or feeling hot or shivery.
  • a severe headache.
  • pain behind the eyes.
  • muscle and joint pain.
  • feeling or being sick.
  • a widespread red rash.
  • tummy pain and loss of appetite.
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18
Q

diagnosis: dengue

A
  • PCR
    • Serology e.g. IgM and IgG
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18
Q

diagnosis: dengue

A
  • PCR
  • Serology e.g. IgM and IgG
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19
Q

management of dengue fever

A

There is no specific treatment for dengue fever. Fever reducers and pain killers can be taken to control the symptoms of muscle aches and pains, and fever. The best options to treat these symptoms are acetaminophen or paracetamo

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20
Q

prevention : dengue

A
  • Vaccine (only in people over certain age)
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21
Q

demographic affected: typhoid and paratyphoid fever

A
  • Disease of poor sanitation
    • Mainly Asia, Africa, S america
    • Travel related in UK
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22
Q

pathogen: typhoid and para

A
  • Salmonella typhi/paratyphi A,B, or C- Gram negative bacilli- Enterobacteriaceae
    • Virulence= low infectious dose
    • Survives gastric acid
    • Fimbriae adhere to ileal lymphoid tissue (Peyers patches)  RE system/blood
    • Reside within macrophages (liver/spleen/ bone marrow)
    • Faecal-oral from contaminated food/water
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23
Q

course of illness: typhoid

A
  • Incubation period: 7-14 days
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24
Q

signs and symptoms: typhoid

A
  • Systemic disease
    • Fever, headache, abdominal discomfort, dry cough
    • Relative bradycardia
    • Complications
      • Intestinal haemorrhage and perforation; seeding
    • Paratyphoid is generally milder
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25
Q

Diagnosis/investigations : typhoid

A
  • Blood culture x 2
    • Blood (+ve in 40-80%)
    • Faeces
  • FBC
    • Moderate anaemia
    • Relative lymphopenia, raise CRP
    • Raised LFTs (transaminase and bilirubin)
    • Culture
  • No serological test
26
Q

management of typhoid

A
  • Ceftriaxone (resistant starting- having to use meropenem)
27
Q

prevention of typhoid

A
  • Vaccine
  • Eating and drinking
28
Q

Non-typhoidal salmonella infections

A
  • Food poisoning salmonellas
  • Widespread distribution including UK
    • S. typhimurium, S enteridis
  • Symptoms
    • Diarrhoea
    • Fever
    • Vomiting
    • Abdominal pain
  • Generally self limiting but bacteraemia and deep-seated infections may occur in the immunosuppressed
29
Q

Pathogen: Amoebic liver disease (Amoebiasis)

A
  • Caused by Entamoeba histolytica
  • Faeco-oral spread- ingestion of cysts
30
Q

Course of illness: amoeebiasis

A
  • Incubation- 2-4 weeks
  • Colonic infection
    • Asymptomatic (90%) may persist for years
31
Q

signs and symptoms: amoebiasis

A
  • Ab pain, bloody diarrhoea (due to invasion of intestinal lining. May lead to:
    • Ulceration/ bowel perforation and peritonitis
    • If invades blood stream: liver/ lung abscess
32
Q

investigations: amoebiasis

A
  • Stool OCP (Ova Cyst Parasite)
    • Not shed constantly, need x 3 stools
    • Usually absent with invasive disease
    • Amoebic serology, stool PCR
33
Q

Management: amoebiasis

A
  • IV ceftriaxone (gram positive and negative)
  • PO metronidazole (anaerobic infections and amoebic)
  • US guided hepatic train
34
Q

demographic affected: TB

A
  • Endemic in parts of Asia, Africa, SA and eastern Europe and was common in the UK until the 1950s (when isoniazid was first developed)
  • Common for people immigrating to the UK for endemic areas to experience reactivation of latent TB after their arrival (maybe Vitamin D deficiency)
35
Q

pathogen: TB

A
  • Mycobacterium tuberculosis

(acid fast stain)

