Infection Flashcards

1
Q

Candidiasis
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication

A

Candida albicans (dimorphic fungus) lives in low numbers in healty skin, oropharyngeal cavity and GI and GU tracts
Causes diease in :
- immunosuppressed (HIV, diabetes, steroid use)
- Imbalance of local flora ( antibiotic, steroid use)
- Compromised skin

Causes infection in two eays:
1) Local: imbalance in local flora so C albicans overgrows
2) Systemic infection: breach in skin barrier so dirrectly goes into the blood stream

CLINICAL FEATURES
1) Oral thrush : white plaque in oral cavity that when scraped off show inflamed areas, feels cottony in mouth, see fissuring at mouth corners, patient may have been on ICS (beclomethasone in asthma)

2) Oesophageal candidiasis: AIDS, gget odynophagia (pain on swallow)

3) Vulvovaginitis: vaginal yeast infection, cottage cheese, non-offensive dyscharge, get dysuria and dyspareunia (sexual pain)

4) Systemic candidiasis: fever, fatigue, skin rash, neuro deficits

INVESTIGATIONS
Superficial smear of lesion for microscopy- may be positive for Candida hyphae
Vaginal swab not routinely needed if clinical features there
Blood culture, ABG, rotuine bloods if systemic: high lactate,hypoxia, high WBC, high creatinine, high PT APTT

MANAGEMENT
Vaginal candidiasis or immunosuppressed like HIV: Oral fluconazole
Oral candidiasis (2nd line vaginal) : Topic Antifungals: Clotrimazole, miconazole, nystatin
Severe/systemic disease: Oral fluconozole (echinocandin or fluconazole)

COMPLICATIONS
of oral candidiasis:
- oesophageal candidiasis
- disseminated candidiasis (sepsis)

PRONGOSIS
not bad even if recurrent, but aggressive treatment needed to preent recurrent

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2
Q

Herpes Simplex Virus
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication

A

Strains: HSV-1, HSV-2
Transmitted via direct contact with mucosal tissue or secretions of another person

HSV-1: in childhood via saliva. Causes herpes labialis (cold sores/oral herpes), HSV encephalitis
HSV-2: genital contact, Causes genital herpes

Risk Factors:
HIV
Immunosuppressive medication

CLINICAL FEATURES
Primary infection: severe gingivostomatitis (erythema and painful ulcerations on perioral skin and oral mucosa)
- painful genital ulcers with dysuria and pruritis
- tender inguinal lymphadenopathy
- oral ulcer, may have tingling sensation before
- erythema multiforme

Eczema hepeticum: infection of skin by HSV1 or 2. Seen in children with atopic eczema. Is a rapidly progressing painful rash with punched out erosions

Herpes simplex keratitis: painful red eye, photophobia, epiphoria, fluorescein stain shows liniar blanchin epithelial ulcer. (green little sprout looking thing in eye)

INVESTIGATIONS
If lesions present: VIral PCR
If none: viral culture
If suspect genital herpes: NAAT with swab from base of ulcer

MANAGEMENT
First line (gngivistomatic and genital herpes) : oral acicovir
Cold sores or herpes simplex keratitis: topical aciclovir
Symptom relief: IV fluid, barrier cream, pain relief (topical lidocane), antipyretics, antibiotics
Referral to opthalmologist immediately if herpes simplex keratitis

Pregnant woman with third trimester/28 weeks: Oral aciclovir until delivery and C section

Eczema Hepeticum : IV acyclovir

COMPLICATIONS
- oesophagitis
- meningitis
- encephalitis
- hepatitis
- bell’s palsy

PROGNOSIS
genital herpes and oral herpes are chronic viral infections with a highly variable course. Some people may have frequent outbreaks of disease, whereas others will be completely asymptomatic

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3
Q

Hospital Acquired Infections
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication

A

aka nosocomial Infections, are infections that are contracted 48 hours after hospitalisation and that were not present or incubating at the time of admission

risk factors:
- Age >70 years
- Lengthy hospital stays
- Foreign bodies: catheters or mechanical ventilation
- Recent antibiotic use
- Metabolic diseases (esp diabetes)
- Immunosuppression

COMMON CAUSATIVE PATHOENS AND INFECTION TYPES
Surgical site: E.coli, S.aureus
Nosocomial/HAP Pneumonia: S.aureus, p.aeruginosia or ventilator associated pneumonia
Nosocomal UTI: E.coli
Blood stream: S.aureus
GI: C.diff
Catheter related

Main multidrug resistant is: Methicillin-Resistant Staphylococcus Aureus (MRSA)

