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Year 2 MCD 2 > Microbiology > Flashcards

Microbiology Flashcards

1
Q

What is a virus?

A

Viruses are obligate intracellular parasites that use cell machinery to create more viral components and genomes.

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2
Q

What are the benefits of a DNA genome over a RNA one for a virus?

A

DNA genomes are more stable, less error prone and can therefore be more complex than RNA genomes. They can even have accessory genes which allow them to evade the immune response.

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3
Q

How long can a RNA virus be?

A

30 base pairs

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4
Q

Which family of viruses tend to be large DNA viruses?

A

Large DNA viruses such as Herpesviruses tend to cause latent infection by surviving in the host for a long period of time. To do this they need to interact intricately with the host immune response to avoid detected.

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5
Q

List the popular members of the Herpes virus family

A

Members of the Herpesviridae include:

  • Varicella zoster virus
  • Epstein-Barr virus
  • Cytomegalovirus
  • Herpes Simplex Viruses.

These are extremely widespread amongst humans.

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6
Q

What is required in order to activate the innate immune system against a virus?

A

In order for a pathogen to initiate any type of response, be it innate (which then leads to adaptive), it needs to activate PRRs (Pathogen Recognition Receptors). After PAMPs (Pathogen Associated Molecular Patterns) bind to PRRs, they can transduce a signal with a cascade of events to mount an immune response.

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7
Q

Give examples of PRRs

A

PPRs can be cytoplasmic like RIG-I like receptors (RLRs) or on the cell surface like Toll-like receptors (TLRs).

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8
Q

How can PRRs detect viral DNA?

A

They don’t have a 5’ cap nor 3’ poly-A tail.

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9
Q

What are interferons?

A

Interferons are soluble cytokines which comprise our innate immunity against viruses (as well as physical barriers).

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10
Q

What are type 1 interferons, and what cells secrete them?

A

Type 1 interferons are secreted from all infected cells, these include IFN-α and IFN-β.

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11
Q

What are the three major functions of type 1 interferons?

A
  1. Induce antimicrobial state in infected and neighbouring cells.
  2. Modulate innate response to promote antigen presentation and activate natural killer (NK) cells.
  3. Activate the adaptive immune response
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12
Q

How many isotypes of INF-a and INF-b do we have

A

While there is only one gene for INF-β, there are 13/14 isotypes of INF-α.

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13
Q

What are type 2 interferons, and what cells secrete them?

A

Type 2 interferons are produced by activated T-cells and NK cells. IFN-y is the only type 2 interferon

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14
Q

What are the main interferon receptors?

A
  • INFAR (for INF-a and INF-b)

- INFGR (for INF-y)

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15
Q

What molecules respond to type-3 interferons?

A

Type 3 interferons are a group of INF-λ molecules, whose receptors are mainly present on epithelial surfaces.

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16
Q

Explain how type I interferon synthesis is regulated

A
  • Signalling from RIG-1 or TLR (after the detection of viral RNA) is passed through Mavs (Mitochondiral activation of viral signalling).
  • This leads to the nuclear entry of various factors which bind to the promoter region of the IFN-β gene.
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17
Q

Complete the sentence:
- The IFN-β molecule can act through autocrine signalling or paracrine signalling to activate de novo transcription of hundreds of _________.

A

Interferon Stimulated Genes (ISGs)

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18
Q

How does viral DNA activate signalling in a similar way RNA does through RIG-1?

A

foreign DNA can be detected through cGAS. cGAS biochemically modifies bits of DNA so that it can be detected by STING on ER to switch on IFN in the same way as RIG-I does.

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19
Q

Outline the canonical type I interferon signalling pathway.

A

INFa/b binds to a transmembrane INF receptor (INFAR) which heterodimerises [INFAR1 and INFAR2]. Through a series of series of phosphorylation events Tyk2 and Jak1 phosphorylate each other, as well as other proteins in the cytoplasm such as STAT proteins.

The STAT proteins enter the nucleus and bind to the promoter regions of ISGs. These promoter regions are called the Interferon Stimulated Response Elements

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20
Q

Why can the IFN response only be maintained for several hours?

A

The interferon stimulated genes (ISGs) have a drastuc effect on the cell and can’t be left switched on.

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21
Q

List some important ISGs

A
  • Mx
  • PKR
  • IFITM3
  • APOBECs
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22
Q

Explain the mechanisms of action of IFITM3

A

IFITM3 (Interferon Induced TransMembrane Protein 3) is an important protein transcribed by a ISG. It inhibits entry of enveloped viruses (such as influenza) which enter the cell via endosomes.

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23
Q

Explain the mechanisms of action of Mx

A

Mx is a GTPase that can form multimers which wrap around the nucleocapsids of incoming viruses – therefore nullifying incoming virus genomes.

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24
Q

Which viruses are particularly prone to Mx1 and Mx2?

