Infection Flashcards

(121 cards)

1
Q

Define candidiasis

A

Candidiasis refers to a mucocutaneous fungal infection with a Candida species, most commonly Candida albicans*

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2
Q

What is the aetiology of candidiasis?

A

The single-celled yeast Candida albicans is a normal commensal in the mouth, GI tract and vagina. However, certain factors can contribute to excessive Candida growth and a spectrum of clinical manifestations, ranging from local symptoms to severe invasive disease.

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3
Q

Name some risk factors for candidiasis:

A

Site: moist body folds, damage to skin/mucosal barriers, indwelling medical devices
Systemic: immunosuppression, recent antibiotics, diabetes mellitus, iron deficiency anaemia, pregnancy
Exposure: hospitalisation

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4
Q

What are the signs and symptoms of candidiasis:

A

Vulvovaginal: pruritis, thick white discharge, burning sensation
Cutaneous: erythematous, scaling macules with smaller outlying lesions
Oral: mucosal erythema with white flecks
yellowish plaques on the oral mucosa that are fairly adherent to the mucosa. On scraping, there is an erythematous base and mild bleeding
Systemic: severe illness in a vulnerable patient e.g. patients

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5
Q

What are the investigations for candidiasis?

A

Swabs - fungal and/or bacterial (especially if unresponsive to treatment or severe)
Bloods - FBC, iron studies, U&E, LFT’s, clotting,CRP, HbA1c, HIV testing, ABG/VBG (if ?sepsis)
Specific investigations for differential diagnoses e.g. STI screen, urine dip
Pregnancy test if appropriate

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6
Q

What is the overall management for candidiasis?

A

If a patient is systemically unwell, adopt an A-E approach, get help early and consider initiating the sepsis six. Patients with systemic candidiasis often have underlying conditions that put them at higher risk, so escalate early. Treatment involves systemic antifungals such as echinocandin, fluconazole or amphotericin B, alongside supportive measures.

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7
Q

What is the management for cutaneous candidiasis?

A

Conservative: advice on skincare, changing nappies regularly, weight loss if appropriate
Topical imidazole which is antifungal

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8
Q

What is the management for vulvovaginal candidiasis?

A

Conservative: washing with soap substitute, avoiding tight clothing, avoiding irritants
Medical: oral fluconazole or clotrimazole cream or pessary (in pregnancy)
An induction & maintenance regime of oral fluconazole may be needed
These treatments may be given with or without topical imidazole for vulval symptoms

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9
Q

What is the management for oral candidiasis?

A

Conservative: advice on good oral hygiene
Medical: miconazole oral gel first line, nystatin suspension second line
If HIV positive: oral fluconazole 200 mg on day one, followed by 100-200mg daily for 14 days

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10
Q

What are the complications of candidiasis?

A

Worsening of symptoms
Recurrence
Secondary bacterial infection
Invasive disease, organ dysfunction & shock

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11
Q

If oral miconazole is contraindicated (e.g. drug interaction such as simvastatin by inhibiting CYP3A4, increasing the risk of statin-induced myopathy and rhabdomyolysis), what is the preferred treatment for oral candidiasis.

A

Oral nystatin suspension

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12
Q

Define herpes simplex virus?

A

Herpes simplex viruses are large double-stranded DNA viruses. They are part of the herpes virus family, and predominantly cause oral, genital and ocular manifestations.
Primary infection is the first-time exposure to HSV in a seronegative (unexposed) person.
Recurrent infection is the reactivation of HSV, causing repeated symptoms.

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13
Q

What are the two types of herpes simplex virus and what do they cause?

A

HSV-1, causing oral, genital or ocular herpes
HSV-2, which usually causes genital herpes
Following initial infection, HSV becomes latent in the sensory ganglia and can subsequently reactivate, known as shingles.

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14
Q

What are the signs and symptoms of herpes simplex virus?

A

Oral: single painful ulcer along the lip border or gingivostomatitis
Genital: multiple painful vesicular lesions progressing to ulceration & crusted lesions, dysuria
Ocular: eye pain, irritation or photophobia, eye watering, blurred vision, acute red eye, visible vesicles around the eye, corneal abnormalities
Lymphadenopathy, malaise, fever
Tingling sensation or painful before lesion appears

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15
Q

What are the investigations for herpes simplex virus?

A

Methods of diagnosis depends on the site and severity of infection. For simple oral lesions, a clinical diagnosis will usually suffice. Genital herpes infection is usually confirmed with a viral swab for PCR. Higher risk circumstances requiring further work-up are:
Recurrent or unresolving lesions - suggesting an underlying cause or alternative diagnosis
If the patient is immunocompromised
Ocular herpes - requiring an examination with fluoroscein stain and visual acuity testing with subsequent slit-lamp examination & viral culture/PCR
During pregnancy - serology may be needed to differentiate between primary infection and reactivation

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16
Q

What is the treatment for herpes simplex virus?

A

Antivirals are the mainstay of treatment. Topical treatments are available over-the-counter.
Genital herpes requires oral aciclovir and a referral to GUM services. Recurrence with no risk of complications can be managed with self-care measures alone.
Oral herpes is usually treated with topical antivirals
Ocular herpes requires specialist management typically involving oral or topical antivirals.
Symptomatic management may involve analgesia, topical lidocaine, maintaining adequate hydration and wearing loose clothing. Measures to reduce risk of transmission are also important.

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17
Q

What is the guidance for herpes simplex virus when pregnant?