Treatment:
HAP pneumonia: co-amoxiclav for 5 days

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4
Q

Human Immunodeficiency Virus
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication

A

Retrovirus that infects and replicates primarily in human CD4+ T cells (lymphocytes) and macrophages, resulting in immunodeficiency

Transmitted via:
- Sexual fluids (majority of cases)
- Blood (IV drugs users sharing contaminated needles or blood transfusions)
- Breast milk

Risk Factors:
- HIV-infected blood transfusion
- IV drug use
- unprotected sexual intercourse
- percutaneous needle prick injury

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5
Q

What is toxoplasmosis

A

Happens in 50% of cerebral lesions in HIV pations

CLINICAL PRESENTATION
- Constitutional symptoms
- Headache
- Confusion
- Drowsiness

IMAGING
CT showing single or multiple ring-enhanced lesions

MANAGEMENT
Pyrimethamine + sulphadiazine for 6 weeks

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6
Q

Infectious Diarrhoea
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication

A

3 or more loose or watery stools per day or more frequent than normal
- Acute diarrhoea <14 days
- Chronic diarrhoea >14 days

Viral: norovirus, rotavirus, adenovirus
Bacterial: Campylobacter jejuni (poultry, gram - curved rod species best at 42 degrees), E.coli (travellers diarrhoea gram-) , C.diff (antibiotic and PPI associated gram +), Shigella (gram -), salmonella (gram -), bacillus cereus (6 hours then vomiting and diarrhoea)
Parasitic: Giardiasis (can cause lactose intolerance), enterobiasis, amebiasis

RF
- Recent travel (traveller’s diarrhoea)
- Exposure to outbreak
- Recent hospitalisation (c diff)
- Medication use

CLINICAL FEATURES
- Sudden onset watery/fatty/bloody stool
- Fever
- Abdo pain and cramping
- Nausea and vomiting

Norovirus
projective vomiting, incubation 12-24 hours highly infective

Salmonella
spread through eggs, poultry, contaminated food. Typhoid fever symptoms: fever, abdominal pain, non-bloody, yellow-green ‘pea soup’ diarrhoea, rose spots over abdomen

Campylobacter jejuni:
raw meat, incubation of 1-6 days, have prodromal headache and malaise, bloody diarrhoea, about pain mimics appendicitis

s.aureus
1-6 hours after exposure, profuse vomiting (ild diarrhoea)

bacillus cereus
spread through rice and pasta

entamobea histolytica
spread through contaminated water

giardisis
after ongoing diarrhoea and recent travel get abdominal pain, bloating/flatulence (lactose intolerance development), steatorrhoea, lethargy

INVESTIGATIONS
Bacterial infection - stool culture
Viral- PCR test
U&E and CRP and ESR

MANAGEMENT
if no systemic signs:
- Bed rest
- Fluids
- Electrolyte replacement with oral rehydration therapy

Systemic signs:
- Admit
- IV fluids
- Stool culture

For diarrhoea
Anti-diarrhoeal agents e.g. loperamide

ABx
c.diff: oral vancomycin (add IV metronidazole if severe)
campylobacter: clarithromycin
salmonella: ciprofloxacin

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7
Q

Necrotising Fasciitis
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication

A

Life-threatening subcutaneous soft tissue infection that requires a high index of suspicion for diagnosis
Most common site is the perineum (fourniers gangrene: is a risk of SGLT-2 inhibitors in T2DM)

Type 1: polymicrobial infection cause by mixed aerobes and anaerobes (common in post-surgery diabetics)
Type 2: mono microbial infection by streptococcus pyogenes

RF
- skin factors: recent trauma, burns or soft tissue infections
- diabetes mellitus: the most common preexisting medical condition, particularly if the patient is treated with SGLT-2 inhibitors
- intravenous drug use
- immunosuppression
- Varicella zoster infections

CLINICAL FEATURES
- Acute onset
- Anaesthesia or severe pain over site of infection
- Oedema (swelling) and erythema
- Systemic signs of infection:
- Fever
- Palpitations
- Tachycardia
- Tachypnoea
- Hypotension
- Lightheadedness
- Nausea and vomiting
- Delirium and crepitus (advanced cases)

Often presents as: Rapidly worsening cellulitis with pain out of keeping with physical features

INVESTIGATIONS
Surgical exploration to get blood and tissue cultures

MANAGEMENT
Urgent surgical debridement repeated until patient has no necrotic tissue

