Infection Flashcards
Cellulitis
severe inflammation of dermal and subcutaneous layers of the skin
Candidiasis
Candida albicans and other Candida species
infections have various manifestations, depending on the site and the degree of immune-incompetence of the patient.
Oral candidiasis (thrush)
yeast Candida albicans and other Candida species
raised, white plaques on the oral mucosa, tongue, or gums. The plaques can become confluent and ulcerated and spread to the throat
treated topically with nystatin or clotrimazole
Vaginal candidiasis
yeast Candida albicans and other Candida species
itching and burning pain of the vulva and vagina, accompanied by a white discharge.
treated topically with nystatin or clotrimazole
Pneumonia
- Definition
- Pathenogenesis
- Clinical features
Pneumonia is infection of the terminal air sacs (“alveoli”) and tissue of the lung.
Pneumococci, characteristically in pairs (diplococci), multiply rapidly in alveolar spaces and induce extensive oedema =incite an acute inflammatory
response in which neutrophils and congestion are prominent. As the inflammatory process progresses, macrophages replace the neutrophils and ingest debris. The
process usually resolves.
fever, malaise, tachypnea (increased respiratory rate),
and tachycardia, cough
Pneumonia
- Definition
- Pathenogenesis
- Clinical features
Pneumonia is infection of the terminal air sacs (“alveoli”) and tissue of the lung.
Pneumococci, characteristically in pairs (diplococci), multiply rapidly in alveolar spaces and induce extensive oedema =incite an acute inflammatory
response in which neutrophils and congestion are prominent. As the inflammatory process progresses, macrophages replace the neutrophils and ingest debris. The process usually resolves.
fever, malaise, tachypnea (increased respiratory rate),
and tachycardia, cough
Community-Acquired Pneumonia
pneumonia (infection of the lung parenchyma seen on chest X-ray) which develops outside the hospital
2 years old+: S.pneumoniae
Under 2 years old: Respiratory syncytial virus (RSV)
No causative agent is found in up to 40% of patients with CAP.
X ray patterns of acute pneumonia
Lobar pneumonia is pulmonary consolidation demarcated by border of lung segment or lobe.
Bronchopneumonia is seen as patchy consolidation around the larger airways
Interstitial pneumonia is demonstrated by fine areas of shadowing in the lung fields and there is usually no sputum production at presentation. It is usually seen in mycoplasma, legionella, and viral pneumonia
Meningitis
Meningitis is inflammation of the meningeal lining of the brain and spine.
A patient will have:
General features of an infection such as fever, increased pulse rate
Symptoms and signs due to inflammation of the meninges:
a. headache
b. photophobia (difficulty looking at bright lights)
c. vomiting
d. neck stiffness on flexion of the neck
e. irritable (progressing to reduced level of consciousness)
f. Other findings dependent on severity (e.g. sepsis) or complications.
Sepsis
a syndrome of life-threatening organ dysfunction caused by a dysregulated host response to infection. It is usually caused by a bacterial infection.
Septic shock: subset of sepsis where particularly profound circulatory, cellular and metabolic abnormalities substantially increase mortality.
Causative agents depend on the syndrome, host and clinical context. Gram-negative infections account for an increasingly large proportion of cases,
particularly of healthcare-associated infections
Common presenting syndromes include pneumonia, intra-abdominal and urinary sepsis, and skin and soft tissue infections.
Management and treatment: prompt recognition, early appropriate
antimicrobial therapy and supportive treatment- Sepsis 6 bundle
Neisseria meningitidis infection
Neisseria meningitidis is a Gram negative diplococcus that may be found within polymorphonuclear leukocytes (neutrophils)
Rates of meningococcal disease are highest for young children and increase again
for adolescents and young adults.
Neisseria meningitidis causes both meningitis and septicaemia. They can occur
together or separately.
Septicaemia
the bacteria in the blood
Neisseria meningitidis in the blood triggers an intense host immune response.
- Fever:
- Sepsis: reduced level of consciousness, tachycardia, low blood pressure, poor peripheral circulation,
reduced urine output.
- Disseminated Intravascular Coagulation (DIC)
- Non-blanching Rash (30-75% pts)
Management: Early recognition Early administration of antibiotics. Urgent investigation Supportive care, often in an intensive care unit to manage organ dysfunction and DIC. Notify Public Health Prevention
Treatment: ceftriaxone
Disseminated Intravascular Coagulation (DIC)
syndrome of widespread intravascular activation of coagulation.