36
Q

Course of illness: TB

A
  • Transmitted by aerosol inhalation and causes pulmonary infection, then spreads via haematogenous spread to any site in the body
  • Initial infection can be asymptomatic and then lie dormant (Latent TB) for many years before reactivating later in life to the active infection
    • Reactivation risk (10-15%) due to immunosuppression, advancing age or HIV)
37
Q

signs and symptomd: TB

A
  • Symptoms:
    • Non resolving cough
    • Unexplained persistent fever
    • Drenching night sweats
    • Weight loss
    • Signs
      • Clubbing
      • Cachexia
      • Lymphadenopathy
      • Hepato/splenomegaly
      • Erythema nodosum
      • Crepitation or bronchial breathing if PE
38
Q

Diagnosis/investigations: TB

A
  • CXR
  • sputum sample
  • Biopsy
39
Q

management: latent TB

A
  • 3 months of rifampicin and isoniazid or 6 months rifampicin alone
    • Treatment reducing risk of reactivation needs to be balanced against hepatotoxicity risk (>35 yo at high risk)
40
Q

Treatment: Active TB

A
  • Standard ATT ( Anti-TB Therapy) used for all sites of TB except for CNS TB
  • 2 months (intensive phase) of RIPE, then 4 months (continuation phase) of rifampicin and isoniazid plus pyridoxine
  • Monitor LFTs before and after treatment- if LFTS deranged treatment can either be stopped and drugs gradually reintroduced once they have normalised
41
Q

prevention: TB

A
  • BCG
  • Contact tracing
42
Q

Latent TB

A
  • By definition latent TB is asymptomatic. It is identified by screening.
  • Screening involves chest x-ray and measurement of interferon gamma (quantiFERON or T-spot)
43
Q

QuantiFERON

A

Assesses the amount of interferon gamma released by T cells when they are exposed to proteins found on mycobacteria.

44
Q

why is Quantiferon not used to diagnose TB

A

BUTTTTT

  • 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.
45
Q

T-SPOT test

A

Similar principle, but rather than testing whole blood the lymphocytes are isolated and tested directly. Theoretically meaning if there is a deficiency of lymphocytes the quantiFERON might be indeterminate but the t spot may be positive.

A POSITIVE INTERFERON GAMMA TEST DOES NOT MEAN THE PATIENT HAS ACTIVE TB AND A NEGATIVE INTERFERON GAMMA TEST DOES NOT MEAN THAT A PATIENT DOESN’T HAVE ACTIVE TB

46
Q

Screening for TB

A
  • Interferon gamma tests used in asymptomatic patients with risk factors for latent TB
    • Immigrants from high prevalence countries
    • Healthcare workers
    • HIV positive patients
    • Patients starting on immunosuppression
47
Q

MDR and non-MDR resistant TB

A
  • Consider in patients who have had incomplete treatment for TB previously
  • Usually seen in patients from abroad
  • Treatment is specialised and is based on sensitivities. Treatment regimen is usually decided by consultant
    • Infection control is paramount, especially for MDR TB and these patient should be managed in a negative pressure room and staff should wear masks/PPE when dealing with them.
48
Q

Disseminated/ Miliary TB

A
  • Characteristic appearance on CXR/CT- widespread throughout patient (CNS/ bone marrow/ pericardium)
  • Requires neuroimaging and lumbar puncture to exclude CNS involvement
  • Treatment for miliary TB shouldn’t be delayed whilst awaiting biopsies
49
Q

TB contact tracing

*

A
  • Once a patient has been diagnosed they should be referred to the TB nurses
  • They will perform contact tracing and will test household contacts with either CXR or QuantiFERON testing and will treat any latent TB
  • Usually if household contacts were going to catch TB it would be before the patient was admitted so visitors are allowed – unless they have resistant TB
50
Q

