7- Infectious diseases (3/3) Flashcards

1
Q

influenza background

A

RNA virus
- A and B most common
–>A has different H and N subtypes e.g.
* H1N1 – swine flu
* H5N1 – avian flu
- Outbreaks typically in winter
- Spread via respiratory droplets
- Most contagious 24 hours before symptoms start
- Become less infective after 5 to 7 days of illness

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2
Q

Presentation of influenza

A
  • Fever
  • Coryzal symptoms
  • Lethargy and fatigue
  • Anorexia (loss of appetite)
  • Muscle and joint aches
  • Headache
  • Dry cough
  • Sore throat
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3
Q

Investigations for influenza

A
  • Diagnosis is based on history, risk factors and clinical presentation
  • Viral nasal or throat swabs – PCR analysis (public health like to monitor cases)
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4
Q

management of influenza: healthy person at no risk of complications

A

NO NEED FOR ANTIVIRALS
Supportive care :
- adequate fluids and rest
- analgesia e.g. paracetamol

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5
Q

management of influenza: person at risk of complications

A
  • Antivirals must be started within 48h of symptom onset to be effective
  • Oral oseltamivir 75mg twice daily for 5 days
  • Inhaled zanamivir 10mg twice daily for 5 days
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6
Q

influenza post exposure prophylaxis

A

can be given to higher risk patients e.g. immunosuppressed, within 48 hours of close contact with influenza
- Oral oseltamivir 75mg once daily for 10 days
- Inhaled zanamivir 10mg once daily for 10 days

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7
Q

Influenza Vaccination

A

Every year the vaccine is changed to target multiple strains of influenza that are likely to cause flu. It needs to be given yearly to keep the person protected.
It is given free on the NHS people at higher risk of developing flu:

  • Aged 65
  • Young children
  • Pregnant women
  • Chronic health conditions such as asthma, COPD, heart failure and diabetes
  • Healthcare workers and carers
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8
Q

Complications of flu

A
  • Otitis media, sinusitis and bronchitis
  • Viral pneumonia
  • Secondary bacteria pneumonia
  • Worsening of chronic health conditions such as COPD and heart failure
  • Febrile convulsions (young children)
  • Encephalitis
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9
Q

tuberculosis background

A
  • Caused by mycobacterium tuberculosis
  • Most commonly affects the lungs
    o Can also affect lymph glands, brain, kidneys or spine
    o More common in children to have TB which affects multiple parts of the body
  • TB more serious in children
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10
Q

mycobacterium tuberculosis

A
  • Rod shaped bacteria
  • Gram staining is ineffective due to waxy coating – acid fast bacilli
  • Requires Zeihl Neelson stain (turns bright red against blue background
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11
Q

RF for TB

A
  • More common in non-UK born patients e.g. south Asian
  • Immunocompromised e.g. HIV
  • Those with close contact with TB
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12
Q

Presentation TB

A

Tuberculosis usually presents with a history of chronic, gradually worsening symptoms. Most cases are of pulmonary TB (around 70%) but they often have systemic symptoms.
Typical signs and symptoms of TB include:

  • Lethargy
  • Fever or night sweats
  • Weight loss
  • Cough with or without haemoptysis
  • Lymphadenopathy
  • Erythema nodosum
  • Spinal pain in spinal TB (also known as Pott’s disease of the spine)

In children specifically
- Failure to thrive
- Wheezing
- Chronic fever
- Chronic cough

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13
Q

TB in children vs adults

A
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14
Q

BCG vaccine

A

Bacille Calmette-Guerin

Intradermal infection of live attenuated TB

  • Protects against severe and complicated TB – less effective at protecting against pulmonary TB

Prior to vaccine may have a Mantoux test to ensure not already contracted

Who is offered the BCG:

  • Neonates born in areas of the UK with high rates of TB
  • Neonates with relatives from countries with a high rate of TB
  • Neonates with a family history of TB
  • Unvaccinated older children and young adults (< 35) who have close contact with TB
  • Unvaccinated children or young adults that recently arrived from a country with a high rate of TB
  • Healthcare workers
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15
Q

why is diagnosing TB hard

A

Hard to diagnose because cannot be strained with traditional gram stain- requires Ziehl-Neelson stain
Two tests for immune response to TB- caused by previous, latent or active TB
- Mantoux
- interferon gamma release assay