Clostridioides difficile infection
gram-positive, anaerobic, spore-forming bacillus that is
responsible for the development of antibiotic-associated diarrhoea and colitis
(bowel inflammation).
Spore (faecal-oral) transmission
The diagnosis of C. difficile colitis should be suspected in any patient with
diarrhoea who has received antibiotics within the previous 3 months, has been
recently hospitalised, and/or has an occurrence of diarrhoea within 48 hours or more after hospitalisation
CDI clinical picture can vary from the asymptomatic carrier state to life-threatening colitis
Treatment:
-Asymptomatic carriers: No necessary treatment
-Mild, antibiotic-associated diarrhoea without fever, abdominal pain, or
leucocytosis: Cessation of antibiotic(s) may be the only treatment
necessary
-Mild to moderate diarrhoea or colitis: Metronidazole (P.O or IV)
or vancomycin (oral) for 10 days
-Severe or complicated disease: Vancomycin is considered to produce faster symptom resolution and fewer treatment failures than metronidazole; in
fulminant cases, combined therapy with IV metronidazole and
oral vancomycin may be considered
MRSA
a type of Staphylococcus aureus that is resistant to most beta-lactam antibiotics, antistaphylococcal penicillins (e.g., methicillin, oxacillin), and
cephalosporins.
Skin to skin transmission
Treatment:
Norovirus
a small, non-enveloped single stranded RNA virus that is a major cause of acute gastroenteritis outbreaks.
There is no specific treatment available so
treatment consists of supportive measures.
Transmission is mainly faecal-oral and also thought to be respiratory. Can be spread following ingestion of contaminated food, direct person-to-person contact or through contact with contaminated surfaces.
HIV
Retrovirus that infects cells with CD4 surface receptor. It destroys the cell, causes inflammation and spreads to/infects to more cells
Clinical features: oral candidiasis, Kaposi’s sacroma, PCP
Transmission: contact of infected bodily fluids with mucosal tissue/blood/broken skin
Treatments: anti-retroviral drugs
Malaria
One of the most common and deadly infections
Vector transmission: female Anopheles mosquito
Presentation: headache, fever, fatigue, pain, chill, pallor, sweating, dry cough, splenomegaly, nausea, vomiting] bite marks, low BP, high HR (110bpm)
Treatment dependant of species:
P. faciparum= artesunate, quinine + doxycycline
P. vivax, ovale, malariae = chloroquine,
Endocarditis
Formation of vegetation that binds to valves or mural endocardium. Aberrant flow predisposes to a collection of fibrin, platelets and scant inflammatory cells
Clinical features of Endocarditis
Fever
Heart murmur
Other cardiac complications
Embolic features: These are small bits of the vegetation (or biofilm) that become loose and travel to small capillaries where they can block the
capillary or cause local infection at that site.
e.g Janeway lesions, splinter haemorrhages, roth spots in the eye, oslers nodes
Chicken pox/shingles
Chicken pox: varicella
Shingles: Herpes zoster
Presentation: fever, malaise, headache, and abdominal pain. The exanthem begins on the scalp, face, or trunk as erythematous macules, which evolve into virus-containing vesicles that begin to crust over after about 48 hours
Treatment: acyclovir
Examples of disease caused by healthcare infection viruses
blood borne viruses (hepatitis B, C, HIV)
norovirus
influenza
chickenpox
Examples of disease caused by healthcare infection bacteria
Staph aures including MRSA Clostridium difficle Escherichia coli, Klebsiella pneumoniae Pseudomonas aeruginosa Mycobacterium tuberculosis
Describe the role of E.coli in health and disease
Gra m-negative rods, typically lactose-fermenting, facultatively anaerobic
normal part of large bowel microbiota
Possibly protects against invasion by pathogenic species
Can cause:
intestinal infections
toxin-mediated disease
extra-intestinal infections
disease is linked to the presence of virulence factors, frequently restricted to specific E.coli strains
Hepatitis B
Inflammation of the liver
Chronic: persistence of HBsAg after 6 months
Double-stranded eveloped DNA virus
Transmission: vertical (75% cases globally), sexual contact, drug injection, needlestick injuries
Presentation: jaundice, fatigue, abdominal pain, anorexia/nausea/vomiting, arthralgia
