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Infection Flashcards

1
Q

what is catalase? describe some microorganisms that are positive and negative

A
  • enzyme produced by bacteria that respire using oxygen . catalase protects them from the toxic by products of oxygen metabolism
    streptococci is catalase negative
    staphylococci is catalase positive
    both gram (+)
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2
Q

name the antibiotics used for streptococcus pyogenes

A

penicillin V

Clarythromycin- if resistant (macrolide)

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3
Q

how do macrolides work?

A

inhibit protein synthesis

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4
Q

how do quinolones work?

A

inhibit nucleic acid synthesis

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5
Q

how do Polymixins work?

A

inhibit cell membrane function

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6
Q

how do Beta lactams work?

A

inhibit cell wall synthesis

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7
Q

how do glycopeptides work?

A

inhibit cell wall synthesis

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8
Q

what are some virulence factors of Streptococcus pyogenes?

A

Capsule- hyaluronic acid not recognised as foreign (same as in CT)= non immunogenic and antiphagocytic
cell wall- M proteins are antiphagocytic and form a coat that interferes with complement binding
- protein F mediates attachment to fibronectin to the pharyngeal epithelium

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9
Q

describe streptococcus pyogenes

A

gram (+) cocci, in chains
spread by skin contact and via the resp tract
- grow and secrete toxins -> damages surrounding cells, invading the mucosa and eliciting an inflammatory response

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10
Q

what is the difference between cellulitis and fascilitis?

A

cellulitis- acute inflammation of subcutaneous tissue
- treated with Flucloxacilin (effective against both Staph. aureus and Strep. pyogenes)
fascilitis- inflammation of tissue under the skin that covers a surface of underlying tissue - require surgery and antibiotics
impetigo- also treat with Flucloxacilin but usually self resolving

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11
Q

describe Streptococcus Pneumoniae

A

gram (+) encapsulated cocci- usually in pairs

most common cause of community- acquired pneumonia

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12
Q

describe the virulence factors of Streptococcus Pneumoniae

A

capsule- antiphagocytic and antigenic

pili- can attach to epithelial cells of the upper respiratory tract

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13
Q

what is the treatment for Streptococcus Pneumoniae?

A

mild: Amoxicillin (doxycycline)
moderate: amoxicillin and doxycycline
severe: co-amoxiclav and doxycycline
all cell wall synthesis inhibitors

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14
Q

how is Streptococcus Pneumoniae managed in the community?

A

Pneumococcal polysaccharide vaccine- for high risk individuals over 2 years old - protect against pneumococcal (penicillin resistant) strains
Pneumococcal conjugate vaccine 13- effective in infants and toddlers (6 weeks- 5 years)- herd immunity

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15
Q

why are antibiotics not used for Streptococcal pharyngitis?

A

no shortening of treatment time and enhances antibiotic resistance

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16
Q

what is a risk factor for endocarditis?

A

a bicuspid aortic valve (usually has 3 cusps)

  • increased risk of development as there is abnormal flow of blood over the valve and abnormal valve tissue
  • means a greater risk of microbes in the blood sticking to the valve cusp and setting up a local infection (biofilm)
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17
Q

Describe the pathogenesis for the development of endocarditis

A
  • viridians streptococci- gram (+) in chains
  • enter blood stream from skin, mucosa or other sites of focal infection
  • bind to vegetation (aberrant flow predisposes to a collection of fibrin, platelets and scant inflammatory cells)
  • local infection leading to pro-coagulant state
  • further fibrin deposition, platelet aggregation and bacterial invasion
  • infective endocarditis
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18
Q

what are the clinical features of endocarditis?

A
  • fever, heart murmur, cardiac complications,
  • Janeway lesions- haemorrhagic nodular lesions with an irregular border on palms/ soles
  • mico- abscess formation and localised necrosis
  • Osler nodes
  • Roth spots in eyes
  • splinter haemorrhages
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19
Q

which antibiotics are used for Viridans Streptococci?

A 
IV penicillin (prophylactic)
Gentamicin - broad spec
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20
Q

Describe Clostridium Difficile

A

Gram (+) bacillus (rod shaped), anaerobic that produces spores
minor component of the normal flora of the large intestine
produces 2 toxic polypeptides

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21
Q

What does Clostridium Difficile produce?