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16
Q

Two tests for immune response to TB- caused by previous, latent or active TB

A

Mantoux
- Looks for previous immune response to TB: vaccination or latent or active TB
- Induration of 5mm or more is a positive test result after intradermal injection of tuberculin

Interferon-gamma release assay
- Involves taking a sample of blood and mixing with antigens from TB bacteria
- If person has had previous contact with TB the WBC will be sensitised to those antigens and will release interferon-gamma as part of an immune response
- IGRA test is used in patients who do not have features of active TB but do have a positive Mantoux test to confirm a diagnosis of latent TB

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17
Q

investigations if active TB suspected

A
  • Chest x-ray
  • cultures
  • NAAT
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18
Q

TB chest x-ray

A

Primary TB
- May show patchy consolidation, pleural effusions and hilar lymphadenopathy

Reactivated TB
- May show patchy or nodular consolidation with cavitation (gas filled spaces in the lungs) typically in the upper zone

Disseminated miliary TB
- Millet seeds uniformly distributed throughout the lung fields

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19
Q

culturing TB

A

Cultures
- Bacterial culture useful prior to starting treatment
- Allows testing for resistance to abx
- HOWEVER Cultures can take several months to take several months to grow organisms
Culture collection
- Sputum
- Mycobacterium blood cultures
- Lymph node aspiration

Nucleic acid amplification test: quicker than cultures

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20
Q

Management latent TB

A

Otherwise healthy patients do not necessarily need treatment for latent TB. Patients at risk of reactivation of latent TB can be treated with either:
* Isoniazid and rifampicin for 3 months
* Isoniazid for 6 months

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21
Q

management acute pulmonary TB

A

RIPE is the mnemonic used to remember the treatment for TB. It involves a combination of 4 drugs used at the same time:

R – Rifampicin for 6 months
- Red urine and tears
- Inducer of cytochrome P450 – reduces effectiveness of combined pill
- Hepatotoxicity (less likely than adults)

I – Isoniazid for 6 months
- Peripheral neuropathy (pyridoxine (vit B6) should be co-prescribed)
- hepatotoxicity

P – Pyrazinamide for 2 months
- High uric acid levels- gout
- Hepatotoxicity

E – Ethambutol for 2 months
- Colour blindness
- Reduced visual acuity

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22
Q

other managements of TB

A

Other management

  • Test for other infectious diseases (HIV, hepatitis B and hepatitis C).
  • Test contacts for TB.
  • Notify Public Health of all suspected cases.
  • Patients with active TB should be isolated to prevent spread until they are established on treatment (usually 2 weeks). In hospital negative pressure rooms are used to prevent airborne spread. Negative pressure rooms have ventilation systems that actively remove air to prevent it spreading out on to the ward.
  • Management and followup should be guided by a specialist MDT.
  • Treatment is slightly different for extrapulmonary disease and often includes using corticosteroids.
  • Individualised drug regimes are required for multidrug resistant TB.
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23
Q

malaria background

A
  • Infectious disease caused by Plasmodium – protozoan parasite
  • Spread through bites from female Anopheles mosquitos that carry the disease
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24
Q

Types of plasmodium

A
  • Plasmodium falciparum is the most severe and dangerous form
  • Plasmodium vivax
  • Plasmodium ovale
  • Plasmodium malariae
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25
Q

life cycle of plasmodium parasite

A
  • Infected blood sucked by by female anopheles mosquito (at night0
  • Malaria in anopheles reproduces in gut- sporozoites
  • When mosquito bites human sporozoites are injected by mos
  • Sporozoites travel to the liver of newly infected person and can lie dormant as hypnozoites for several years (P. vivax and P.ovale)
  • Mature into merozoites-> enter blood and infect RBC -> rupture -> release more merozoites -> haemolytic anaemia
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26
Q

Risk factors for malaria

A
  • Young children <5 most vulnerable
  • Those with no immunity to malaria e.g. travellers from areas with no malaria are more likely to become very sick and die
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27
Q

protective factors for malaria

A

recessive trait for SS

28
Q

Presentation of malaria

A

Non-specific Symptoms
* CylicalFever, sweats and rigors (every 48 hours)
* Malaise
* Myalgia
* Headache
* Hypoglycaemia
* Vomiting
Signs
* Pallor due to the anaemia
* Hepatosplenomegaly
* Jaundice as bilirubin is released during the rupture of red blood cells