A

Mx1 inhibits influenza and Mx2 inhibits HIV

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25
Q

Explain the mechanisms of action of PKR

A

PKR (Protein Kinase R) phosphorylates the alpha subunit of eIF2 and prevents translation in the infected host cells. It also activates IKKb leading to NFkb release – an important transcription factor in the antiviral response.

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26
Q

What are the general ways viruses control or evade the type I interferon system?

A
  • Avoiding detection by hiding the PAMP. This results in a failure to initiate the innate and this interferon response.
  • Interfere globally with host cell gene expression and/or protein synthesis.
  • Block IFN induction cascades by destroying or binding.
  • Inhibit IFN signalling
  • Activate SOCS (Suppression of Cytokine Signalling)
  • Use a replication strategy that is insensitive to IFN
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27
Q

How does HCV control or evade the type I interferon system?

A

Hepatitis C Virus contains an accessory gene that codes for the NS3/4 protease which cleaves MAVS and therefore prevents interferon induction.

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28
Q

How does Influenza virus control or evade the type I interferon system

A

Influenza virus contains an accessory gene that codes for the NS1 protein which binds to RIG-I preventing activation of signalling pathway and preventing nuclear processing of newly induced genes.

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29
Q

How do the Pox viurses control or evade the type I interferon system?

A

The Pox viruses are also large DNA viruses. More than half of their genome is comprised of accessory genes that modify the immune response. Some pox viruses encode soluble cytokine receptors that mop up interferon so that they don’t reach their receptors.

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30
Q

How does HIV control or evade the type I interferon system?

A

Through accessory genes Vif and Vpu:
• The Vif protein product targets the APOBEC system. APOBEC3G is a mRNA-editing enzyme which is involved in innate resistance to retroviruses and hepadendoviruses. It usually deaminates dC to dU in minus strand viral cDNA during reverse transcription.
•The Vpu, Env and Nef genes target Tethrin which is a cell surface molecule that normally stops viral budding from the plasma membrane.

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31
Q

How can viruses modulate the immune system to cause us more harm?

A
  • skewing the effects of interferon from protective to immunopathologic by induce different ISG expression profiles
  • Viral induction of interferon can lead to a cytokine storm. This is the release of toxic anti-viral mediators such as massive amounts of TNF-α, which causes harm to the host.
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32
Q

Which viral infections are characterised by a dangerous cytokine storm?

A

Dengue haemorrhagic fever, severe influenza and Ebola viral infections

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33
Q

How is INF used in treatment against viruses?

A

Pegylated IFN is used as a treatment for hepatitis C.

Normal INF has too may side-effects and is very dangerous

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34
Q

Why are viruses that lack the ability to control infection useful?

A

Viruses that lack the ability to control interferon, produce high INF levels. This is useful in generation of live attenuated vaccines as the high IFN levels can also induce and recruit useful immune cells; Interferon can act as an adjuvant.

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35
Q

Why is it a good thing that the antigen target of the immune system tends to be a internal viral protein as opposed to an external viral protein.

A

This is good because they vary less than surface antigens, and also allows for the formation of good immunological memory.

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36
Q

Describe viral protein processing

A

Viral (and cellular) peptides are fed into a proteasome which chops the peptide before it is fed into the endoplasmic reticulum through TAP proteins. Here it is complexed with MHC molecules which are presented on the cell surface.

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37
Q

How does EBV escape the host cellular immune response?

A

The Epstein-Barr Virus encodes a protein (EBNA1) that cannot be processed by the proteasome, and therefore cannot be loaded by TAP.

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38
Q

How does HSV escape the host cellular immune response?

A

Herpes-Simplex Virus produces a protein (ICP47) that blocks access of the processed peptide to TAP.

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39
Q

How does CMV escape the host cellular immune response?

A
  • encodes a protein (US6) which stops ATP binding to TAP, preventing translocation.
  • protein (US3) which binds to tapasin and prevents peptides being loaded into MHC
  • also encode MHC analogues (gpUL40) or upregulate MHC.
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40
Q

How does KSHV escape the host cellular immune response?

A

encoded protein kK3 induces polyubiquitinylation and internalisation of MHC. Because it is ubiquinated, it is also marked for degradation by lysosomes.

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41
Q

How does Adenovirus escape the host cellular immune response?

A
  • Adenovirus prevents recruitment of TAP to tapasin (through E3-19K protein).
  • It also retains the MHC molecule in the ER preventing it from reaching the cell surface.
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42
Q

Which viruses attack the immune system and how?

A
  • HIV – targets CD4+ T-cells and depletes the ability to support an immune response
  • Ebola virus infection also results in destruction of target dendritic cells and macrophages by direct infection. As these cells present to T-cells, Ebola also infect T-cells by bystander response. Because Ebola is much more acute than HIV, we do not see the long-term sequelae of immunosuppression caused by it.
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43
Q

Explain how antigenic variation may lead to viral evasion

A

Antigenic variation is a form of continued rapid evolution driven by antigen pressure from the host. An example of this is the influenza antigenic drift where the influenza cell surface antigens change over time.