A

two toxic polypeptides:
Toxin A- enterotoxin that causes excessive fluid secretion and stimulates a inflammatory response and has some cytopathic effect in tissue culture
Toxic B- cytotoxin- disrupts protein synthesis and causes disorganisation of the cytoskeleton

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22
Q

what is the treatment for Clostridium Difficile

A

discontinuance of predisposing drug and fluid replacement
- diarrhoea is a common complication of antimicrobial drug treatment
- reconstitution of host’s normal colonic flora may aid in recovery
oral administration of Metronidazole (damage DNA)
treatment= metronidazole, oral vancomycin, fidaxomicin (to stop recurrent), faecal microbiota transplantation

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23
Q

Describe Staphyloccus Aureus

A

Gram (+) coccus - grape like, coagulase (+)
frequently carried on skin and mucous membranes
virulence factors :
- capsule
- Protein A- anti-opsonin (and antiphagocytic) effect
- Fibronectin- binding protein
- clumping factor
- pore forming toxin
majority resistant to penicillin G. use beta lactamase resistant penicillins (methicillin/ oxacillin)

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24
Q

What is MRSA?

A

Meticillin Reststant Staphyloccus Aureus - resistant to most beta- lactam antibiotics (cell wall synthesis), antistaphyloccal penicillins (methicillin, etc) and cephalosporins
- produces penicillin binding protein 2a- confers resistance
- some strains only sensitive to glycopeptides- Vancomycin
usually spread via skin to skin contact
can include syndromes of: bacteraemia, pneumonia, endocarditis, joint infections

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25
Q

what is Norovirus?

A
  • small, non enveloped single stranded RNA virus
  • transmission usually by faecal oral route, respiratory
  • acute gastroenteritis outbreaks (nausea, vomiting and diarrhoea)
  • adults and school age children usually acquire (not infants)
  • no specific treatment -> supportive measures (usually 24-48hrs)
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26
Q

what are biofilms?

A

microbial communities attached to surfaces and encased in an extracellular matrix of microbial origin
lifestyle helps bacteria survive and persist within the environment
- Coagulase (-) Staphylococci and Staphylococcus aureus- predominant bacterial species device- associated infections

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27
Q

what is the coagulase virulence factor?

A

converts fibrinogen into fibrin, forming a micro clot wound the bacteria
this protects from phagocytosis

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28
Q

Define sepsis

A

syndrome of life- threatening organ dysfunction caused by a dysregulated host response to infection
usually caused by bacterial infection (mostly gram (-))
normal immune response becomes greatly exaggerated/ dysregulated so that the consequence for the patient is damage inflicted by their own immune response

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29
Q

Define septic shock

A

severe sepsis leads to circulatory failure and metabolic abnormalities
- persisting hypotension requiring active medical treatment and biochemical evidence of disturbed metabolism (increased lactate)

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30
Q

what is the sepsis 6 bundle?

A

take 3:

  • blood culture
  • urine output
  • lactate and bloods

give 3:

  • oxygen - treat hypoxia
  • antibiotics
  • fluid - optimise tissue perfusion
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31
Q

how is the immune system activated in sepsis?

A

bacterial cel wall products -> lipopolysaccharide (endotoxin) binding to host receptors ( Toll like receptors TLRs) which are widely found on monocytes, macrophages and some endothelial cells
pro inflammatory cytokines (TNF) and ILs 1 & 6 are released -> active immune cells
complement system activated -> mediates activation of leukocytes, attracting them to site of infection

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32
Q

what happens to the endothelium and coagulation system during sepsis?

