Case 3 : HAIs Flashcards

1
Q

What are hospital acquired infections ?

A
  • Infections patients get while receiving treatment for medical or surgical conditions.
  • Many are preventable.
  • Infections can be associated with procedures (like surgery) and the devices used in medical procedures, such as catheters or ventilators.
  • Healthcare associated infection: diff between the two, this is a more general term than hospital acq inf, because healthcarre encompasses healthcare facilities not just hospitals
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2
Q

What is a central line-associated bloodstream infection (CLABSI)

A

Serious HAI that occurs when germs (e.g., bacteria) enter the bloodstream through the central line (a long flexible tube placed in a large vein that empties out near the heart).

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3
Q

What is Methicillin-resistant Staphylococcus aureus (MRSA)

A

A type of bacteria that is resistant to many antibiotics. In medical facilities, MRSA causes life-threatening bloodstream infections, pneumonia, and surgical site infections.

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4
Q

Sources of HAIs :

A
  • CLABSI
  • MRSA
  • Catheter-associated urinary tract infections
  • Surgical site infections
  • Bloodstream infections
  • Pneumonia
  • Clostridium difficile
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5
Q

Why Are Healthcare-Associated Infections Important?

A
  • Source of complications
  • Transmission between different health care facilities
  • Medical cost saving
  • Education and training of health care workers increases compliance with and adoption of best practices (e.g., infection control, hand hygiene, attention to safety culture, and antibiotic stewardship) eg careful insertion, maintenance, and prompt removal of catheters, and careful use of antibiotics and getting rid of MRSA in patients with an evidence-based method to reduce transmission of MRSA in hospitals.
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6
Q

Chain of infection

A
  1. Infectious agent
  2. Reservoir
  3. Portal of exit
  4. Mode of transmission
  5. Portal of entry
  6. Susceptible host
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7
Q

Reservoir meaning

A
  • The habitat in which the infectious agent normally lives, grows, and multiplies.
  • Can be humans, animals, and the environment.
  • The reservoir may or may not be the source from which an agent is transferred to a host eg reservoir of Clostridium botulinum is soil, but the source of most botulism infections is improperly canned food containing C. botulinum spores.
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8
Q

Human reservoirs

A
  • include the sexually transmitted diseases, measles, mumps, streptococcal infection, and many respiratory pathogens.
  • Because humans were the only reservoir for the smallpox virus, naturally occurring smallpox was eradicated after the last human case was identified and isolated.
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9
Q

Types of human reservoir

A
  • A carrier : person with inapparent infection who is capable of transmitting the pathogen to others.
  • Asymptomatic or passive or healthy carriers : never experience symptoms despite being infected.
  • Incubatory carriers : can transmit the agent during the incubation period before clinical illness begins.
  • Convalescent carriers : recovered from their illness but remain capable of transmitting to others.
  • Chronic carriers : continue to harbor a pathogen such as hepatitis B virus or Salmonella Typhi, the causative agent of typhoid fever, for months or even years after their initial infection.
  • Carriers commonly transmit disease because they do not realize they are infected, and consequently take no special precautions to prevent transmission.
  • Symptomatic persons who are aware of their illness, on the other hand, may be less likely to transmit infection because they are either too sick to be out and about, take precautions to reduce transmission, or receive treatment that limits the disease.
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10
Q

Animal reservoirs and zoonosis

A

Zoonosis refers to an infectious disease that is transmissible under natural conditions from vertebrate animals to humans.

Long recognized zoonotic diseases include brucellosis (cows and pigs), anthrax (sheep), plague (rodents), trichinellosis/trichinosis (swine), tularemia (rabbits), and rabies (bats, raccoons, dogs, and other mammals).