29
Q

investigations for malaria

A

Malaria blood film
- Sent in EDTA bottle (red top bottle used for FBC)
- Will show parasites, the conc and what type they are
- 3 samples sent over 3 consecutive days to exclude malaria
o 48 hour cycle of malaria being released into the blood from red blood cells

30
Q

maanagement of TB depends

A

type and severity

31
Q

Falciparum malaria management

A

Admitted for treatment since they can deteriorate quickly

32
Q

management of simple/uncomplicated malaria

A

Oral options in uncomplicated malaria:
- Artemether with lumefantrine (Riamet)
- Proguanil and atovaquone (Malarone)
- Quinine sulphate
- Doxycycline

33
Q

management of severe or complicated malaria

A

IV
 Artesunate (most effective not licensed)
 Quinine dihydrochloride

34
Q

Complications of falciparum infection

A
  • Cerebral malaria
  • Seizures
  • Reduced consciousness
  • Acute kidney injury
  • Pulmonary oedema
  • Disseminated intravascular coagulopathy (DIC)
  • Severe haemolytic anaemia
  • Multi-organ failure and death
35
Q

prophylaxis for malaria

A
  • Mosquito spray (50% DEET)
  • Mosquito nets and abrriers in sleeping
  • Antimalarials (several options)
    o Proguanil and atovaquone (malarone)
    -> Best side effects, most expensive
    o Mefloquine
    -> Bad dreams, rarely psychotic disorders or seizures
    o Doxycycline
    ->Diarrhoea and thrush
    -> Sensitivity to sun
36
Q

Viral gastroenteritis

A
  • Gastroenteritis is inflammation all the way from the stomach to the intestines and presents with nausea, vomiting and diarrhoea.
  • Common in children
  • Most commonly viral
  • Very easily spread
37
Q

main concern with viral gastroenteritis

A

Main concern
- Dehydration!!!!
- Need to establish if they can hydrate themselves or require admission for IV fluids

38
Q

Investigations for viral GE

A
  • Stool sample – microscopy, culture and sensitivity
39
Q

main types of viral gastroenteritis

A
  • Rotavirus
    o Most common cause of infantile gastroenteritis
    o immunity long lasting (vaccinations)
    o Faecal oral route
  • Norovirus
    o Commonest cause of gastroenteritis in all age groups
    o Faecal oral route
  • Adenovirus less common
40
Q

causes of bacterial gastroenteritis

A
  • E.coli
  • Campylobacter jejuni
  • Shigella
  • Salmonella
  • Bacillus cereus
41
Q

E.coli

A

o Only certain strains cause gastroenteritis e.g. E.coli 0157 -> shiga toxin
o Faecal oral route
o Blood diarrhoea -dysentry
o RBC destruction -> haemolytic uraemic syndrome

42
Q

Campylobacter jejuni

A

o Most common
o Travellers diarrhoea
o Spread via faecal oral route
o Symptoms: abdominal cramps, bloody diarrhoea, vomiting, fever

43
Q

shigella

A
  • Shigella
    o Faecal oral route
    o Bloody diarrhoea, abdominal cramps and fever
    o Can also produce Shiga toxin -> haemolytic uraemic syndrome
44
Q

salmonella

A

o Raw eggs, poultry or food contaminated with infected faeces of small animals
o Water diarrhoea , abdominal pain and vomiting

45
Q

Bacillus cereus

A

o Most typically spread via fried rice (food left at room temp before refrigerating)
o Water diarrhoea

46
Q

managment of gastroenteritis egneral

A

Supportive

1) Fluids

  • Keep patient hydrated whilst waiting for d and V to settle
  • Fluid challenge – give small volume of fluid orally every 5-10 mins to ensure they can tolerate it
  • If they can tolerate oral fluids -> can be managed at home
  • Rehydration fluids e.g. dioralyte can be used if tolerate
  • Once oral intake tolerated a light diet can be slowly reintroduced
  • If refuse oral-NG before IV

2) Good hygiene

  • Barrier nursing
  • Children off school until 48 hours after symptoms have resolves

3) If viral -> antibiotics usually not required

4) if bacterial ->only give antibitocis ocne the causative organism is confirmed and only if patient is at risk of complications e.g. campylobacter

47
Q

what are not recommended in the treatment of gastroenteritis

A
  • Antidiarrheals and antiemetics not recommended
48
Q

why not give immediatley antibiotics if you suspect bacterial GE

A

E.coli and other Shiga-producing bacteria -> avoid abx – increases risk of haemolytic uraemic syndrome.

