7- Infectious diseases (3/3) Flashcards
influenza background
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
Presentation of influenza
- Fever
- Coryzal symptoms
- Lethargy and fatigue
- Anorexia (loss of appetite)
- Muscle and joint aches
- Headache
- Dry cough
- Sore throat
Investigations for influenza
- Diagnosis is based on history, risk factors and clinical presentation
- Viral nasal or throat swabs – PCR analysis (public health like to monitor cases)
management of influenza: healthy person at no risk of complications
NO NEED FOR ANTIVIRALS
Supportive care :
- adequate fluids and rest
- analgesia e.g. paracetamol
management of influenza: person at risk of complications
- 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
influenza post exposure prophylaxis
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
Influenza Vaccination
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
Complications of flu
- 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
tuberculosis background
- 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
mycobacterium tuberculosis
- Rod shaped bacteria
- Gram staining is ineffective due to waxy coating – acid fast bacilli
- Requires Zeihl Neelson stain (turns bright red against blue background
RF for TB
- More common in non-UK born patients e.g. south Asian
- Immunocompromised e.g. HIV
- Those with close contact with TB
Presentation TB
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
TB in children vs adults
BCG vaccine
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
why is diagnosing TB hard
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
Two tests for immune response to TB- caused by previous, latent or active TB
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
investigations if active TB suspected
- Chest x-ray
- cultures
- NAAT
TB chest x-ray
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
culturing TB
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
Management latent TB
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
management acute pulmonary TB
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
other managements of TB
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.
malaria background
- Infectious disease caused by Plasmodium – protozoan parasite
- Spread through bites from female Anopheles mosquitos that carry the disease
Types of plasmodium
- Plasmodium falciparum is the most severe and dangerous form
- Plasmodium vivax
- Plasmodium ovale
- Plasmodium malariae
life cycle of plasmodium parasite
- 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
Risk factors for malaria
- 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
protective factors for malaria
recessive trait for SS
Presentation of malaria
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
investigations for malaria
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
maanagement of TB depends
type and severity
Falciparum malaria management
Admitted for treatment since they can deteriorate quickly
management of simple/uncomplicated malaria
Oral options in uncomplicated malaria:
- Artemether with lumefantrine (Riamet)
- Proguanil and atovaquone (Malarone)
- Quinine sulphate
- Doxycycline
management of severe or complicated malaria
IV
Artesunate (most effective not licensed)
Quinine dihydrochloride
Complications of falciparum infection
- Cerebral malaria
- Seizures
- Reduced consciousness
- Acute kidney injury
- Pulmonary oedema
- Disseminated intravascular coagulopathy (DIC)
- Severe haemolytic anaemia
- Multi-organ failure and death
prophylaxis for malaria
- 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
Viral gastroenteritis
- 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
main concern with viral gastroenteritis
Main concern
- Dehydration!!!!
- Need to establish if they can hydrate themselves or require admission for IV fluids
Investigations for viral GE
- Stool sample – microscopy, culture and sensitivity
main types of viral gastroenteritis
-
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
causes of bacterial gastroenteritis
- E.coli
- Campylobacter jejuni
- Shigella
- Salmonella
- Bacillus cereus
E.coli
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
Campylobacter jejuni
o Most common
o Travellers diarrhoea
o Spread via faecal oral route
o Symptoms: abdominal cramps, bloody diarrhoea, vomiting, fever
shigella
- Shigella
o Faecal oral route
o Bloody diarrhoea, abdominal cramps and fever
o Can also produce Shiga toxin -> haemolytic uraemic syndrome
salmonella
o Raw eggs, poultry or food contaminated with infected faeces of small animals
o Water diarrhoea , abdominal pain and vomiting
Bacillus cereus
o Most typically spread via fried rice (food left at room temp before refrigerating)
o Water diarrhoea
managment of gastroenteritis egneral
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
what are not recommended in the treatment of gastroenteritis
- Antidiarrheals and antiemetics not recommended
why not give immediatley antibiotics if you suspect bacterial GE
E.coli and other Shiga-producing bacteria -> avoid abx – increases risk of haemolytic uraemic syndrome.
Post Gastroenteritis Complications
The are possible post-gastroenteritis complications:
* Lactose intolerance
* Irritable bowel syndrome
* Reactive arthritis
* Guillain–Barré syndrome
Haemolytic uraemic syndrome
Background
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
cause of HUS
- Associated with gastroenteritis and travels e.g. Shiga toxin-producing E.coli
o Rarely shigella
o Streptococcus
o Pneumonia - G6PD deficiency
Risk factors for HUS
- Children <5 years, people >75
- Genetic predisposition to endothelial cell damage
Presentation of HUS
- Bloody diarrhea
- Weakness, fatigue, lethargy, jaundice due to RBC destruction
- Fever
- Blood clots
Investigations for HUS
- Bloods
o FBC
o Thrombocytopenia - Urine dip
o Proteinuria
o Haematuria - Stool sample e.g. schistocytes/hemet cells
Management HUS
- Supportive
Toxic shock syndrome background
- 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
Pathophysiology of toxic shock syndrome
- Staphylococcus or streptococcus release exotoxins which work as superantigens
- Sets off inflammatory cascacde, mediated predominantly by tumour necrosis factor alpha and IL-1
causes of toxic shock syndrome
- 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
Risk factors for toxic shock syndrome
- DM
- Gynaecological infections
- Puerperal sepsis
- HIV
- IVDU
- Alcoholism
- Surgical procedures
Presentation of toxic shock syndrome
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
examination for toxic shock
Examination
- Examination of skin
- Check for tampons- gynaecological exam
- Resp exam
Investigation for toxic shock
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
Management of toxic shock syndrome
- 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
Management of toxic shock syndrome
- 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
prognosis of TSS
Prognosis
- 5-15% mortality