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11
Q

Environmental reservoirs

A
  • Plants, soil, and water
  • Many fungal agents eg those that cause histoplasmosis, live and multiply in the soil.
  • Outbreaks of Legionnaires disease often traced to water supplies in cooling towers and evaporative condensers, reservoirs for the causative organism Legionella pneumophila.
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12
Q

Portal of exit

A
  • influenza viruses and Mycobacterium tuberculosis exit the respiratory tract, schistosomes through urine, cholera vibrios in feces, Sarcoptes scabiei in scabies skin lesions, and enterovirus 70, a cause of hemorrhagic conjunctivitis, in conjunctival secretions.
  • Some bloodborne agents can exit by crossing the placenta from mother to fetus (rubella, syphilis, toxoplasmosis), while others exit through cuts or needles in the skin (hepatitis B) or blood-sucking arthropods (malaria).
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13
Q

Modes of transmission

A

Direct

  • Direct contact
  • Droplet spread

Indirect

  • Airborne
  • Vehicleborne
  • Vectorborne (mechanical or biologic)
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14
Q

Direct contact

A
  • skin-to-skin contact, kissing, sexual intercourse, contact with soil or vegetation harboring infectious organisms.
  • Thus, infectious mononucleosis (“kissing disease”) and gonorrhea are spread from person to person by direct contact.
  • Hookworm is spread by direct contact with contaminated soil.
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15
Q

Droplet spread

A
  • spray with relatively large, short-range aerosols produced by sneezing, coughing, or even talking.
  • Droplet spread is classified as direct because transmission is by direct spray over a few feet, before the droplets fall to the ground.
  • Pertussis and meningococcal infection are examples of diseases transmitted from an infectious patient to a susceptible host by droplet spread.
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16
Q

Airborne transmission

A
  • when infectious agents are carried by dust or droplet nuclei suspended in air.
  • Airborne dust includes material that has settled on surfaces and become resuspended by air currents as well as infectious particles blown from the soil by the wind.
  • Droplet nuclei are dried residue of less than 5 microns in size.
  • In contrast to droplets that fall to the ground within a few feet, droplet nuclei may remain suspended in the air for long periods of time and may be blown over great distances.
  • Eg measles
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17
Q

Vectors

A
  • mosquitoes, fleas, and ticks may carry an infectious agent through purely mechanical means or may support growth or changes in the agent.
  • Eg of mechanical transmission are flies carrying Shigella on their appendages and fleas carrying Yersinia pestis, the causative agent of plague, in their gut.
  • in biologic transmission, the causative agent of malaria or guinea worm disease undergoes maturation in an intermediate host before it can be transmitted to humans.
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18
Q

Portals of entry examples

A
  • skin (hookworm),
  • mucous membranes (syphilis),
  • blood (hepatitis B, human immunodeficiency virus).
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19
Q

Susceptibilty

A
  • Depends on genetic or constitutional factors, specific immunity, and nonspecific factors that affect an individual’s ability to resist infection or to limit pathogenicity
  • persons with sickle cell trait seem to be at least partially protected from a particular type of malaria.
  • Specific immunity : protective antibodies that are directed against a specific agent; may develop in response to infection, vaccine, or toxoid (toxin that has been deactivated but retains its capacity to stimulate production of toxin antibodies) or mtransplacental transfer from mother to fetus or by injection of antitoxin or immune globulin.
  • Nonspecific factors that defend against infection include the skin, mucous membranes, gastric acidity, cilia in the respiratory tract, the cough reflex, and nonspecific immune response.
  • Factors that may increase susceptibility to infection by disrupting host defenses include malnutrition, alcoholism, and disease or therapy that impairs the nonspecific immune response.
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20
Q

Interventions

A
  • Controlling or eliminating agent at source of transmission
  • Protecting portals of entry
  • Increasing host’s defenses
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21
Q

What is given to protect against malaria

A

prophylactic use of antimalarial drugs, recommended for visitors to malaria-endemic areas, does not prevent exposure through mosquito bites, but does prevent infection from taking root.

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22
Q

Difference between vector and carrier

A

a vector carries the infection but is not affected by it, a carrier actually has the disease.

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23
Q

How do altered target sites arise in resistant bacteria?