A

Genital herpes during pregnancy carries a risk of neonatal herpes simplex infection, which can be very serious if left untreated. Management depends on the stage of pregnancy and whether this is a primary or recurrent infection. Below is a summary of the RCOG/BASHH guidelines (2014):
Primary infection at less than 28 weeks’ gestation: aciclovir initially and regular prophylactic aciclovir from 38 weeks. Can consider vaginal delivery (specialist decision).
Primary infection at greater than 28 weeks’ gestation: aciclovir during initial infection followed by regular prophylactic aciclovir. Usually requires caesarean section delivery.
Recurrent HSV typically carries a lower risk of neonatal infection, but it is important to avoid a prolonged rupture of membranes and prophylactic aciclovir may be considered on specialist advice.

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18
Q

What are the complications of herpes simplex virus?

A

Oral: dehydration, eczema herpeticum, adhesions, erythema multiforme, spread to trachea/lungs/oesophagus
Progressive multifocal coalescing lesions, urinary retention, increased risk of HIV infection, neonatal HSV

Ocular: corneal scarring damage & visual impairment

Secondary infection
Autoinoculation of other areas
Systemic infection including meningitis, encephalitis, hepatitis

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19
Q

What is a hospital acquired infection?

A

A hospital-acquired infection, or healthcare-associated infection, is an infection which occurs due to contact with a healthcare setting or healthcare interventions.

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20
Q

What are the common hospital acquired infections?

A

Common pathogens are:
Meticillin-resistant Staphylococcus aureus
Meticillin-sensitive Staphylococcus aureus
PVL - Staphylococcus aureus
Clostridium difficile
Escherichia coli
Pseudomonas - common cause of hospital acquired pneumonia

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21
Q

Which risk factors can increase the risk of healthcare associated infections?

A

Healthcare-specific: indwelling urinary catheters, vascular access devices
Person-specific: genetics, specific immunity, comorbidities such as malnutrition, alcoholism, immunocompromise
Specific risk factors exist for each pathogen

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22
Q

Name some common types of hospital acquired infections?

A

Common types of healthcare-associated infection are:
Respiratory, including hospital-acquired pneumonia
Urinary tract infections
Surgical site infections
There must be a temporal link between healthcare interaction and infection developing. For example, hospital-acquired pneumonia is a pneumonia with onset more than 48 hours after admission.

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23
Q

What do we treat hospital acquired pneumonia?

A

co-amoxiclav is used first-line where there is less risk of resistance. For severe cases or increased risk of resistance, options include piperacillin with tazobactam, cephalosporins or meropenem. If MRSA is a possibility, add a glycopeptide like vancomycin or teicoplanin.

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24
Q

What do we treat Catheter-associated urinary tract infections

A

can usually be managed with a 7 day course of nitrofurantoin or trimethoprim (for lower UTI’s) or cefalexin (for upper UTI’s).