IV ABx : start as empirical until blood cultures

COMPLICATIONS
- Mortality
- Skin loss
- Scarring

PROGNOSIS
if shock and high-end organ damage 50-70% mortality

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8
Q

Notifiable diseases

A
  • Acute encephalitis
    • Acute infectious hepatitis
    • Acute meningitis
    • Acute poliomyelitis
    • Anthrax
    • Botulism
    • Brucellosis
    • Cholera
    • COVID-19
    • Diphtheria
    • Enteric fever (typhoid or paratyphoid fever)
    • Food poisoning
    • Haemolytic uraemic syndrome (HUS)
    • Infectious bloody diarrhoea
    • Invasive group A streptococcal disease
    • Legionnaires’ disease
    • Leprosy
    • Malaria
    • Measles
    • Meningococcal septicaemia
    • Monkeypox
    • Mumps
    • Plague
    • Rabies
    • Rubella
    • Severe Acute Respiratory Syndrome (SARS)
    • Scarlet fever
    • Smallpox
    • Tetanus
    • Tuberculosis
    • Typhus
    • Viral haemorrhagic fever (VHF)
    • Whooping cough
    • Yellow fever

The ‘Proper Officer’ at the Local Health Protection Team needs to be notified by the medical practitioner
They in turn will notify the Health Protection Agency on a weekly basis
‘immediately on diagnosis of a suspected notifiable disease’ and not to ‘wait for laboratory confirmation of a suspected infection or contamination before notification’

HIV is an exception on the list

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9
Q

Sepsis
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication

A

Life-threatening organ dysfunction caused by a dysregulated host response to an infection
Suspect sepsis based on acute deterioration in patient who has infection

RF:
- Age >65 years
- Immunocompromise
- Recent surgery
- Haemodialysis
- Diabetes
- IV drug use
- Breached skin integrity

CLINICAL FEATURES
- Signs associated with specific infection e.g. cough, dysuria, abdo pain
- NEWS2 ≥5 → indicates sepsis
- High >38 or low <36 temp
- Tachypnoea (20/min)
- Hypotension
- Tachycardia
- Altered mental status
- Low O2 sats
- Oliguria
- Poor CRT

INVESTIGATIONS AND MANAGEMENT
BLUOAF : take 3 give three
Take:
- blood culture (immediately before ABx)
- serum lactate levels ( determines severity, may show metabolic acidosis with raised lactate)
- hourly urine output

Give:
- O2: 94-96% sats to be maintained
- Broad spectrum ABx
- IV Fluid: 500ml crystalloid

also: Vasopressor + inotrope + corticosteroid

COMPLICATIONS
- renal dysfunction
- hypotension
- ARDS
- multiple organ system failure

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10
Q

Varicella Zoster (Human Alpha Herpes Virus)
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication

A

Varicella (chickenpox)
Exclusively human virus- over 80% of people have been infected by the age of 10 years

When susceptible person is exposed to VZV either by direct contact with lesions or through airborne spread from respiratory droplets
Incubation period is 14 days

After primary infection: can become latent in dorsal root ganglia and trigeminal ganglia. Later in lifer it may reactivate and cause shingles. HIV use or immunocompromised (steroid use of chemo) have higher chances.

Groups at highest risk of complications of infection:
- Adults
- Pregnant women
- Immunosuppressed patients
- Neonates

RF
- Exposure to VZV
- Age 1-9 years
- Unimmunised status
- Occupational exposure

CLINICAL FEATURES
- Fever
- Vesicular rash: appears centrally first then spreads to extremities
- Vesicles on mucous membranes e.g. nasopharynx
- Pruritus
- Headache
- Fatigue/malaise
- Sore throat

INVESTIGATIONS
PCR- positive for virus DNA
pregnant women: US to look if foetus affected

MANAGEMENT
supportive: paracetamol
mod-severe: oral aciclovir
severe: IV antiviral therapy

post exposure prophylaxis:varicella-zoster immunoglobulin (VZIG)
give if exposed to chickenpox or varicella zoster, if immunosuppressed, neonates, pregnant women, if have no antibodies to varicella virus

COMPLICATIONS
- Varicella pneumonia
- Encephalitis
- Meningitis
- Hepatitis
- Severe infection in the newborn

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11
Q

What are two issues that are caused by reactivation of Varicella Zoster Virus

A

1) Ramsay Hunt Syndrome: LMN facial nerve palsy due to reactivation of varicella zoster virus in geniculate ganglion of facial nerve.
Get auricular pain and can get unilateral facial nerve palsy and vesicular rash around ear, some get blisters on anterior 2/3 of tongue
Treat with oral cicilovir and prednisolone