A
  • Bact gets alternative gene or a gene that encodes a target-modifying enzyme.
  • MRSA encodes an alternative PBP (PBP2a) with low affinity for beta-lactams, enables bacterium to resist them.
  • Streptococcus pneumoniae resistance to erythromycin becasue it acquires erm gene, which encodes an enzyme that methylates the AB target site in the 50S ribosomal subunit.
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24
Q

How do resistant bacteria inactivate antibiotics?

A
  • Enzymatic degradation or alteration : renders antibiotic ineffective.
  • Examples include beta-lactamase (bla) and chloramphenicol acetyl-transferase (cat).
  • ESBL and NDM-1 are examples of broad-spectrum beta-lactamases (can degrade a wide range of beta-lactams abs, including newest).
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25
Q

How does penicillin resistance come about

A
  • B-lactamase breaks a bond in the b lactam ring of penicillin to disable the molecule -
  • Bact with this enz can resist effects of penicillin and other B lactam ab
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26
Q

How do bacteria alter their metabolism to resist the effects of antibiotics?

A
  • Increased production of enzyme substrate can out-compete antibiotic inhibitor (e.g. increased production of PABA confers resistance to sulfonamides).
  • Alternatively, bacteria switch to other metabolic pathways, reducing requirement for PABA. Eg bact that have access to thymidine are not inhibited by trimethoprim because bact can bypass the inherited metabolic pathway.
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27
Q

How do resistant bacteria decrease drug accumulation?

A

Reduced penetration of AB into bacterial cell (permeability) and/or increased efflux of AB out of the cell – drug does not reach concentration required to be effective.

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28
Q

How is resistance conferred

A
  1. The cell wall consists of peptidoglycan
  2. Gram positive build thick sheath of this but gram neg has thin sheath of this sandwiched between two membranes.
  3. Osmosis - peptid prevents pressure build-up
  4. Penicillin weakens this, prevents bact building the peptid layer so that overcomes to pressure
  5. two Sugars assembled into chains with amino acids, crosslinked via peptide bridge to - tough matrix
  6. Penicillin assembling protein assembles chain , Enzyme D - alanyl-Dalanine Carboxypeptidase / transpeptidase, also known as penicillin - Binding protein, assists with peptid matrix assembly by creating the crosslinks between the chains.
  7. Penicillin blocksthis enzyme by making a direct bond to key serine amino acid in its active site. Active portion of penicillin is a beta lactam ring, chemically reactive and opens up to form a bond to active site serine.
  8. Inactivates enzyme and prevents proper formation of peptid matrix
  9. some bact have developed resistance mechanisms to pen.
  10. For example MRSA - expresses penicillin binding protein 2a which has an altered active site that doesn’t bind beta lactam antibiotics.
  11. Bact can also express special Beta lactamase enzymes which bind to beta lactam antibiotics and break the beta lactam ring making antibiotic ineffective
  12. New drugs block beta lactamases so that ab can break down the bact.
  13. some block beta lactamase directly leaving antibiotic free to inhibit penicillin binding proteins, other beta lactam drugs are either not recognized or not broken down by some beta lactamases.
  14. Many genes crucial in ab resistance are encoded on small circular pieces of DNA called plasmids - these plasmids can be passed on from one generation of bact to another.
  15. One particularly dangerous gene is NDM-1, bact possessing this gene can build the New Delhi metallo beta lactamase enzyme - these types of enzymes can break down almost all known beta lactam drugs posing a major global threat
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29
Q

Sequence of events for infection with C. Difficile

A
  1. Treatment with Co-amoxiclav
  2. Disruption of gut microbiome
  3. Activation of toxigenic C . Difficile
  4. Toxins cause diarrhoea, they can cause inflammation by damaging lining of guts.
  5. Positive for C. Difficile diarrhoea
  6. Encourage to stay well hydrated, and possibly take laxatives to avoid constipation.
  7. Don’t necessarily need ab to treat C difficile - check with microbiologist whether diff ab needed to treat the C diificile
30
Q