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25
What do we treat Indwelling line sepsis?
usually treated with vancomycin, with or without a broad-spectrum beta-lactam (see below).
26
How do we prevent healthcare associated infections?
Hand hygiene: correctly washing hands or using alcohol gel before & after any contact with a patient or healthcare environment (see the 5 steps of hand hygiene) Personal protective equipment: use of gloves, aprons, face masks & eye protection as indicated by local protocols for patient contact Safe use & disposal of sharps Use of aseptic non touch technique for procedures Correct waste disposal & laundry management Prompt and appropriate management of blood & body fluid spillages Equipment decontamination Regular cleaning of the healthcare environment Specific precautions for vascular access devices & urinary catheters
27
What do we treat Undifferentiated hospital-acquired septicaemia
should be treated with a broad-spectrum beta-lactam antibiotic with pseudomonas cover. Examples include piperacillin with tazobactam, ceftazidime or meropenem. Vancomycin or metronidazole may be needed for MRSA or anaerobic cover respectively.
28
Define Primary HIV infection
Primary HIV infection, or HIV seroconversion illness, is the phase that commences immediately after the initial exposure to the Human Immunodeficiency Virus (HIV). This phase is characterised by a surge in viral replication and often coincides with the onset of clinical symptoms. Advanced HIV disease, also known as AIDS, is defined as very low CD4 cell levels and the development of opportunistic infections or malignancies also known as AIDS-defining illnesses.
29
What is the aetiology of HIV infections?
HIV, specifically HIV-1 and HIV-2, are retroviruses that cause primary HIV infection. They are predominantly transmitted through sexual contact, parenteral exposure (e.g., injection drug use, needlestick injury), or from mother to child during childbirth or breastfeeding. HIV infects the CD4+ T-cells, integrating its DNA into the host genome which is then transcribed into viral proteins.
30
What are the distinct stages of HIV infections?
Primary HIV infection, which is associated with symptoms and high infectivity along with immune activation. Asymptomatic phase, associated with a low transmission risk. As viral diversity increases, the virus befins to evade the immune response. Advanced HIV disease (AIDS) whereby the immune system is compromised giving rise to opportunistic infections and malignancies
31
What are some of the initial signs and symptoms of HIV infections?
Typically, individuals with primary HIV infection experience a mild flu-like illness 2-6 weeks post-exposure. The range of clinical manifestations can span from a mild glandular fever-like syndrome to an evolving encephalopathy. Classic presentations include: Fever Lymphadenopathy Maculopapular rash (commonly found on the upper chest) Mucosal ulcers Myalgia Arthralgia Fatigue Symptom onset within 3 weeks of infection, lasting longer than 2 weeks or involving the central nervous system (CNS), is associated with rapid progression to AIDS. It's worth noting that some individuals might remain asymptomatic.
32
What are the long standing HIV symptoms?
Constitutional symptoms Respiratory conditions such as pneumocystis pneumonia (classically causes reduced SpO2 on exertion), tuberculosis or recurrent respiratory infections Neurological symptoms of cryptococcal meningitis, cerebral toxoplasmosis, cerebral lymphoma, cytomegalovirus retinitis Malignancies including lymphoma, Kaposi's sarcoma (dark purple/brown skin lesions), cervical cancer Skin conditions: fungal skin & nail, viral and bacterial infections - especially severe or recurrent Oral conditions such as candidiasis, ulcers, oral hairy leukoplakia Gastrointestinal: oesophageal candidiasis, diarrhoea, hepatitis infections Genital: candida, genital herpes & warts - especially if severe Unexplained FBC abnormalities
33
What are the investigations for a primary HIV infection?
Laboratory tests: a venous blood sample is taken and sent to a laboratory for testing. Third-generation tests detect IgM and IgG antibodies, with highest sensitivity during the initial seroconversion period. The window period for third-generation tests is 60 days. Fourth-generation tests also detect serology as well as the p24 antigen, with a window period of 45 days. Point of care tests: these are similar to third-generation laboratory tests but can be performed in the community with a fingerprick testing kit. The window period for these is 90 days. A confirmatory laboratory test is required for diagnosis. Where there is uncertainty, molecular assays are sometimes used. A range of tests are then performed to facilitate treatment decisions. These may include: FBC, U&E, LFT's, liver, bone profile, lipids, HbA1c, TB testing, CXR, ECG, toxoplasma serology Sexual health screen Viral load, genotype testing, tropism tests, HLA testing, CD4 count and CD4:8 ratio
34
What is the treatment for a primary HIV infection?
All patients diagnosed with primary HIV infection should be offered combination antiretroviral therapy (cART), regardless of their CD4 count. This may involve a combination of three drugs, including: Reverse transcriptase inhibitors Nucleoside (NRTIs) e.g. Tenofovir, Abacavir, Emtricitabine, Lamivudine, Zidovudine Non-nucleoside (NNRTIs) e.g. Efavirenz, Nevirapine, Rilpivirine Protease inhibitors e.g. Darunavir, Lopinavir/ritonavir, Saquinavir Integrase inhibitors e.g. Dolutegravir, Raltegravir CCR5 antagonist e.g. Maraviroc Fusion inhibitors e.g. Enfuvirtide A typical regime will include two nucleoside reverse transcriptase inhibitors and one additional drug. Contact tracing is necessary to identify and notify individuals who may have been exposed to the virus. Regular monitoring and appropriate management of any comorbid conditions are also integral to the care of these patients. Pre- or post- exposure prophylaxis can be offered to those who may be/have been exposed to reduce transmission risk.
35
Name some opportunistic infections due to HIV:
Pneumocystis pneumonia This is a fungal infection caused by Pneumocystis Jirovecii and affects immunocompromised people, including those with HIV. Typically patients present with a subacute onset of fever, dry cough and exertional breathlessness. Patients desaturate on walking short distances, and chest X-ray may be normal or show bilateral infiltrates. Definitive diagnosis requires a sputum or broncho-alveolar lavage sample with silver staining. Management is with co-trimoxazole, with steroids for moderate-severe cases, and supportive care. Patients may be offered prophylactic co-trimoxazole if they have very low CD4 counts or have had a previous pneumocystis pneumonia. Candidiasis While this is a common condition in the general population, those with HIV may develop more severe or widespread infections. They may develop oesophageal candidiasis which causes painful or difficult swallowing. It is usually treated with oral fluconazole. They may require referral for biopsy if unresponsive to treatment due to malignancy risk. Cytomegalovirus This is a common viral infection remains latent in the body following primary infection. In immunocompromised states - such as advanced HIV - it can reactivate and cause a range of problems. Patients may experience visual changes due to CMV retinitis, polyradiculopathy, respiratory problems or gut symptoms. Ganciclovir is