2) Herpes Zoster Opthalmicus: Reactivation of varicella zoster virus in area supplied by ophthalmic division of trigeminal nerve
Vesicular rash around the eye, hutchinson’s sign (rash on tip or side of nose (indicated ocular involvement like anterior uveitis)
urgent opthalmology review, antivirals 7-10 days

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12
Q

Clinical features of shingles

A
  • acute, unilateral, painful blistering rash: erythematous, macular, vesicular rash
  • prodromal period of burning pain over affected dermatome for 2-3 days
  • infectious until vesicles have crusted over (5-7 days from onset)

paracetamol and NSAIDs, can give antivirals within 72 hours.
Antivirals to reduce chances of post herpetic neuralgia, especially in old people

should avoid contact with immunocompromised and pregnant women whilst infectious

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13
Q

Viral Exanthema
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication

A

Widespread skin rash due to a viral illness
Very common in childhood- especially:
- Chickenpox (varicella)
- Measles
- Rubella
Immunisations with MMR have decreased cases

CLINICAL FEATURES
- spots/blotches on skin with widespread rash usually on trunk
- Fever
- Malaise
- Headache
- Loss of appetite
- Muscular aches and pains

INVESTIGATIONS
- Viral swab
- Blood tests

MANAGEMENT
antipyretics - paracetamol for the fever
moisturising emollients for the itch

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14
Q

Viral Gastroenteritis
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication

A

Acute inflammation of the lining of the stomach and intestines caused by enteropathogenic viruses

Norovirus > sapovirus > rotavirus

Bacterial causes:
- Campylobacter
- E. coli
- Salmonella

RF
- Exposure to contaminated food
- Close contact with infected people
- Poor hygiene
- Extremes of age
- Immunocompromisation

CLINICAL PRESENTATION
- Sudden onset diarrhoea
- Blood or mucus in stool
- Vomiting
- Nausea
- Abdo pain
- Fever and malaise
- Signs of dehydration: dry mucous membrane, skin turgor decrease, cap refill, dec urine output

If norovirus: abrupt onset short lived so 24-48 jours. self limiting but can cause AKI in frail people. Strict hand washing with soap and warm water to prevent spread

INVESTIGATIONS
FBC before starting IV fluid
U&E as can cause dehydration
Stool viral culture

MANAGEMENT
No systemic signs:
bed rest, fluids, electrolyte replacement with oral rehydration

Systemic sign:
Admit + IV fluids + stool culture

C diff: oral vancomycin (add IV metronidazole if severe)

COMPLICATIONS
- Electrolyte abnormalities (metabolic acidosis)
- acute renal failure
- transient lactose intolerance
- Guillain-Barre syndrome

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15
Q

Guillain Barre syndrome

A

Acute autoimmune demyelinating polyneuropathy affecting the PNS. Occurs after gastroenteritis caused by campylobacter jejuni

CLINICAL PRESENTATION
- back/leg pain in initial stages of illness
- ascending weakness, paraesthesia and pain (i.e. legs are first)
- areflexia (completely absent reflexes)

Can progress and affect respiratory muscles leading to rest failure and death (so must do spirometry test)

INVESTIGATIONS
- CSF (Lumbar Puncture) will show high protein + normal WCC (autoimmune condition, antibodies are proteins, hence increased proteins)
- Nerve conduction studies = decreased motor nerve conduction due to demyelination
- Spirometry test

MANAGEMENT
- IV immunoglobulins (normal antibodies to dilute autoantibodies)
- plasmapheresis (filter antibodies out of plasma)

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16
Q

Viral Hepatitis A+E
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication

A

A+E
A caused by RNA picornavirus
E caused by calcivirus

Both faecal oral route and 3-6 weeks incubation
Hep A usually in shellfish, Hep E in undercooked pork

Hep A endemic in developing world, sub clinical so tests can’t pick up. Better sanitisation in developed world so less common, associated more with travellers
Hep E endemic in Asia, Africa, Central America. Causes severe hepatitis in pregnant women

CLINICAL FEATURES
- Acute
- Prodromal period- malaise, anorexia, fever, N&V
- Hepatitis- dark urine, pale stools, jaundice, itching
- RUQ abdo pain
- Pyrexia
- Hepatomegaly
- 85% recover in 3 months

INVESTIGATIONS
LFT- raised ALP, AST, ALT, GGT, billirubin
Bloods: high ESR, low albumin, high platelets
Hep A:
- Anti-Hep A IgM present during acute illness, disappears after 3-5 months
- Anti-Hep A IgG persists indefinitely after infection or vaccination