Hand hygiene

A
  1. Before toucing patient
  2. Before procedures
  3. Washing hands after putting in catheters , touching bodily fluids etc
  4. After touching patient
  5. After changing sheets handling equipment etc.
31
Q

Most common HAI in US

A
  1. urinary tract infections
  2. surgical site infections
  3. Lung infections
  4. Blood stream infections
32
Q

what % of patients in ENgland get HAIs

A

6.14 %

33
Q

Ab resistance

A

Ab are important for ;

  • Sepsis treatment, without timely treatment with ig, sepsis can rapidly lead to tissue, organ failure, death.
  • Surgery, treat surgical site infections and things like C section to prevent infection
  • Chronic conditions (put people at increased risk of infection like sickle cell and diabetes)
34
Q

REsistance can spread between

A
  • people, animals, and the environment. ( water and soil)
  • Some types of ig resistant can spread person to person eg nightmare bact (carbapenem resistant Enterobacteriaceae (CRE), can also survive and grow in sink drains at healthcare facilities and spread to patients thru wastewater
  • Resistant germs can spread between animals and people thru food or contact with animals
  • Ig resistant germs can spread in environment. Crop fields can be treated with fungicides that are similar to antifungals used in human med
35
Q

Side effects of ig

A
  • Rash
  • Nausea
  • Diarrhea
  • Yeast infections
  • C. diff infection, which causes diarrhea that can lead to severe colon damage and death
  • Severe and life-threatening allergic reactions
  • Antibiotic-resistant infections
36
Q

Resistnace mechanisms

A
  • Restrict access of the antibiotic
  • Get rid of the antibiotic
  • Change or destroy the antibiotic
  • Bypass the effects of the antibiotic
  • Change the targets for the antibiotic
37
Q

Risk factors of HAIS

A

Medical procedures

Ab use

Patient characteristics eg age

Behaviour of healthcare staff

Healthcare facility

Length of hospital stay

38
Q

Restriction of access of ab example

A

Gram-negative bacteria : outer layer (membrane) that protects them from their environment

can use this membrane to selectively keep antibiotic drugs from entering.

39
Q

GEtting rid of ab example

A
  • Germs get rid of antibiotics using pumps in their cell walls to remove antibiotic drugs that enter the cell.
  • eg Some Pseudomonas aeruginosa bacteria can produce pumps to get rid of several different important antibiotic drugs, including fluoroquinolones, beta-lactams, chloramphenicol, and trimethoprim.
40
Q

Changing or destroying the ab eg

A

Klebsiella pneumoniae bacteria produce enzymes called carbapenemases, which break down carbapenem drugs and most other beta-lactam drugs

41
Q

BYpassing the effects of the ab eg

A

Some Staphylococcus aureus bacteria can bypass the drug effects of trimethoprim

42
Q

Changing the targets for the ab

A

Many antibiotic drugs are designed to single out and destroy specific parts (or targets) of a bacterium. Germs change the antibiotic’s target so the drug can no longer fit and do its job.

Example: Escherichia coli bacteria with the mcr-1 gene can add a compound to the outside of the cell wall so that the drug colistin cannot latch onto it.

43
Q

Resistant traits can pass directly from germ to germ by

A

mobile genetic elements:

  • plasmids
  • transposons (small pieces of DNA that can go into and change overall DNA of cell, can move from chromosomes to plasmids and back)
  • Phages (viruses that attack germs and can carry DNA from germ to germ)
44
Q

HOw do mobile genetic elements work

A
  • Transduction (resistance genes can be transferred via phages)
  • Conjugation ( transfer between germs when they connect)
  • Transformation (released from nearby live or dead germs)
45
Q

Carbapenem-resistant Acinetobacter

A
  • URGENT
  • Bacteria
  • CAuses pneumonia and wound, bloodstream, and urinary tract infections. Nearly all these infections happen in patients who recently received care in a healthcare facility.
46
Q

Drug-resistant Candida auris (C. auris)