Infection control

A
  • Patients with non-resistant pulmonary TB should be nursed in a side room.
  • After 2 weeks of treatment patients are generally 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 positive or negative (there are criteria by which they can come out but they are very stringent)
  • Smear positive patients can still be discharged home but would need to quarantine themselves at home until they have completed 2 weeks of treatment.
  • NICE guidance is that staff do NOT need to wear masks/aprons unless MDR TB is suspected or they are performing an aerosol generating procedure such as giving a nebuliser.
  • Patients with smear positive TB DO need to wear a mask when leaving their room until they have completed 2 weeks of treatment.
51
Q

pathogen: HIV

A

Retrovirus ssRNA

52
Q

course of illness : HIV

A
  • Stage 1: Acute HIV infection (2-4 weeks after infection) – flu like illness
  • Stage 2: Clinical latency/ chronic HIV infection- usually symptomless (some people without HIV treatment can 10-15 years without symptoms
  • Stage 3: AIDS
53
Q

Signs and symptoms: HIV

A
  • Patients with HIV may present with infections not commonly seen in the general population.
  • Flu like symptoms (fever, chills, rash, night sweats, muscle aches, sore throat, fatigue, swollen lymph nodes, mouth ulcers)
  • AIDs
    • Rapid weight loss
    • Recurring fever
    • Extreme and unexplained tiredness
    • Swelling of lymph glands in armpits, groin or neck
    • Diarrhea that lasts for more than a week
    • Sore of the mouth, anus, or genitals
    • Pneumonia
    • Memory loss, depression…
54
Q

diagnosis : HIV

A
  • Confirmatory HIV test
  • CD4 count
  • HIV viral load
  • HIV resistance profile
  • HLA B*5701 status
  • Serology for syphilis, hepatitis B (sAg, cAb, sAb), hepatitis C, hepatitis A
  • Toxoplasma IgG, measles IgG, varicella IgG, rubella IgG
  • FBC, U&Es, LFTs, bone profile, lipid profile
  • Schistosoma serology (if has spent >1 month in sub-Saharan Africa)
  • Women should have annual cervical cytology.
55
Q

management of HIV

A
  • Support for PTs
    • HIV clinical nurse speciliast team offers advice, education and medical/social support
    • Antiretroviral (ARV) medication
      • Dispensed by hospital pharmacy and not GPs
        • Important dose is correct and not missed
        • Many drug interactions
56
Q

Prevention : HIV

A
  • Vaccination
    • HepB
    • Pneumococcus
    • Annual influenza vaccination
  • Post-exposure prophylaxis (PEP)
57
Q

HIV patients with low CD4 count

*

A

HIV patients with low CD4 count

  • Susceptible to opportunist infections
  • CD4 <200 should be prescribed Co-trimoxazole 480mg PO OD as primary prophylaxis against PCP.
  • CD4 <50 Azithromycin 1250mg PO once weekly to protect against MAI
    • Should be assessed by ophthalmology with dilated fundoscopy to look for evidence of intra-ocular infections such as CMV retinitis
58
Q

STI

A

All patients admitted to IDU, regardless of age, history or perceived risk factors, should be offered a blood-borne infection screen to test for HIV, syphilis, hepatitis B and hepatitis C. Verbal consent from the patient for these tests should be recorded in the medical notes.

Important to exclude pregnancy in all women of child-bearing age → for women with abdominal pain a bimanual examination should be performed in addition to speculum examination.

59
Q

Types of testing methods: STI

A
  • first pass urine (men only) – urethral GC/CT (can be sent in white universal pot)
  • vulvo-vaginal swab – vaginal/cervical GC/CT (use chlamydia swab pack and break pink swab tip into NAAT medium)
  • pharyngeal swab – GC/CT of the throat (use plain purple swab and break tip into NAAT medium)
  • rectal swab – GC/CT of the rectum (send as for pharyngeal swab)
60
Q

Pyrexia of unknown origin on IDU

Classical definition:

A
  • Temperature > 38 degrees on multiple occasions
  • Illness of >3 weeks duration
  • No diagnosis despite >1 week’s worth of inpatient
61
Q

Common causes of POUO

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
62
Q

pyrexia of unknown origin history and exam

A
  • Chronology of symptoms
  • Pets/animal exposure
  • Travel
  • Occupation
  • Medication
  • Family history
  • Vaccination history
  • Sexual contacts

Examinations

  • Lymph nodes
  • Stigmata of endocarditis
  • Evidence of weight loss
  • Joint abnormalities
63
Q

pyrexia of unknown origin: investigations

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

medicine block (y3) (38 decks)

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