the first-line treatment for CMV infection. Cryptococcal meningitis Cryptococcus is a fungal infection that primarily affects immunocompromised people. This usually presents as a subacute meningitis involving headache, fever, altered mental status and cranial nerve deficits. Diagnosis is with CSF analysis cultured and stained with India ink. Treatment involves an induction regime with amphotericin B alongside supportive treatment, followed by a maintenance regime of fluconazole. Cerebral toxoplasmosis This occurs due to reactivation of a toxoplasmosis infection. It typically presents with altered mental state, headache, seizures, focal neurology and fevers. MRI is most sensitive for diagnosis and will show multiple ring enhancing lesions of toxoplasma abscesses. Treatment is with pyrimethamine, sulphadiazine and folinic acid for 6 weeks followed by a maintenance regime. Mycobacterial disease Patients may with severe tuberculous disease, and the two often co-exist. However, patients with HIV are also susceptible to non-tuberculous mycobacterial disease including disseminated M. avium complex. Patients often present non-specifically with fever, night sweats, gastrointestinal upset, fatigue and anorexia. Diagnosis is based on cultures and treatment is with combination antibiotic regime.
36
Name some HIV associated malignancies:
Kaposi's sarcoma This is caused by human herpes virus 8 (HHV-8). It causes multiple lesions on the skin, mucous membranes and internal organs, which may be purple, red or brown. It is often recognised clinically, though definitive diagnosis requires biopsy. Treatment generally involves combination antiretroviral therapy to manage the underlying immunodeficiency, though systemic anticancer therapy may be needed. LANA1 (latent nuclear antigen 1) is usually expressed by Kaposi's sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus 8 (HHV-8). Lymphoma EBV-associated lymphomas are more common in HIV patients as their immune system is less effective at clearing the EBV virus. They may present with enlarging lymph nodes, night sweats, fevers and weight loss. Diagnosis is with biopsy and management is with systemic chemotherapy in conjunction with oncology. Cervical cancer Patients with HIV are less able to clear HPV infections that can lead to cervical cancer. As a consequence, they are at increased risk of developing cervical cancer and undergo annual cervical screening.
37
Name some additional complications of HIV:
Progressive muscle wasting & weakness Diarrhoea Neurological problems Mental health problems Metabolic abnormalities and cardiovascular disease Renal disease Osteoporosis
38
Define AIDS:
AIDS is the terminal stage of HIV infection where combination antiretroviral therapy (cART) has not halted the spread of the virus. It is defined by the presence of an AIDS-defining illness alongside a CD4 count of less than 200 cells/mm³.
39
In immunocompromised patients, such as those with HIV and a low CD4 count, Mycobacterium avium intracellulare can cause abdominal pain due to lymph node enlargement. What does this show on blood tests:
resulting in elevated levels of alkaline phosphatase and lactate dehydrogenase.
40
Define gastroenteritis:
Gastroenteritis: an enteric infection causing acute-onset diarrhoea, with or without associated symptoms
41
Define food poisoning:
Food poisoning: illness caused by eating or drinking substances contaminated with disease-causing pathogens, toxins or chemicals.
42
Define acute diarrhoea:
Acute diarrhoea: 3+ episodes liquid/semi-liquid stools in in a 24h period, lasting less than 14 days
43
Define prolonged diarrhoea:
acute-onset diarrhoea lasting over 14 days
44
Define dysentery:
is acute infectious diarrhoea with blood & mucus, often with associated symptoms
45
What are the three most common viruses causing gastroenteritis:
Most cases of infectious diarrhoea are spread by the faeco-oral route and are caused by viruses. These include: Norovirus: most common cause in the population, and often causes outbreaks. Typically causes projectile vomiting and non-bloody diarrhoea. Rotavirus: the most common cause of gastroenteritis in children. Adenovirus: typically causes respiratory tract infections but may cause gastrointestinal symptoms in children.
46
Name some common bacterial causes of gastroenteritis:
Campylobacter: often associated with contaminated food & drink (in exams: a recent barbeque!), this is the most common cause of bacterial gastroenteritis in the UK. On microscopy, gram-negative rods are seen with characteristic 'seagull' shape, which release enterotoxin in the gut and invade the mucosa. Incubation period is 16-48 hours and may cause bloody diarrhoea, though vomiting is rare. E. coli: the most common cause of traveller's diarrhoea. In the UK, O157:H7 is the most common type and may cause bloody diarrhoea. Sources include improperly cooked meat. Associated complications include haemolytic uraemic syndrome, which typically affects the very young are old and can be fatal. Salmonella is associated with consumption of contaminated foods, particularly poultry, eggs and milk. These are gram negative bacteria with an incubation of 16-48 hours. Salmonella can cause bloody diarrhoea and is associated with complications such as sepsis, endocarditis, mycotic aneurysm and osteomyelitis. Cholera is associated with contaminated water supplies and causes very watery diarrhoea associated with dehydration. Shigella and Yersinia tend to occur in children. The former can cause severe, bloody diarrhoea. Bacillus cereus are gram-positive rods that produce two toxins causing diarrhoea and vomiting within hours of eating contaminated food (in exams, this is usually reheated rice). Staphylococcus aureus produces a heat-stable enterotoxin that causes profuse vomiting with mild diarrhoea and abdominal pain. The incubation period is short (under 6 hours) after eating contaminated foods. The bacteria are usually introduced from the skin of the person preparing the food. Foods which do not require cooking carry greater risk.
47
Name some parasites causing gastroenteritis:
Cryptosporidium: a protozoal infection which may cause prolonged symptoms Entamoeba histolytica: most cases are mild but severe cases cause dysentery Giardia: causing diarrhoea, constitutional symptoms and bloating which may be prolonged
48
What are the signs and symptoms of gastroenteritis:
Sudden-onset diarrhoea, with or without blood Faecal urgency Nausea & vomiting Fever, malaise Abdominal pain Associated symptoms specific to the cause
49
What are the investigations for gastroenteritis:
Often, infectious diarrhoea is a clinical diagnosis and, providing the patient is not systemically unwell, may not need further investigation. It is important to assess hydration status and consider whether the person can tolerate oral fluids. A stool culture may be needed if there are any higher risk features. These include if the person is systemically unwell, is immunocompromised, presents with dysentery or prolonged diarrhoea, there is increased risk of transmission, food poisoning is suspected or symptoms are associated with recent travel. If a person is unwell presenting to secondary care, consider performing blood tests to include FBC, U&Es, CRP, LFTs and TFTs. Consider a VBG, blood cultures and monitoring urine output if they appear septic.
50
Name some notifiable diseases which cause gastroenteritis:
Food poisoning Haemolytic uraemic syndrome Dysentery Enteric fever Cholera
51