A
  • URGENT
  • Fungus
  • emerging multidrug-resistant yeast.
  • It can cause severe infections and spreads easily between hospitalized patients and nursing home residents.
47
Q

Clostridioides difficile (C. difficile)

A
  • URGENT
  • Bacteria
  • Also known as: C. difficile or C. diff, previously Clostridium difficile
  • Causes life-threatening diarrhea and colitis (an inflammation of the colon), mostly in people who have had both recent medical care and antibiotics.
48
Q

Carbapenem-resistant Enterobacteriaceae (CRE)

A
  • URGENT
  • Bacteria
  • Also known as: Nightmare bacteria
  • Major concern for patients in healthcare facilities. Some Enterobacteriaceae (a family of germs) are resistant to nearly all antibiotics, leaving more toxic or less effective treatment options.
49
Q

Drug-resistant Neisseria gonorrhoeae (N. gonorrhoeae)

A
  • URGENT
  • Bacteria
  • Also known as: Drug-resistant gonorrhea
  • Causes the sexually transmitted disease gonorrhea that can result in life-threatening ectopic pregnancy and infertility, and can increase the risk of getting and giving HIV.
50
Q

Drug-resistant Campylobacter

A
  • Serious
  • Bacteria
  • Also known as: Campy
  • Usually causes diarrhea (often bloody), fever, and abdominal cramps, and can spread from animals to people through contaminated food, especially raw or undercooked chicken.
51
Q

Drug-resistant Candida Species

A
  • Serious
  • Fungus
  • Dozens of Candida species—a group of fungi—cause infections, ranging from mild oral and vaginal yeast infections to severe invasive infections. Many are resistant to the antifungals used to treat them.
52
Q

ESBL-producing Enterobacteriaceae

A
  • Serious
  • Bacteria
  • Also known as: Extended-spectrum β-lactamase
  • Concern in healthcare settings and the community. They can spread rapidly and cause or complicate infections in healthy people.
  • ESBL stands for extended-spectrum beta-lactamase. ESBLs are enzymes that break down commonly used antibiotics, such as penicillins and cephalosporins, making them ineffective.
53
Q

Vancomycin-resistant Enterococcus (VRE)

A
  • Serious
  • Bacteria
  • can cause serious infections for patients in healthcare settings, including bloodstream, surgical site, and urinary tract infections.
54
Q

Multidrug-resistant Pseudomonas aeruginosa (P. aeruginosa)

A
  • Serious
  • Bacteria
  • usually occur in people with weakened immune systems, and can be particularly dangerous for patients with chronic lung diseases.
55
Q

Drug-resistant nontyphoidal Salmonella

A
  • Serious
  • Bacteria
  • Nontyphoidal Salmonella can spread from animals to people through food, and usually causes diarrhea, fever, and abdominal cramps. Some infections spread to the blood and can have life-threatening complications.
56
Q

Drug-resistant Salmonella serotype Typhi

A
  • Serious
  • Bacteria
  • Also known as: Typhoid fever
  • causes a serious disease called typhoid fever, which can be life-threatening. Most in US become infected while traveling to countries where the disease is common.
57
Q

Drug-resistant Shigella

A
  • SERIOUS
  • Bacteria
  • About: Shigella spreads in feces through direct contact or through contaminated surfaces, food, or water. Most people with Shigella infections develop diarrhea, fever, and stomach cramps.
58
Q

Methicillin-resistant Staphylococcus aureus (S. aureus) (MRSA)

A
  • serious
  • Type: Bacteria
  • Also known as: Resistant staph (short for Staphylococcus)
  • About: S. aureus are common bacteria that spread in healthcare facilities and the community. MRSA can cause difficult-to-treat staph infections because of resistance to some antibiotics.
59
Q

Drug-resistant Streptococcus pneumoniae (S. pneumoniae)

A
  • SERIOUS
  • Type: Bacteria
  • Also known as: Pneumococcus
  • About: S. pneumoniae causes pneumococcal disease, which can range from ear and sinus infections to pneumonia and bloodstream infections.
60
Q