A
  • activated endothelium becomes porous to large molecules (proteins) -> oedema
    coagulation system - increased procoagulant factors and decreased circulating levels of natural anticoagulants -> clotting in small vessels and tendency to blood at other sites
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33
Q

describe the organ dysfunction that occurs during sepsis

A

vasodilation ad increased capillary permeability decreases circulating volume
hypovolaemia and decreased LV contractility created hypotension
increased HR and CO initially- compensatory mechanism becomes exhausted- hypoperfusion and shock may result
impaired tissue oxygen delivery - precapillary oedema- capillary micothrombus formation

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34
Q

describe Neisseria Meningitidis

A

gram (-) bacteria- diplococcus (occurs in pairs)

  • encapsulated (antiphagocytic)
  • piliated ( allow attachment of organism to nasopharyngeal mucosa- in carriers and with disease)
  • inhalation of resp droplets from carrier/ patient with disease in early state
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35
Q

describe the pathogenesis of Neisseria Meningitis

A
  • initially colonises the nasopharynx
  • largely asymptomatic meningococcal pharyngitis

young children-

  • disseminated disease by spreading through the blood
  • meningitis and/or septicaemia
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36
Q

what is the difference between meningitis and septicaemia?

A

meningitis- bacteria in cerebrospinal fluid that surrounds the brain and spine and attaches to meningeal lining- intense inflammation
- headaches, photophobia, vomiting
- treatment= Ceftriaxone (inhibit cell wall synthesis)
septicaemia- bacteria in the blood triggers host immune response
- fever, sepsis, DIC (widespread intravascular activation of coagulation- small clots form while bleeding occurs), petechiae (platelet count decreases and small bleeds into the skin), rash
- management= Ceftriaxone - early recognition and administration with supportive care

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37
Q

Describe Escherichia Coli

A

Gram (-) rod shaped
Stain (-) as cell wall is composed of a thin peptidoglycan layer and outer membrane
facultative anaerobe
- part of the normal flora of the colon
- usually transmitted via the fecal- oral route
- most common case of UTI (and cystitis and pyelonephritis)
- treat UTI with Trimepathrim (inhibits folic acid synthesis for DNA production) or Nitrofrantoin if resistant

38
Q

what is community acquired pneumonia usually due to?

A

Streptococcus pneumonia
Haemophilus influenzae

  • both treated with Co- amoxiclav (penicillin- Beta lactamase inhibitor )
39
Q

what is the pathogenesis for Epstein- Barr Virus (EBV)

A

glandular fever
initial site for virus replication= oropharyngeal epithelium
- B lymphocytes
- B cell receptor for EBV= complement component C3b receptor
- induce cell multiplication and immortalisation
- increase in total IgM, IgG, IgA

40
Q

what other neoplastic diseases are associated with Epstein - Barr Virus?

A
  • Burkitt lymphoma

- Epstein- Barr- associated nasopharyngeal carcinoma

41
Q

what do labs usually show and what is the treament for EBV?

A

labs: atypical lymphocytes (cytotoxic T cells) and elevation of all Igs
treatment= Acyclovir- inhibits EBV replication

42
Q

what causes pharyngitis ?

A 
Streptococal pharyngitis (strep throat)
- treat with penicillin- co amoxiclav or amoxicillin
43
Q

what is the treatment for HIV?

A
  • nucleoside reverse transcriptase inhibitor (NRTI) x2
    +
    non-nucleotide reverse transcriptase inhibitor (NNRTI)
    or
    protease inhibitor / integrase inhibitor / CCR5 (entry) inhibitor
  • 3 anti- retroviral drugs are given as there are millions of rounds of replication each day and therefore virus mutates
  • resistance to dugs occurs in days
44
Q

what are the typical infections associated with HIV?

A
  • oral candidiasis
  • Kaposi’s sarcoma
  • PCP: pneumocystis pneumnia - pneumocystis jirovecii ( fungal)
45
Q

what is Aspergillus

A

opportunistic fungus that usually resides in dust- breathe in fungal spores
- treatment = Amphotericin - anti fungal agent given IV

46
Q

what is Varicella- Zoster?

A
  • double stranded DNA virus which causes chicken pox - has an envelope layer which makes it difficult to clear
    via resp droplets spreads to infect resp mucosa and regional lumps nodes - endothelial cells of capillaries infected -> chicken pox appearance
  • belongs to the herpes family
  • treatment= Acyclovir IV (antiviral)
    reactivation causes shingles (Herpes zoster)
  • decreased T cell - usually prevents dorment virus from reactivating
  • lately established in multiple sensory ganglia - distribution of vesicular lesions is dermatomal
47
Q

what is hepatitis?