Treatment: no cure, life-long anti-virals
Vaccine available
Pharyngitis
Streptococcus pyogenes
• Peak incidence 5-15 years • Droplet spread • Association with overcrowding • Untreated patients develop M protein specific antibody
Clinical features Abrupt onset sore throat Malaise, fever, headache Lymphoid hyperplasia Tonsillopharyngeal exudates Throat swab -> Group A strep
Scarlet fever
Due to infection with streptococcal pyrogenic exotoxin strain of S.pyogenes • Local or haematogenous spread • High fever, sepsis, arthritis, jaundice
Typhoid and paratyphoid (enteric fever)
Systemic disease
Salmonella typhi, Salmonella paratyphi= rod shaped Gram-negative bacteria
Faecal-oral transmission from contaminated food/water
-poor sanitation, limited access to clean water
Presentation: fever headache, abdominal discomfort, dry cough, relative bradycardia
Treatment: fluoroquinolones (increasing resistance), IV ceftriaxone or azithormycin for 7-14days Vaccine available (50-75% effective)
Dengue fever
commonest arbovirus
Vector transmission: Aedes aegytpo
Presentation: first infection ranges from asymptomatic to non-specific febrile illness
Dengue fever
commonest arbovirus
Vector transmission: Aedes aegytpo
Presentation: first infection ranges from asymptomatic to non-specific febrile illness
- lasts 1-5 days: intense headache, fever, muscle/joint pain, widespread red rash
Supportive treatment only: paracetamol, fluids
Schistosomaisis/bilharzia
Parasitic worms in fresh water snails (cercariae)
- Schistosoma mansoni
Presentation: fever, chills, cough, muscle aches, rash, itchy skin
Treatment: praziquantel
Ebola
Filovirus
Presentation: flu-like illness with vomiting, diarrhoea, headaches, confusion, rash, internal/external bleeding at 5-7 day
Transition: direct contact with body fluids
Zika virus
Arbovirus (flavivrius)
Vector transmission: Aedes mosquito and sexual transmission
Presentation: 20% get symptoms which are mild, dengue-like
No treatment, no vaccine
Primary immunodeficiency disease
due to intrinsic gene defect: missing protein, missing cell, non-functional components
Secondary immunodeficiency disease
due to an underlying disease/treatment:
Primary immunodeficiency disease
due to intrinsic gene defect: missing protein, missing cell, non-functional components
65% caused by Ab defects
Secondary immunodeficiency disease
due to an underlying disease/treatment: decrease production/function of immune components, increased loss of catabolism of immune components
X-linked agammaglobulinaemia
Primary immunodeficiency disease
due to intrinsic gene defect: missing protein, missing cell, non-functional components
Patient lacks B cells- defect in B cell development
Primary immunodeficiency disease
due to intrinsic gene defect: missing protein, missing cell, non-functional components
Presentation: age of symptom onset, type of microbes/sites
Management: supportive treatment (infection prevention, nutritional support), specific treatment ( regular Ig therapy), comorbidities
Common Variable Immunodeficiency (CVID)
Primary immunodeficiency disease
due to intrinsic gene defect: missing protein, missing cell, non-functional components
Patient has B cells but do not produce any antibodies
Selective IgA deficiency
Primary immunodeficiency disease
due to intrinsic gene defect: missing protein, missing cell, non-functional components
Most common - slight raised risk of autoimmune conditions
90% of patients are asymptomatic
prevalence 1:100 to 1:1000
Hyper-IgM syndrome
Primary immunodeficiency disease
due to intrinsic gene defect: missing protein, missing cell, non-functional components
no type switching in B cells= IgG is not produced. IgM continues to be produced leading to unusually high levels in serum
Severe combined immunodeficiency (SCID)
Primary immunodeficiency disease
due to intrinsic gene defect: missing protein, missing cell, non-functional components
T cells are defective. B cells are not activated
Di George syndrome (thymus)
Primary immunodeficiency disease
due to intrinsic gene defect: missing protein, missing cell, non-functional components
5-10% of all PID
deletion syndrome on chr22p11.2
absence of hypoplastic thymus= no T cell maturation
Chronic granulomatous disease (CGD)
Primary immunodeficiency disease
due to intrinsic gene defect: missing protein, missing cell, non-functional components