Hep E:
- Anti-Hep E IgM for active infection
- Anti-Hep E IgG for past infection

MANAGEMENT
Prevent : Hep A vaccine (no vaccine for Hep E)
Treat: symptoms and avoid alcohol and too much paracetamol

COMPLICATIONS
- acute liver failure (more common in pregnant women)
- cholestatic hepatitis
- post-hepatitis syndrome (no increased risk of hepatocellular carcinoma)

PROGNOSIS
recovery usually within 3-6 weeks

17
Q

Viral Hepatitis B+D
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication

A

Notifiable disease
Hep B: double stranded DNA hepadnavirus
Transmitted through sexual contact, blood, vertical transmission (mother to baby.
- Core antigen (HBcAg)
- Surface antigen (HBsAg)
- Envelope antigen (HbeAg) - marker of high infectivity

Hep D: single stranded RNA virus coated with HBsAg. Defective virus, it needs Hep B surface antigen to complete its replication and transmission cycle, Can only co-infect with Hep B or superinfection people who’re already carriers of Hep B (if chronic Hep B patient with flare up then suspect Hep D)

RF:
- IV drug use
- Unscreened blood products
- Infants of HbeAg-positive mothers
- Sexual contact with hep B carriers
- Southeast Asia, Africa and Mediterranean countries

CLINICAL FEATURES
- Incubation period of 3-6 months
- prodromal : malaise, headache, anorexia, N+V, diarrhoea, RUQ pain
- jaundice
- dark urine (high conj bilirubin)
- hepatomegaly

INVESTIGATIONS
Acute Hep B: surface antigen and IgM core
HBsAg positive & IgM anti-HBc positive

Chronic Hep B: surface antigen and IgG core antibody
anti-HBs antibody positive & IgG anti-HBc positive

Cleared Hep B: surface antibody and IgG core antibody
anti-HBs antibody positive & IgG anti-HBc positive

Vaccinated against Hep B: only surface no core
Anti-HBs antibody positive and everything else negative (won’t have IgG antibody)

HBeAg: Marker of infectivity → higher means more infectious so more likely to transmit it

PCR used to detect Hep D

LFT : Raise ALT, AST, ALP, bilirubin
PT: may be high is a marker of significant liver damage

MANAGEMENT
Acute- supportive treatment
Chronic- interferon alpha (antiviral
HIV screening
Prevent:
- Blood screening
- Safe sex
- Instrument sterilisation
- Hep B vaccine

COMPLICATIONS
- Hepatocellular carcinoma
- Fulminant liver failure
- Chronic Hep B infection

PROGNOSIS
10% of infections in adults become chronic. Of these, 20-30% will develop cirrhosis.

18
Q

Viral Hepatitis C
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication

A

small, enveloped, single-stranded RNA virus. Sexual or vertical (mother to baby). 2weeks -6 months incubation period. No vaccine

Acute- less than 6 months
chronic- over 6 months (hep C is most likely to be chronic out of all hepatitis infections)

Rf
- IV drug users
- Needlestick injury (healthcare workers)
- Blood transfusion (esp before 1992)

CLINICAL FEATURES
90% asymptomatic
- Malaise
- Fever
- RUQ pain
- Hepatomegaly
- Jaundice
- Nausea and vomiting
- Diarrhoea

Hep C can lead to
- arthritis
- arthralgia
- eye problems (sjogren’s syndrome)
- cirrhosis
- hepatocellular cancer
- cryoglobulinemia
- membranoproliferative glomerulonephritis (leading to renal dysfunction)

INVESTIGATIONS
Anti-Hep C antibodies
- IgM → acute
- IgG → past exposure or chronic

RT- PCR
LFT
Liver biopsy : assess degree of inflammation and liver damage (diagnose cirrhosis)

MANAGEMENT
Antivirals: Interferon alpha, ribavirin
HIV screen
Prevent: screen blood, blood products and organ donor screen, instrument sterilisation

COMPLICATIONS
- chronic hepatitis C
- hepatocellular carcinoma
- fulminant hepatic failure

19
Q

Hepatocellular carcinoma- most common causes, risk factors and investigations

A

Chronic Hep B most common worldwide
Chronic Hep C most common in Europe

RF:
- Main risk factor is liver cirrhosis secondary to hep B and C
- Alcohol
- NAFLD
- α-1-antitrypsin deficiency
- Haemochromatosis

INVESTIGATIONS
AFP raised
Screening with USS and AFP test for people with cirrhosis secondary to Hep,c, haemochromatosis or alcohol

20
Q
A