A 
inflammation of the liver
- replication of virus in hepatocytes 
- destruct liver
- break down RBCs
- metabolism haem
- bilirubin produced -> conjugated bilirubin in liver-
excreted in urine or feces
48
Q

what are the liver function tests for hepatitis?

A
  • bilirubin
  • liver transaminases- alanine (ALT)
    • aspartate aminotransferase (AST)
  • albumin
  • test for coagulation (clotting factors synthesised in the liver)
  • > INR , PT
49
Q

how to determine if chronic Hep B?

A
  • persistence of HBsAg after 6 months
  • no cure- integrates into host genome
  • require life- long antiviral to suppress viral replication
50
Q

what serology is present with acute hep?

A

surface antigen HBsAg
core antibody HBcAb (IgM)
surface antibody ABsAb - will not clear

51
Q

what serology is present with chronic hep?

A

surface antigen HBsAg
core antibody HBcAb (IgG)
no surface antigen HBsAb- wanted response

52
Q

what serology is present if vaccinated against hep?

A

no surface antigen HBsAg
no core antibody HBcAb
surface antibody ABsAb - wanted immune response

53
Q

what is the history for a patient with malaria?

A

fever, chills and sweats may have slenomegaly

tachycardia, hypotension, diarrhoea, acute kidney injury, DIC

54
Q

how does the malaria parasite infect?

A
  • plasmodium sporozoites injected into the bloodstream and migrate to liver
  • form cyst- like structures containing thousands of merozoites
  • merozoites can invade other erythrocytes and case RBC lysis => anaemia
55
Q

what are the investigations and treatment for malaria?

A

investigations:

  • blood film x3
  • FBC, U & E, LFTs, glucose, coagulation - anaemia, decreased lymphocytes, increased eosinophils
  • head CT if neurological symptoms
  • chest x ray

treatment:
Plasmodium falciparum- lots of resistance
- Artusunate
- Quinine + doxycycline

Plasmodium viva, ovale, malariae

  • Chloroquine
  • Dormant hypnozoites (liver )
56
Q

describe Salmonella Typhi

A

aerobic gram (-) bacillus
human pathogen only via faecal oral route
virulence factors :
- low infectious dose
- survives gastric acid
- resides within macrophages- liver/ spleen/ bone marrow
- fimbrae adhere to epithelium over ileal lymphoid tissue (Peyer’s Patches) -> RE system/ blood

57
Q

what does Salmonella Typhi cause?

A

Enteric / Typhoid fever

  • fever, headache abdominal discomfort, dry cough, bradycardia
  • moderate anaemia, lymphopaenia, increased LFTs

Treatment= IV Ceftriaxone or azithromycin (macrolide)

58
Q

What is Dengue fever?

A

caused by an arbovirus

  • severe myalgia and headache - no other specific features
  • Dengue PCR and serology (IgM)
59
Q

what is Schistosmoiasis?

A
  • Helminth- rash after swimming in lake (Malawi) - increased eosinophils
  • mostly no symptoms - abdomen pain, diarrhoea, blood in stool/ urine

treatment= Praziquantel- wait 4-6 weeks as only works on adult worms

60
Q

Describe the structure of the Influenza virus

A
  • spherical, enveloped virus containing a segmented (-) strand RNA genome
  • 3 RNA polymerases- high error rates
  • 2 surface antigens :
    H- binds to cells of the infected person (via sialic acid on glycoprotein/ glycolipid- acts as a receptor and entry via receptor mediated endocytosis)
    N- releases the virus from the host cell surface
61
Q

what are the different types of influenza?

A

A-usual cause of outbreaks
- live and multiple in humans, swine, equine, birds etc

B- less severe disease and smaller outbreaks
- found in humans with burden of disease mostly in children

C- humans and swine

62
Q

how does the influenza virus replicate

A 
(-) SSRNA not infective by itself as needs to be translated into (+)
- produces (+) SSRNA and mRNAs 
(+)SSRNA -> (-) SSNRA 
mRNA -> viral proteins 
assemble into nucleocapsids 
leave host cells and infect others
63
Q

how does the influenza virus transmit and how does the body protect itself?