~10% of all PIDs
Chronic granulomatous disease (CGD)
Primary immunodeficiency disease
due to intrinsic gene defect: missing protein, missing cell, non-functional components
~10% of all PIDs
phagocytes lack killing machinery and are ineffective as a result
Describe the serological antigensof E.coli
Capsule (K) LPS (O) Cell membrane Fimbriae (F) Flagella (H) production of toxins
Describe E. coli as a cause of diarrhoea including its pathogenesis, role of
toxins and clinical features
Enterotoxigenic E.coli (ETEC) is the most important cause of bacterial diarrohoeal illness
Faeco-oral transmission
ETEC produces two toxins, a heat-stable toxin (ST) and heat-labile toxin (LT)
Toxins stimulate the lining of the intestines to secreted excessive fluid =watery diarrhoea and abdominal cramping
other less common features: fever, nausea, chills, loss of appetite, headache, muscle aches and bloating
Cystistis
Lower UTI
Risk factors: female, history UTI, secual activity, vaginal infection, diabetes, obesity, genetic susceptibilyt
Clinical features: frequent and urgent urination, dysuria, suprapubic pain, nocturia, hematuria, malaise
Causative organisms: Uropathogenic E.coli (UPEC)
Virulence factors:
Adhesins (type 1 & other chaperone-usher pili_
toxins (HIyA, CNF1)
Siderophores (aerobactin, enterobactin, yersinabactin)
capsule
Pyelonephritis
Upper UTI
Risk factors: diabetes, HIV/AIDS, iatrogenic immunosuppression
Clinical symptoms: back and/or flank pain
fever, chills, malaise, nausea, vomiting, anorexia
Causative organisms: Uropathogenic E.coli (UPEC)
Virulence factors: Adhesins (type 1 & P pili) toxins (HIyA, CNF1) Siderophores flagella
Describe UPEC virulence factors
Adhesins:
Type 1 fimbriae have adhesive tips that bind to alpha-D-mannosylated proteins on uroepithelium= adhesion, invasion of uroepitheilum and the formation of intracellular bacterial communities (IBCs)
Toxins:
Lipopolysaccharide (LPS)
alpha-Hameolysin (HIyA) is a secreted, pore-forming toxin, cytotoic towards epithelial cells in the urinary tract
bacteria produce their own iron-complexing proteins (siderophores) to acquire iron
Describe E. coli as a cause of blood stream infections and sepsis
E.coli are the commonest cause of bacterial bloodstream infection in England
~50% of E.coli bloodstream infections occur in patients older than 75 years
Describe the management of E. coli infections - Diarrhoea
Prevention:
avoid contaminated food and water
eating raw fruits, veg, seafood or undercooked meat or poultry in areas lacking adequate chlorinate
Treatment: most recover without any specific treatments,
clear liquids to prevent deydration
oral rehydration solutions
avoid antibiotics
Describe the management of E. coli infections - UTI
Antibiotics: trimethoprim and nitrofurantoin
Describe the management of E. coli infections - bloodstream infections
increasing resistance to a wide range of antibiotic classes
Describe the management of E. coli infections - bloodstream infections
increasing resistance to a wide range of antibiotic classes
Describe the structure of the Influenza virus
orthomyxovirus- spherical, enveloped viruses containing a segmented, negative strand RNA genome
Genetic material:
• (-) ssRNA – 8 genes
• encoding 11 proteins
• include 3 RNA polymerases (high error rates)
Two surface antigens:
• Haemagglutinin (H) – 18 types – binds to cells
of the infected person
• Neuraminidase (N) – 11 types - releases the
virus from the host cell surface
Define the concept of an animal reservoir for type A influenza (including
poultry, horses, pigs, and other animals) and its major surface antigens -
hemagglutinin (HA) and neuraminidase (NA)
a) influenza type A viruses in many animals, including horses, pigs, and wild migrating waterfowl.
b) reassortment can occur between influenza A viruses that
infect different animal and avian species, e.g., pigs can be infected by human- and avian-specific influenza viruses
c) In environments where pigs, birds and humans coexist,
it is possible for a pig to be simultaneously infected with
multiple influenza subtypes.
d) “Reassortants” can, therefore, be produced within one
host animal (the pig), in which the mRNAs encoding the H
and N antigens have been reassorted into unique
combinations.
e)The reassortant virus then has the potential to
spread among humans, birds, and pigs.