What is the management for gastroenteritis:
If a person is systemically unwell, or severely dehydrated, adopt an A-E approach and consider initiating the sepsis six. Admit the patient and seek senior help early. They may need IV fluids, antiemetics or antibiotics. The most appropriate initial management for a patient presenting with gastroenteritis and symptoms of dehydration is oral rehydration therapy (ORT) Conservative: advise regular fluids, with or without rehydration salts, and safetynet for signs of dehydration. Antidiarrhoeal drugs are not routinely used, and should be avoided if the patient has symptoms of dysentery or suspected E. coli 0157. Medical: antimicrobials are not routinely indicated, but clinical suspicion or positive cultures of the following may prompt initiation of antibiotics: Campylobacter: macrolide e.g. clarithromycin Amoeba, Giardia: anti-protozoal e.g. metronidazole Cholera: tetracycline If a patient is systemically unwell, immunosuppressed or elderly, consider empirical antibiotics following local pathways and microbiology advice. Infectious diarrhoea can be prevented by avoiding foods that are undercooked or prepared in unsanitary conditions, and handwashing at appropriate times and hygiene measures. Enhanced precautions such as isolation and barrier nursing along with handwashing can prevent spread in clinical settings. People should not return to work until 48 hours after their symptoms have resolved.
52
What are the complications of gastroenteritis:
Young children, elderly, people with comorbidities or immunocompromised and pregnant women are at highest risk of complications. These include: Dehydration, electrolyte disturbance, acute kidney injury Haemorrhagic colitis, haemolytic uraemic syndrome, thrombotic thrombocytopenic purpura Reactive arthritis Toxic megacolon Sepsis Longer-term complications include: faltering growth, irritable bowel syndrome and lactose intolerance.
53
Define necrotising fasciitis:
Necrotising fasciitis is a life-threatening infection of the soft tissue.
54
Causes of necrotising fasciitis?
Bacteria causing necrotising fasciitis include: Polymicrobial infection - typically afffecting those with immunocompromise or comorbidities Group A streptococcus - can appear in any age Gram-negatives - occuring due to seawater contamination Fungal infections - affecting wound or burns patients or in the immunocompromised
55
What are the signs and symptoms of necrotising fasciitis?
Early in the disease: only minor skin changes with pain, swelling and erythema, often poorly defined Pain, tenderness, systemically unwell patient disproportionate to the clinical signs Bullae & ecchymoses Tense oedema, discoloration and necrosis occur after a couple of days On palpation, tissues may appear wooden-hard and there may be crepitus Hypotension, shock and altered mental status occur later in the disease Rapidly worsening cellulitis with pain out of keeping with physical features
56
What are the investigations for necrotising fasciitis?
Necrotising fasciitis is a clinical diagnosis. Surgery is used to confirm the diagnosis as part of management. Additional tests include: Blood tests: FBC, U&E's, CRP, CK (may be raised due to muscle breakdown) Blood cultures, wound swab, fungal culture Histology of excised tissue
57
What is the management for necrotising fasciitis?
In an acutely unwell patient, adopt an A-E approach, get senior help early & consider initiating the sepsis six. Patients may need ICU input. Once resuscitated, urgent surgical debridement is needed. This is repeated daily until the infection is controlled. The wound is closed by secondary intention (left open to repair with appropriate dressings), though skin grafts may be required. Empirical antibiotics covering possible organisms will be required, and will depend on local policies and microbiology advice Supportive measures include adequate nutrition, supporting the organ systems with careful monitoring and providing sufficient symptom control it is important to first debride the necrotic tissue before initiating IV antibiotics.
58
What are the types of necrotising fasciitis?
- What is type I necrotising fasciitis? polymicrobial infection caused by mixed aerobes and anaerobes - Who does it occur more commonly in? post-surgery in diabetics - What is type II necrotising fasciitis? monomicrobial infection caused by *Streptococcus pyogenes*
59
Define a notifiable infectious disease?
A notifiable infectious disease is any disease which healthcare practitioners are legally required to report to the UK Health Security Agency (UKHSA). The legislation underpinning this is: Public Health (Control of Disease) Act 1984 Health Protection (Notification) Regulations 2010 Reporting infectious diseases is a statutory requirement and one of the overriding public interests in which confidentiality can be broken - but only in the limited capacity as required by UKHSA. It is good practice to discuss with the patient first, but disclosure must take place regardless. This is to control the spread of potentially serious infectious diseases, and monitor cases.
60
What is the list of notifiable diseases?
Acute encephalitis Acute infectious hepatitis Acute meningitis Acute poliomyelitis Anthrax Botulism Brucellosis Cholera COVID-19 Diphtheria Enteric fever Food poisoning Haemolytic uraemic syndrome Dysentery Invasive group A streptococcal disease Legionnaire's disease Leprosy Malaria Measles Meningococcal septicemia Monkeypox Mumps Plague Rabies Rubella Severe acute respiratory distress syndrome Scarlet fever Smallpox Tetanus Tuberculosis Typhus Viral haemorrhagic fever Whooping cough Yellow fever
61
Define sepsis
defined as a syndrome of life-threatening organ dysfunction due to a dysregulated host response to infection.
62
Define septic shock:
is another term used to describe some patients with sepsis who are at greater risk of death. To be classified as having septic shock, patients need to be persistently hypotensive, requiring vasopressors to maintain a mean arterial pressure of 65 mmHg or more and have a lactate of over 2 mmol/L despite adequate fluid resuscitation.
63
What are the risk factors for sepsis:
Pregnancy Recent miscarriage or abortion Frailty Immunocompromise due to chronic comorbidities e.g. HIV, diabetes, sickle cell disease Immunosuppression secondary to medications e.g. chemotherapy, steroids Recent surgery or trauma Skin breaks or infections Drug or alcohol misuse Indwelling lines or catheters
64
What are the symptoms for sepsis:
General malaise Fevers, sweats or chills Localising signs of infection e.g. rashes, dysuria Decreased urine output Confusion Breathlessness Nausea and vomiting Myalgia
65
What are the signs for sepsis:
Tachycardia Hypotension Pyrexia or hypothermia Dehydration e.g. dry mucous membranes Altered mental state including delirium Irritability Respiratory distress e.g. tachypnoea, accessory muscle usage Cyanosis and hypoxia Delayed capillary refill time Cool extremities Skin appears mottled or ashen
66
What is the sepsis 6?
Blood cultures ideally prior to antibiotic administration Lactate (i.e. a blood gas - venous or arterial) Urine output (which may involve inserting a urinary catheter) IV fluid resuscitation (usually a 500ml bolus over 15 minutes initially) Supplementary oxygen to target saturations of 94-98% (88-92% if at risk of type 2 respiratory failure) Broad-spectrum IV antibiotics (as per local guidelines) In septic patients with potential for anuria, it is important to insert a urinary catheter to accurately monitor fluid balance