A
  • small particle aerosols, larger particles/ droplets, viral particles land on surfaces
  • resp epithelial cells covered by thick glycocalyx and tracheobronchial mucus - trap virus particles
  • ciliated resp epithelial cells- sweep music from lower resp tract to upper so can be swallowed
  • lung: immunological defences -> secretory IgA, NK cells and macrophages
64
Q

what are the complications of influenza?

A
  • viral pneumonia
  • secondary (bacterial) pneumonia
  • meningitis
  • pharyngitis
    immune system overreacts- T cells attack and destroy tissues in which virus is replicating- particularly the lungs
    opportunistic secondary infections- Strep or Staph usually in the lungs
65
Q

what is the treatment for influenza ?

A

Antivirals - rimantadine and amantadine
- inhibit viral uncaring after uptake
influenza A

Neuraminidase inhibitors - Tamiflu, Relenza
- inhibit viral release from infected cell and cause aggregator of viral particles
influenza A and B

Prevention
- formalin- inactivated vaccine by injection
- live, attenuated, cold- adapted vaccine by nasal spray
both against Influenza A and B

66
Q

What is the issue with the RNA polymerases in influenza?

A

high error rates
lack of proof reading ability
creates mutations

67
Q

what is the difference between antigenic drift and antigenic shift? (in relation to influenza)

A

antigenic drift: minor changes (natural mutations) in the genes of the flu virus that occur gradually over time - cause seasonal epidemics
minor changes in the H and N proteins
random mutations in viral RNA and single/ small number of AA substitutions in H and N Proteins

antigenic shift (influenza A): major changes in the genes of flu virus that occur suddenly when 2 or more different strains combine 
new subtype cause widespread epidemics/ pandemics
change in viral subtype results in different H and N proteins 
potentially no previous immunity to new subtype
68
Q

what is the difference between epidemic and pandemic?

A

epidemic- prevalent among a people/ community at a special time

pandemic- epidemic over a larger area- affecting a large proportion of a population

69
Q

Describe Pseudomonas aeruginosa , including treatment

A

gram (-) bacilli- aerobic
has flagella
opportunistic infection
causes biofilms - cycle of inflammation in CF damages local epithelium- good setting to produce biofilm
often resistant to antibiotics due to multiple virulence factors - give multiple antibiotics
Treatment= Ciprofloxacin, Tazocin, Gentamycin, Ceftazidime

70
Q

how to prevent Pseudomonas aeruginosa in CF patients?

A
  • encourage mucus clearance ( chest physio, nebulisers, brochodilators )
  • steroids to reduce inflammation
  • prophylactic antibiotics (present colonisation)
  • avoid mixing with other CF patients
  • good hand hygiene and nutrition
71
Q

What is Cystic Fibrosis?

A
  • autosmal recessive defect in CFTR gene in exocrine glands
  • codes for cAMP regulated CL- channels
  • reduced secretion of CL- means that more water is reabsorbed therefore thicker secretions
  • impair body’s clearance mechanisms - reduced ciliary action, airway remodelling
72
Q

What can Diabetes Mellitus result in?

A
  • hyperglycaemia and academia impair humoral immunity, neutrophil and lymphocyte function
  • diabetic microvascular and microvascular disease result in poor tissue perfusion and increased risk of infection
  • diabetic neuropathy causes diminished sensation
73
Q

why do diabetics get UTIs?

A

-diabetic neuropathy leads to defects in bladder emptying (stasis)
glycosuria= increased bacterial infections

  • usually E. coli
    or Pseudomonas aeruginosa
74
Q

what is the difference between exotoxin and endotoxin?

A

exotoxin- toxins that are released extracellularly as the organism grows

  • may travel from a focus of infection to distant part of the body and cause damage
  • specific mode of action on cells/ tissues

endotoxin- lipopolysaccharides toxin produced by gram (-) bacteria

  • generally cell bounded released only when the cell lyses
  • general mode of action- fever, diarrhoea, vomiting
75
Q

What is a microbiome vs microbiota?

A 
microbiome= all genome within the gut environment
microbiota= all organisms within the gut environment
76
Q

what is microbiota useful for in the GI?