49
Q

Post Gastroenteritis Complications

A

The are possible post-gastroenteritis complications:
* Lactose intolerance
* Irritable bowel syndrome
* Reactive arthritis
* Guillain–Barré syndrome

50
Q

Haemolytic uraemic syndrome
Background

A

Small blood clots in tiny vessels of the kidney cause RBC breakdown -> reduced kidney function -> urea levels in blood increase

Triad of
- Anaemia - Microangiopathic haemolytic anaemia
- Low platelets- Thrombocytopenia
- Kidney damage- Acute kidney injury

51
Q

cause of HUS

A
  • Associated with gastroenteritis and travels e.g. Shiga toxin-producing E.coli
    o Rarely shigella
    o Streptococcus
    o Pneumonia
  • G6PD deficiency
52
Q

Risk factors for HUS

A
  • Children <5 years, people >75
  • Genetic predisposition to endothelial cell damage
53
Q

Presentation of HUS

A
  • Bloody diarrhea
  • Weakness, fatigue, lethargy, jaundice due to RBC destruction
  • Fever
  • Blood clots
54
Q

Investigations for HUS

A
  • Bloods
    o FBC
    o Thrombocytopenia
  • Urine dip
    o Proteinuria
    o Haematuria
  • Stool sample e.g. schistocytes/hemet cells
55
Q

Management HUS

A
  • Supportive
56
Q

Toxic shock syndrome background

A
  • Exotoxin-mediated illness caused by bacterial infection
  • Multisystem inflammatory response
  • First associated with highly absorbative tampons- cases have reduced now due to changes in tampon manufacture and increased awareness
57
Q

Pathophysiology of toxic shock syndrome

A
  • Staphylococcus or streptococcus release exotoxins which work as superantigens
  • Sets off inflammatory cascacde, mediated predominantly by tumour necrosis factor alpha and IL-1
58
Q

causes of toxic shock syndrome

A
  • Group A streptococcus
    o Most commonly associated with infected cutaneous site
  • Staphylococcus aureus
    o Menstrual: Most associated with extended tampon use
    o Non-menstrual: Postpartum infections
59
Q

Risk factors for toxic shock syndrome

A
  • DM
  • Gynaecological infections
  • Puerperal sepsis
  • HIV
  • IVDU
  • Alcoholism
  • Surgical procedures
60
Q

Presentation of toxic shock syndrome

A

Non-specific, flu-like symptoms. Toxicity occurs early, resulting in serious life-threatening disease and multi-organ system failure
- Fever
- Rash
- Myalgia
- Hypotension
- Nausea and vomiting
- Headache
- Localised pain e.g. abdominal
- Localised swelling
- Hypotension- shock
- Acute mental state changes- confusion

61
Q

examination for toxic shock

A

Examination
- Examination of skin
- Check for tampons- gynaecological exam
- Resp exam

62
Q

Investigation for toxic shock

A

Microscopy and culture
- Blood
- Wound
- Fluid
- Tissue

Bloods
- FBC
–>High WBC
–> Low platelets
- U&Es
- CK and LCTS elevated
- Prothrombin time

Urinalysis
- Haematuria

Imaging
- CXR if pneumonic feature

63
Q

Management of toxic shock syndrome

A
  • Early diagnosis and rapid intervention
  • Focus of infection should be removed immediately
    o Drainage of abscess
    o Wound pack
    o Tampon
  • Manage shock
    o IV resus
    o Vasopressors
  • Normalise glucose
  • Empirical antibiotics e.g. clindamycin plus vancomycin
  • Corticosteroids
64
Q

Management of toxic shock syndrome

A
  • Early diagnosis and rapid intervention
  • Focus of infection should be removed immediately
    o Drainage of abscess
    o Wound pack
    o Tampon
  • Manage shock
    o IV resus
    o Vasopressors
  • Normalise glucose
  • Empirical antibiotics e.g. clindamycin plus vancomycin
  • Corticosteroids
65
Q

prognosis of TSS

A

Prognosis
- 5-15% mortality