67
What other investigations do we do for sepsis ?
Blood tests should include: FBC and CRP for inflammatory markers U&Es looking for evidence of acute kidney injury LFTs as a baseline prior to giving antibiotics, may be deranged in sepsis Coagulation screen as this may be deranged in sepsis Imaging should include: Chest X-ray as part of a septic screen
68
What is the other management for sepsis?
Other conservative management considerations involve: Close monitoring of observations, fluid balance, clinical condition and bloods including serial lactate measurement Early escalation for senior review and inform intensive care as may require interventions such as inotropes or vasopressors Other medical management involves: Modify antibiotic therapy if a source of infection is identified or microbiological results become available Further IV fluids may be required however this should be done with careful fluid balance monitoring Surgical management involves: Source control, e.g. draining abscesses or debriding infected tissue Infected devices may need to be removed
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What are the complications of sepsis?
Multi-organ failure including renal failure, heart failure, acute respiratory distress syndrome and cholestasis Coagulopathy including disseminated intravascular coagulation Delirium which may be associated with long-term cognitive impairment e.g. difficulty concentrating and memory loss Mental health impacts including anxiety, depression and post-traumatic stress disorder Secondary infections which are often hospital-acquired Polyneuropathy i.e. critical illness polyneuropathy, characterised by generalised weakness and sensory loss Death
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What is the prognosis for sepsis?
Overall mortality has been estimated at around 20-30% This increases to 64% in patients aged over 85 years Patients with septic shock also have higher mortality (40-60%) Risk of death in survivors remains raised after recovery (15% of sepsis survivors die within a year of discharge, with 6-8% more dying each year for the following 5 years)
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In fluid-refractory septic shock, what is the treatment of choice to maintain blood pressure and organ perfusion, as fluids alone are insufficient.
intravenous noradrenaline infusion
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Define varicella zoster virus?
Varicella zoster virus (VZV) or human alpha-herpesvirus 3 (HHV-3) causes the skin infection 'chickenpox' in children. Following initial infection, the virus lies dormant in the dorsal root ganglia and may be reactivated in later life, manifesting as shingles. Disseminated disease occurs in immunocompromised hosts.
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What does chicken pox present as?
Chickenpox typically presents with a vesicular rash, often accompanied by fever and fatigue. The vesicles typically described as 'Dew drop on a rose petal' initially being pruritic macules and papules and becoming** pustular, before drying out and crusting over within a week. starts on the scalp and gradually spreads down the face, trunk, and extremities. Patients often complain of itching and fever.
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What is the treatment for chicken pox?
Chickenpox is usually self-limiting and does not require any treatment. Self-care measures include calamine lotion, antipyretics, chlorphenamine for itching. In immunocompromised patients, there is the risk of pneumonia, encephalitis and hepatitis, which would likely require admission.
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What might primary infection of varicella zoster cause in pregnant women?
Primary infection within the first 20 weeks may result in foetal varicella syndrome characterised by limb hypoplasia, cutaneous scarring, eye defects and neurological abnormalities (e.g. microcephaly)
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What is the treatment for pregnant women who have a primary infection of varicella zoster virus?
Pregnant women may be provided Post exposure prophylaxis if they are found to have no detectable VZV IgG on testing with aciclovir from day 7-14 post exposure. This regime is also used in immunosuppressed individuals.
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Define shingles and the signs and symptoms?
Shingles is a reactivation of the VZV that causes chickenpox. Shingles presents with a unilateral vesicular rash that follows a dermatomal distribution. The rash can be painful, and pain can persist beyond resolution of the rash (post-herpetic neuralgia). nose tip vesicles which is known as Hutchinson’s sign. This means the virus is three times more likely to cause ocular complications and must be taken very seriously. Intravenous antivirals are warranted
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What is the treatment for shingles?
Oral antiviral therapy with aciclovir can be initiated within 72 hours of rash onset to reduce the risk of post-herpetic neuralgia. Pain can be managed with simple analgesia, such as paracetamol and NSAIDs.
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Define post-herpetic neuralgia?
Post-herpetic neuralgia is persistent pain following shingles infection. The pain is neuropathic in nature and localised to a dermatomal distribution; it may also manifest as allodynia, hyperalgesia or pruritus. Treatment is primarily supportive and most cases resolve within a few months. Some oral anticonvulsants can be used in the management of shingles pain and postherpetic neuralgia. The most commonly used are gabapentin and pregabalin.
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What is Ramsay hunt syndrome?
LMN facial nerve palsy due to reactivation of varicella zoster virus in geniculate ganglion of facial nerve
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What are the signs and symptoms of Ramsay hunt syndrome?
- First is auricular pain - Then unilateral facial nerve palsy and vesicular rash around ear (may also get blisters on anterior 2/3 of tongue)
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What is the treatment for Ramsay hunt syndrome?
Oral aciclovir and corticosteroids (prednisolone)
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What is Herpes Zoster Ophthalmicus?
Reactivation of varicella zoster virus in area supplied by ophthalmic division of trigeminal nerve
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What are the clinical features of herpes zoster opthalmicus?
- Vesicular rash around eye - Hutchinson’s sign (rash on tip or side of nose) → indicates likely ocular involvement e.g. anterior uveitis
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Define viral exanthema?
An exanthem is a widespread rash occurring alongside systemic symptoms of infection.
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Name some common viral causes of exanthema?
Chickenpox Measles Rubella Roseola infantum Parvovirus B19
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What are the investigations for viral exanthema:
Viral swab: culture, immunofluorescence & PCR Blood tests: serology, PCR, ANA, specific antibodies HIV testing
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What is the management for viral exanthema?