A
  • pathogen inhibition
  • immune protection
  • nutrient metabolism
  • drug metabolism
  • gut brain axis
77
Q

what are the two types of acute infectious diarrhoeas and describe them

A

watery diarrhoea

  • small bowel origin
  • large volume
  • abdo bloating and cramping
  • Norovirus, rotavirus, Clostridioides difficile, enterotoxigenic E. coli

inflammatory diarrhoea

  • smaller volume
  • bloody
  • pain when opening bowels
  • non typhoidal salmonella, campylobacter, clostiodioides difficile, shigella
78
Q

what is non-typhoidal salmonella?

A

gram - rod

  • usually self limiting
  • primarily gastroenteritis
  • transmission route via food, face-oral, animals
  • complications: bacteraemia, endovascular infections, accesses, osteomyelitis and septic arthritis

treatment= Ciprofloxacin, azithromycin, cetriaxone

79
Q

what is campylobacter?

A

gram - spiral shape
- abdo cramping, diarrhoea, fever and malaise
- treatment= macrolides or fluoroquinolone
complications- reactive arthritis, Guillain- Barle syndrome (ascending paralysis)

80
Q

what is shigella?

A

gram -

  • dysentry = bloody diarrhoea (inflammatory diarrhoea), fever, frequent low volume bloody cools, tenesmus
  • nausea and vomiting usually absent
  • usually self limiting
  • treatment= ciprofloxacin, azithromycin, ceftriaxone ( same as non- typhoidal salmonella)
81
Q

what is E. coli 0157

A
  • bloody diarrhoea, haemolytic uraemia syndrome ( microangiopathic haemolytic anaemia, thrombocytopenia and acute renal failure)
  • children <10y/o and elderly are vulnerable
  • worsened by antibiotics as remove other flora and therefore more toxins are produced
    in children can cause acute renal failure
  • low platelets and haemolysis
  • block renal vasculature
82
Q

norovirus vs rotavirus

A

norovirus: profuse diarrhoea and vomiting but usually self limiting - give supportive measures (hydration)
rotavirus: gastroenteritis in young children
- self limiting with supportive treatments
- rare compilations= seizures, encephalopathy, acute encephalitis

83
Q

define cryptosporidium

A
  • intracellular protozoan parasite
  • think walled so live a long time outside the human
  • sporadic, water associated outbreaks

treatment= nitazoxanide

84
Q

define Giardia

A
  • protozoan parasite
  • usually travellers, infants/ children, immunocompromised, CF
  • malaise, steatorrohea, abdo cramping or asymptomatic

treatment if symptomatic= metronidazole/ nitazoxanide

85
Q

define Entamoeba histolytica

A
  • protozoan parasite
  • can cause amoebic dysentery/ infection at extra intestinal sites but majority are asymptomatic

treatment= metronidazole (high dose but cysts not killed) + intraluminal agent (to kill cysts)

86
Q

uncomplicated UTI treatment

A

3 days

Nitrofurantonin, Trimethoprim, Pirmecillinam, Fosfomycin

87
Q

complicated UTI treatment

A

5-7 days

Nirtofurantonin, Trimethoprim, Cefelexin (pregnant)

88
Q

pyelonephritis/ septicaemia treatment

A 
7-10 day course
agent with systemic activity 
possibly IV:
- co amoxiclav
- ciprofloxacin
- gentamicin IV only - nephrotoxic
89
Q

what is helicbacter pylori and what features does it have

A

helix shaped gram (-) microaerophilic

  • produces urease which converts urea to ammonium - ammonia toxic to epithelia
  • have flagellum for good motility and lives in the mucus layer/ adheres to gastric epithelia
90
Q

what is the significance of where Helicobacter pylori colonises?

A

location leads to intestinal metplasia-> dysplasia

antrum- increase gastrin secretions, can cause duodenal ulceration

antrum and body- more damaging than cancer, can be asymptomatic and lead to cancer

91
Q

how to diagnose Helicobacter pylori?

A
  • urease breath test
  • stool antigen test
  • (upper gastrointestinal endoscopy)
92
Q

what is the treatment for Helicobacter pylori?

A
  • PPI (proton pump inhibitor)

- Amoxicillin + (Clarithromycin/ Metronidazole)

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