Drug-resistant Tuberculosis

A
  • SERIOUS
  • Type: Bacteria
  • Also known as: TB, multidrug-resistant TB (MDR TB), or extensively drug-resistant TB (XDR TB), Mycobacterium tuberculosis (M. tuberculosis)
  • About: TB is caused by the bacteria M. tuberculosis, and is among the most common infectious diseases and a frequent cause of death worldwide.
61
Q

Erythromycin-resistant Group A Streptococcus

A
  • concerning
  • Type: Bacteria
  • Also known as: Resistant group A strep, GAS
  • About: GAS can cause many different infections that range from minor illnesses to serious and deadly diseases, including strep throat, pneumonia, flesh-eating infections, and sepsis.
62
Q

Clindamycin-resistant Group B Streptococcus

A
  • concerning
  • Type: Bacteria
  • Also known as: Resistant group B strep, GBS
  • About: GBS can cause severe illness in people of all ages.
63
Q

Azole-resistant Aspergillus fumigatus

A
  • watchlist
  • fungus that can cause life-threatening infections in people with weakened immune systems.
  • These infections are treated with antifungals called azoles.
  • increasingly used in agriculture to prevent and treat fungal diseases in crops. Azole use in human medicine and agriculture can contribute to resistance to antifungal medicines.
64
Q

Drug-resistant Mycoplasma genitalium (M. genitalium)

A
  • Watchlist
  • M. genitalium bacteria are sexually transmitted and can cause urethritis in men (inflammation of the urethra) and may cause cervicitis in women (inflammation of the cervix).
  • Few antibiotics are available to treat M. genitalium infections. Resistance to azithromycin, which has been recommended for treatment, is high across the globe.
65
Q

Drug-resistant Bordetella pertussis (B. pertussis)

A
  • watchlist
  • respiratory illness commonly known as whooping cough, is a very contagious disease caused by a type of bacteria called B. pertussis.
  • It can cause serious and sometimes deadly complications, especially in babies.
66
Q

Why is herd immunity not always the best form of prevention

A

IN past hasn’t prevented measles outbreaks and rubella even with high immunization rates:

Because, few susceptible people often clustered in small subgroups : defined by socioeconomic and cultural factors

If pathogen introduced into one of these groups- outbreak

67
Q

Explanation of medical notes

A

HIGh CRP: C reactive protein - indicates infection or inflammation

High wbc - infection

Low O2 blood saturation - infection (normal = 95 - 100 % ) these can dip during infection , and need to know if patient has been on O and for how long

HIGh RR (respiratory rate) - infection (norm : 12 -20 bpm) , higher in infection

68
Q

What is sepsis and shock and what are the sequences of septic shock

A

Sespsis : bodys extreme reaction to infection

Shock : imbalance in supply and demand

Sequences of septic shock :

  1. Respiratory rate goes up
  2. Tachycardic
  3. Blood pressure drops
69
Q

IV vs oral for sepsis shock

A

IV as opposed to oral : IV is faster delivery and systemic effect - acts straight away

70
Q

What are B lactamase inhibitor, Co - amoxiclav, Clavulanic acid ?

A
  • B lactamase inhibitors : medication used to inhibit the activity of B lactamases allowing B lactam ab to work properly
  • Co - amoxiclav = amoxicillin (beta lactam ab) and clavulanic acid (beta lactamase inhib ) - prevents breakdown of amoxicillin
  • Clavulanic acid is a B lactamase inhibitor - stops breakdown of amoxicillin
  • If resistant to amoxicillin but receptive to co amoxiclav - beta lactamase driven.
71
Q

Negative side effects of treatment with co amoxiclav

A

Treatment with Co-amoxiclav - disruption of gut microbiome (created perf environment for toxigenic C. difficile)

Ab Killed gut bact which stopped C. difficile from multiplying before because they were out competed , C. difficile was always there, ab wipes out all gut bact and so C. difficile can now flourish and multiply

This causes diarrhoea