Describe the clinical symptoms and complications of influenza
infection
headache, high fever, sore throat, runny nose, muscle aches and pains
complications of influenza:
viral pneumonia, secondary (bacterial) pneumonia,
central nervous system syndromes, or Reye syndrome
Describe how you would diagnose flu in a clinical setting
sample from a nasopharyngeal swab
Briefly outline the management of influenza including treatment options
and prevention Treatment and prevention
including vaccination and how this is determined by WHO each year
antivirals
NA inhibitors- Tamiflu
Prevention: formalin-activated vaccine by injection influenza A&B
live, attenuated, cold-adapted vaccine by nasal spray Influenza A&B
Define the concepts of antigenic shift (acquisition of a novel HA and NA by
the virus) and antigenic drift (yearly accumulation of mutations in the HA
and NA)
antigenic shift= acquisition of a novel HA and NA by the virus
antigenic drift =yearly accumulation of natural mutations in the HA and NA - this causes seasonal epidemics
Define the concepts of antigenic shift (acquisition of a novel HA and NA by
the virus) and antigenic drift (yearly accumulation of mutations in the HA
and NA)
antigenic shift= major changes in the genes of flu vruses that occur suddenly when two or more different strains combine. Acquisition of a novel HA and NA by the virus- cause widespread epidemics/pandemics
antigenic drift =yearly accumulation of natural mutations in the HA and NA - this causes seasonal epidemics
Define the concepts of pandemics and epidemics (seasonality) and how
these may arise in relation to influenza.
Antigentic shift phenomenon can
be easily explained by the reassortment of different RNA segments from each species in a new capsid.
Occurs infrequently - maybe every 10 or 20 years
Only influenza type A viruses show antigenic shift
May not have been seen in circulation in population for
many years
Immune systems of many individuals have no defence
against this new subtype
Epidemic - Prevalent among a people or a community at a special time, and produced by some special causes not generally present in the affected locality
Pandemic - epidemic over a very large area;
affecting a large proportion of a population – often the world
Suppurative complications of streptococcal
pharyngitis
- Peritonsillar cellulitis/abscess
- Retropharyngeal abscess
- Mastoiditis, sinusitis, otitis media
- Meningitis, brain abscess
Acute rheumatic fever
Complications of streptococcal pharyngitis
Inflammation of heart, joints, CNS • Follows on from pharyngitis • Rheumatogenic M types • Possible mechanisms: – Auto-immune – Serum sickness – Binding of M protein to collagen – ASO, ASS induced tissue injury
Acute post-streptococcal
glomerulonephritis
Complications of streptococcal
pharyngitis
Acute inflammation of renal glomerulus
• M type specific but NOT same as ARF M types
• Antigen-antibody complexes in glomerulus
Impetigo
Streptococcus pyogenes skin infections
Childhood infection, 2-5 years
– Initial skin colonisation, followed by intradermal innoculation
– No ARF but impetigo is most common cause of glomeruonephritis
Erysipelas
Streptococcus pyogenes skin infections
– Dermis infection with lymphatic involvement
– Face, lower limbs
– Facial lesions frequently preceded by pharyngitis
– Lower limb infection usually secondary to invasion of skin via trauma, skin disease or local fungal infection
Cellulitis
Streptococcus pyogenes skin infections
Skin and subcutaneous tissue infection
– Impaired lymphatic drainage and illicit injecting drug use important risk factors
Necrotising fasciitis
Streptococcus pyogenes skin infections
Infection of deeper subcutaneous tissues and fascia. – Rapid, extensive necrosis – Usually secondary to skin break – Severe pain, even before gross clinical changes – High fever, fulminant course, high mortality (20-70%)
Streptococcal toxic shock syndrome
Deep tissue infection with
Strep pyogenes AND Bacteraemia AND Vascular collapse AND Organ failure
From health to death in hours
Entry of group A strep into deeper tissues and
bloodstream
Streptococcal pyrogenic exotoxins stimulate T-cells
through binding to MHC class II antigen-presenting
cells and V-β region of T-cell receptor, inducing
monocyte cytokines (TNF-α, IL-1β, IL-6) and lymphokines (TNF-β, IL-2, IFN-γ).
M-protein fibrinogen complex formation
