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
what is Norovirus?
- 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)
26
what are biofilms?
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
27
what is the coagulase virulence factor?
converts fibrinogen into fibrin, forming a micro clot wound the bacteria this protects from phagocytosis
28
Define sepsis
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
29
Define septic shock
severe sepsis leads to circulatory failure and metabolic abnormalities - persisting hypotension requiring active medical treatment and biochemical evidence of disturbed metabolism (increased lactate)
30
what is the sepsis 6 bundle?
take 3: - blood culture - urine output - lactate and bloods give 3: - oxygen - treat hypoxia - antibiotics - fluid - optimise tissue perfusion
31
how is the immune system activated in sepsis?
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
32
what happens to the endothelium and coagulation system during sepsis?
- 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
33
describe the organ dysfunction that occurs during sepsis
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
34
describe Neisseria Meningitidis
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
35
describe the pathogenesis of Neisseria Meningitis
- initially colonises the nasopharynx - largely asymptomatic meningococcal pharyngitis young children- - disseminated disease by spreading through the blood - meningitis and/or septicaemia
36
what is the difference between meningitis and septicaemia?
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
37
Describe Escherichia Coli
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
what is community acquired pneumonia usually due to?
Streptococcus pneumonia Haemophilus influenzae - both treated with Co- amoxiclav (penicillin- Beta lactamase inhibitor )
39
what is the pathogenesis for Epstein- Barr Virus (EBV)
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
what other neoplastic diseases are associated with Epstein - Barr Virus?
- Burkitt lymphoma | - Epstein- Barr- associated nasopharyngeal carcinoma
41
what do labs usually show and what is the treament for EBV?
labs: atypical lymphocytes (cytotoxic T cells) and elevation of all Igs treatment= Acyclovir- inhibits EBV replication
42
what causes pharyngitis ?
``` Streptococal pharyngitis (strep throat) - treat with penicillin- co amoxiclav or amoxicillin ```
43
what is the treatment for HIV?
- 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
what are the typical infections associated with HIV?
- oral candidiasis - Kaposi's sarcoma - PCP: pneumocystis pneumnia - pneumocystis jirovecii ( fungal)
45
what is Aspergillus
opportunistic fungus that usually resides in dust- breathe in fungal spores - treatment = Amphotericin - anti fungal agent given IV
46
what is Varicella- Zoster?
- 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
what is hepatitis?
``` 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
what are the liver function tests for hepatitis?
- bilirubin - liver transaminases- alanine (ALT) - aspartate aminotransferase (AST) - albumin - test for coagulation (clotting factors synthesised in the liver) - > INR , PT
49
how to determine if chronic Hep B?
- persistence of HBsAg after 6 months - no cure- integrates into host genome - require life- long antiviral to suppress viral replication
50
what serology is present with acute hep?
surface antigen HBsAg core antibody HBcAb (IgM) surface antibody ABsAb - will not clear
51
what serology is present with chronic hep?
surface antigen HBsAg core antibody HBcAb (IgG) no surface antigen HBsAb- wanted response
52
what serology is present if vaccinated against hep?
no surface antigen HBsAg no core antibody HBcAb surface antibody ABsAb - wanted immune response
53
what is the history for a patient with malaria?
fever, chills and sweats may have slenomegaly | tachycardia, hypotension, diarrhoea, acute kidney injury, DIC
54
how does the malaria parasite infect?
- 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
what are the investigations and treatment for malaria?
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
describe Salmonella Typhi
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
what does Salmonella Typhi cause?
Enteric / Typhoid fever - fever, headache abdominal discomfort, dry cough, bradycardia - moderate anaemia, lymphopaenia, increased LFTs Treatment= IV Ceftriaxone or azithromycin (macrolide)
58
What is Dengue fever?
caused by an arbovirus - severe myalgia and headache - no other specific features - Dengue PCR and serology (IgM)
59
what is Schistosmoiasis?
- 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
Describe the structure of the Influenza virus
- 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
what are the different types of influenza?
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
how does the influenza virus replicate
``` (-) 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
how does the influenza virus transmit and how does the body protect itself?
- 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
what are the complications of influenza?
- 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
what is the treatment for influenza ?
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
What is the issue with the RNA polymerases in influenza?
high error rates lack of proof reading ability creates mutations
67
what is the difference between antigenic drift and antigenic shift? (in relation to influenza)
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
what is the difference between epidemic and pandemic?
epidemic- prevalent among a people/ community at a special time pandemic- epidemic over a larger area- affecting a large proportion of a population
69
Describe Pseudomonas aeruginosa , including treatment
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
how to prevent Pseudomonas aeruginosa in CF patients?
- 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
What is Cystic Fibrosis?
- 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
What can Diabetes Mellitus result in?
- 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
why do diabetics get UTIs?
-diabetic neuropathy leads to defects in bladder emptying (stasis) glycosuria= increased bacterial infections - usually E. coli or Pseudomonas aeruginosa
74
what is the difference between exotoxin and endotoxin?
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
What is a microbiome vs microbiota?
``` microbiome= all genome within the gut environment microbiota= all organisms within the gut environment ```
76
what is microbiota useful for in the GI?
- pathogen inhibition - immune protection - nutrient metabolism - drug metabolism - gut brain axis
77
what are the two types of acute infectious diarrhoeas and describe them
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
what is non-typhoidal salmonella?
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
what is campylobacter?
gram - spiral shape - abdo cramping, diarrhoea, fever and malaise - treatment= macrolides or fluoroquinolone complications- reactive arthritis, Guillain- Barle syndrome (ascending paralysis)
80
what is shigella?
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
what is E. coli 0157
- 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
norovirus vs rotavirus
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
define cryptosporidium
- intracellular protozoan parasite - think walled so live a long time outside the human - sporadic, water associated outbreaks treatment= nitazoxanide
84
define Giardia
- protozoan parasite - usually travellers, infants/ children, immunocompromised, CF - malaise, steatorrohea, abdo cramping or asymptomatic treatment if symptomatic= metronidazole/ nitazoxanide
85
define Entamoeba histolytica
- 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
uncomplicated UTI treatment
3 days | Nitrofurantonin, Trimethoprim, Pirmecillinam, Fosfomycin
87
complicated UTI treatment
5-7 days | Nirtofurantonin, Trimethoprim, Cefelexin (pregnant)
88
pyelonephritis/ septicaemia treatment
``` 7-10 day course agent with systemic activity possibly IV: - co amoxiclav - ciprofloxacin - gentamicin IV only - nephrotoxic ```
89
what is helicbacter pylori and what features does it have
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
what is the significance of where Helicobacter pylori colonises?
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
how to diagnose Helicobacter pylori?
- urease breath test - stool antigen test - (upper gastrointestinal endoscopy)
92
what is the treatment for Helicobacter pylori?
- PPI (proton pump inhibitor) | - Amoxicillin + (Clarithromycin/ Metronidazole)