Adopt an A-E approach, seek senior help early and initiate the sepsis six if sepsis is suspected. Otherwise, management of exanthems have two aims: Treatment specific to the underlying cause, or giving patient information about the likely course of self-limiting illnesses. Please see the relevant pages for management of specific conditions. Supportive management and self-care, involving antipyretics for fever, emollients to reduce itch, ensuring patients stay hydrated and are safety netted to return for new, worsening or unresolved symptoms.
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Define clostridium difficile:
Clostridioides difficile previously known as Clostridium difficile is a Gram-positive anaerobic bacteria that produce spores which releases exotoxin which causes intestinal damage and can lead to life-threatening complications including pseuodomembranous colitis and toxic megacolon. Infection is often seen in patients who have recently received broad-spectrum antibiotics.
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What are the different classifications of clostridium difficile?
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What causes clostridium difficile:
Recent treatment with broad-spectrum antibiotics – nearly all antibiotics can cause C. difficile infection, with common culprits being: Clindamycin Ciprofloxacin Third-generation cephalosporins (eg. Ceftriaxone) Penicillins including Piperacillin-tazobactam (Tazocin) Carbapenems (eg. Meropenem) Increased length of stay in hospital Age over 65 years Predisposing conditions including inflammatory bowel disease (IBD), cancer or kidney disease, and immunosuppression (diabetes or HIV infection, or as side effect of chemotherapy or steroids) Prolonged proton pump inhibitor (PPI) usage
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What are the signs and symptoms of c.difficile infection
Infection presents as a wide range of clinical disease, ranging from asymptomatic colonisation or trivial diarrhoea to life-threatening illness. The most common symptoms and signs of C. difficile infection are: Watery diarrhoea, which can be bloody Painful abdominal cramps Nausea Signs of dehydration, such as dry mucous membranes, tachycardia and oliguria Fever Loss of appetite and weight loss Confusion Clinical note: classically the white cell count (WCC) rises with little change in C-reactive protein (CRP) – always consider C. difficile if a patient has been on antibiotics and was responding but now has worsening clinical and biochemical results.
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What are the investigations for c.difficile infections?
1st line investigations include a stool culture, which must also be toxin positive (as patients can have C.difficile growth but be asymptomatic) Blood tests including FBC (to determine severity), CRP and U&E's Imaging - abdominal X-ray and erect chest x-ray if concerns of perforation or toxic megacolon, with CT abdomen being a gold standard for picking up these complications. Barium enemas should be avoided as they carry a risk of perforation.
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What is the conservative management for c.difficile infections?
Evaluate current antibiotics and stop if not extremely necessary Move to side room and barrier nurse immediately
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What is the medical treatment for c.difficile infections?
Antidiarrhoeal agents should be avoided and opiate use minimised (the antiperistaltic effects and toxin entrapment can predispose to toxic megacolon) Replace fluid and electrolyte losses as needed with IV rehydration Antibiotics Oral vancomycin (not IV) is the first-line treatment. Antibiotics may be needed for up to 2 weeks Second line – fidaxomicin Third line = oral vancomycin +/- IV metronidazole In patients with recurrent infection, a faecal transplant may be a viable option Surgical: in life-threatening toxic megacolon, a subtotal colectomy may be required
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What are the complications of c.difficile infections?
Pseudomembranous colitis: severe C.difficile infection with a ‘pseudomembrane’ of immune cells, mucous and necrotic tissue. Toxic megacolon: presents with ileus, and has a high risk of perforation. Systemic toxicity and manifestations of the systemic inflammatory response syndrome (SIRS), including leucocytosis (≥15.0 × 109/l), rising serum lactate levels (≥5 mmol/l), hypotension requiring vasopressor therapy, acute renal failure and respiratory distress – all indicators of poor prognosis and high mortality
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Define hepatitis:
Hepatitis refers to the inflammation of the liver. It is typically caused by viral infection but can also result from non-infectious aetiologies such as toxins and alcohol. Hepatitis A and Hepatitis E can lead to acute liver failure, whereas Hepatitis B and Hepatitis C tend to lead to chronic liver failure. Hepatitis D only occurs in individuals who are infected with Hepatitis B.
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What is the epidemiology of hepatitis:
Viral hepatitis is common in the UK with the primary causes being hepatitis A, B, and C viruses. These can cause acute disease, but hepatitis B and C can also lead to chronic infection, liver fibrosis, and hepatocellular carcinoma. The prevalence of Hepatitis A is higher in developing countries, while Hepatitis B is the most common cause of hepatitis globally. Other causes of acute hepatitis include drugs, toxins, alcohol, EBV, CMV, hepatitis E, leptospirosis, and malaria. NB: All infectious hepatitis cases are notifiable diseases in the UK.
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Acute liver failure with prodromal signs such as - Fever - Malaise - Anorexia - Nausea and vomiting are caused by what types of hepatitis:
A and E
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Signs of acute hepatitis:
Right upper quadrant pain Jaundice Tender hepatosplenomegaly (due to swelling of the liver capsule)
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Signs of chronic liver failure:
Hepatic encephalopathy Jaundice Ascites Coagulopathy due to abnormal clotting
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Which virus causes hepatitis A:
RNA picornavirus, transmitted by faecal-oral route (occasionally through food sources or through anal sex)
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Which virus causes hepatitis E:
Calcivirus
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What is the epidemiology of hepatitis A:
Prevalence is high in developing countries. Increasing age is the only real determinant of disease severity, with the greatest morbidity and mortality in those over 50 years old. Travellers and those at risk can be offered immunisation It is transmitted via the faecal-oral route (commonly through shellfish)
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What is the presentation of hepatitis A:
Flu-like symptoms followed by jaundice, pale stools (in some), dark urine and abdominal pain Incubation period of 2-6 weeks, presents only as an acute hepatitis with no chronic phase Complete recovery can take up to 6 months. Manage conservatively
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What are the investigations for hepatitis A:
Hepatitic LFTs, with ALT/AST as high as in the 1000s IgM and IgG antibodies to HAV
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Give an overview of hepatitis E:
Similarly spread via faecal-oral route (commonly undercooked pork) It is extremely dangerous in pregnancy, with a mortality rate up to 20% Similar to Hepatitis A with only an acute presentation and no chronic phase, with management also supportive in nature
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What is the cause of hepatitis B:
dsDNA virus of Hepadnaviridae family Primarily causes an acute hepatitis, with the main and most severe complication being progression to chronic hepatitis infection
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What is the epidemiology of hepatitis B:
Most common cause of hepatitis globally High prevalence regions include sub-Saharan Africa, Asia and the Pacific Islands. Decline of disease in children and adolescents in the UK is due to routine vaccination Incubation period usually 60-90 days.
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How does hepatitis B transmit?
Transmission is via infected blood or body fluids Vaginal/anal intercourse Transfusion Vertical transmission (in 90% of pregnancies where the mother is HBeAg positive, and 10% where this is negative). In developing countries, infection is mostly in childhood through vertical or horizontal transmission. In areas of low endemicity (such as the UK), infections are mostly acquired in adulthood.
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What is the presentation of hepatitis B:
Children - Only 5% of children have jaundice and severe symptoms i.e. it is mostly an asymptomatic primary infection, but the majority (90%) develop chronic disease with only 10% able to clear the virus Adults - more likely to have an acute hepatitis picture with jaundice, fever, malaise, viral prodrome and occasionally darkening of urine and lightening of stool. Some develop fulminant liver failure with decompensation (ascites, encephalopathy etc.). 90% clear the infection, with only around 10% developing chronic disease Chronic features occur when the virus has been unable to be cleared for more than 6 months - development of cirrhosis, decompensated liver failure, and increased risk for hepatocellular carcinoma Rarer features of hepatitis B infection include glomerulonephritis, cryoglobulinaemia and polyarteritis nodosa
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What are the investigations for hepatitis B:
HBsAg is detected 3-5 weeks after infection. If present for >6 months, this defines carrier status (5-10% of infections). In carriers, HBeAg-positive patients are the most infectious. If HBeAg-negative (and anti-HBe-antibody positive), they have lower infectivity. Patients with chronic infection who are HBeAg -ve may get immune escape phase when the virus mutates despite anti-HBe antibodies being present. These patients are the main pool for the spread in the UK, and so all chronically infectious patients need yearly screens to identify this Biopsy of the liver in chronic hepatitis B infection will reveal 'ground-glass' hepatocytes on light microscopy
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What is the serology in hepatitis B:
A positive hepatitis B surface antigen (HBsAg) signifies current infection, either acute or chronic. The anti-HBc antibodies indicate at what stage the infection is. During acute infection, anti-HBc IgM is positive. Then anti-HBc IgG becomes positive in chronic infection or in resolution of infection and remains positive. The HBeAg indicates viral replication. This is negative here and the anti-HBe antibody is positive, indicating a low viral load.
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What is the management for hepatitis B:
There is no cure for chronic hepatitis B, but there is a functional cure as you can prevent liver disease with pegylated interferon Indications for antiviral treatment - Adults aged 30 years and older who have HBV DNA greater than 2000 IU/ml and abnormal ALT on 2 consecutive tests conducted 3 months apart - Adults who have HBV DNA greater than 20,000 IU/ml and abnormal ALT on 2 consecutive tests conducted 3 months apart regardless of age or the extent of liver disease - Adults with cirrhosis and detectable HBV DNA, regardless of HBeAg status, HBV DNA and ALT levels Pegylated interferon alfa-2a is the first line, with tenofovir and entecavir as second-line alternatives - Pegylated interferon can lead to viral suppression which leads to ALT normalisation and improved liver histology
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If a patient with hepatitis B becomes suddenly very unwell with a worsening hepatitic picture, consider if they are now suffering co-infection with
Hepatitis D
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What is the special case for hepatitis D infecting people:
It’s a defective virus- requires Hep B surface antigen to complete its replication and transmission cycle - So which groups can it only infect? **(2)** - Co-infect with Hep B - Superinfect people who’re already carriers of Hep B → we suspect Hep D superinfection in chronic Hep B patients who have flare ups
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What virus causes hepatitis C:
RNA virus of the Flaviviridae family, with 6 major genetic types (genotypes 1 and 3 are most common in the UK, and genotype 1 is associated with longer treatment and worse prognosis) There is no vaccination for Hepatitis C, currently
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What is the transmission route of hepatitis C:
Transmitted via exchange of blood and bodily fluids: Intravenous drug use Blood transfusion Haemodialysis (rare in the UK) Sexual transmission (less than 1% per year of relationship, but rate higher if co-infected with HIV) Needlestick injuries in healthcare facilities - 3% risk of transmission. Perinatal infection from infected mother. Incubation period of 6-9 weeks.
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What is the presentation of hepatitis C infection:
Most infections are asymptomatic, and only 15-25% clear the virus. 75% go on to develop chronic infection Patients with chronic infection have persistently high LFTs, and cirrhosis develops in 20-30% 1-4% of patients with cirrhosis develop hepatocellular carcinoma, and 2-5% develop liver failure Additional features – arthralgia/arthritis, Sjogren’s syndrome, cryoglobulinaemia, porphyria cutanea tarda, membranoproliferative glomerulonephritis
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What are the investigations for hepatitis C:
Anti-HCV serology - 90% are positive 3 months after infection but it may take many months to become positive for some Even if the virus has been cleared, HCV antibodies can remain positive for months afterwards HCV RNA - if positive for more than two months then need to be treated.
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What is the management for hepatitis C:
Symptomatic treatment in the early stages of the disease There is a cure (Hepatitis C for Cure), unlike in Hepatitis B Drug therapy should be considered for all patients and depends on the genotype of the virus. Direct-acting antiviral (DAA) therapy is the standard treatment for chronic hepatitis C. Nucleoside analogs are generally preferred e.g. Sofosbuvir and often lead to undetectable viral loads Sofosbuvir and daclatsavir may be used as combination therapy Antivirals of proven benefit in basically every patient irrespective of the amount of cirrhosis and fibrosis Manage any underlying cirrhosis