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44
Q

Give an example of a virus that exists as many serotypes

A

rhinovirus (120 distinct serotypes)

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45
Q

How can we partially account for influenza antigenic drift?

A

producing multivalent seasonal vaccines for antigens predicted to be popular.

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46
Q

How does ebola evade the immune system?

A
  • Some viruses have glycoprotein antigens that are so heavily glycosylated (mucin like) that antibody access is hindered - eg in HIV and Ebola. Ebola virus particle membranes have a high content of phosphatidyl serine lipids, making them look like apoptotic bodies that are rapidly taken up by pinocytosis away from antibody surveillance.
  • Ebola also codes for sGP (soluble glycoproteins) which act as an antibody decoy. sGP also has immunosuppressive properties, inhibiting neutrophils.
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47
Q

How does measles cause immunosuppression?

A

by infecting CD150 cells

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48
Q

Define infection

A

Infection is the invasion by and growth of pathogenic microorganisms within the body.

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49
Q

Define disease

A

A disease is a disordered or incorrectly functioning organ, part, structure, or system of the body resulting from the effect of
genetic or developmental errors, infection, poisons, nutritional deficiency or imbalance, toxicity, or unfavourable environmental factors; illness; sickness; ailment.

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50
Q

Define parasite

A

Parasite: An organism living in or on the host and dependent on it for nutrition - causing damage.

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51
Q

What are the main categories of parasites?

A
  • Ectoparasites live outside the body of the host
  • Endoparasites live inside the body of the host.
  • Protozoa are endoparasites that are single-celled
  • Metazoan are endoparasites that are multicellular
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52
Q

What are the types of protozoa?

A
  • Amoeba
  • Coccidia
  • Ciliates
  • Flagellates
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53
Q

What are the types of metazoan (helminths)?

A
  • Roundworms
  • Flatworms
  • Flukes
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54
Q

What endoparasites produce eosinophilia?

A

Helminths/Metazoa

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55
Q

List the important ameobae

A
  • Entamoeba histolytica

- Entamoeba dispar (not pathogenic)

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56
Q

How doe amoeba infections occur?

A

Infections occur by ingestion of mature cysts in food or water, or on hands

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57
Q

What percentage of the world is infected with E. histolytica?

A

10%

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58
Q

What organism is responsible for the third most common cause of death from parasite?

A

Entamoeba histolyticia

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59
Q

Where are E. histolytica infections most common?

A

Common in south and central America, and Asia (rare in temperate climates

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60
Q

What are the symptoms of an E.histolytica infection?

A

90% of infections are asymptomatic with the reminder producing a spectrum of disease varying from dysentery to amoebic liver abscess. Invasive amoebas can also affect the lung, heart, brain, urinary tract and skin.

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61
Q

List the important coccidia parasites

A
  • Plasmodium genus
  • Toxoplasma gondii
  • Cryptosporidium
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62
Q

What organisms cause malaria?

A
  • Plasmodium falciparum
  • Plasmodium malariae
  • Plasmodium ovale
  • Plasmodium vivax
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63
Q

What are the symptoms of Plasmodium infection?

A
  • Symptoms include fever, headache, chills, vomiting and muscle pain in a paroxysmal (sudden and intense) cycle.
  • The longer term complication of malaria includes severe anaemia (due to destruction of the red blood cells), and cerebral malaria (due to swelling of the brain) leading to seizures and coma.
  • Other symptoms include liver failure, shock, pulmonary oedema, kidney failure and ruptured spleen
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64
Q

How many cases of malaria were there in 2013?

A

198 million

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65
Q

How many deaths does malaria cause every year?

A

584 000

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66
Q

What hosts carry plasmodium?

A

Humans and Anopheles mosquitos

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67
Q

How can malaria be detected and treated?

A

Plasmodium can be detected on a blood film or a more rapid antigen detection test can be done. Usually treated with chloroquine and doxyclycline.

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68
Q

How does infection by Toxoplasma gondii occur?

A

Humans can become infected by eating undercooked meat of animals harbouring cysts, exposure to cat faeces, blood/organ transplants, and also transplacentally.

69
Q

What are the symptoms produced by toxoplasmosis?

A

Toxoplasmosis is a mild disease in immunocompetent individuals, however can pose a serious danger for the foetus. immunocompromised patients may develop CNS disease, brain lesions, and pneumonitis among other risks.

70
Q

What are the symptoms caused by cryptosporidium infection?

A

Cryptosporidium is a genus of coccidia protozoa that can cause diarrhoea in immunocompetent individuals. However, it usually presents in HIV+ patients with more serious symptoms.

71
Q

List the important ciliates

A
  • Balantidium coli
72
Q

What are the reservoir hosts of Balantidium coli?

A

pigs, rodents, and primates

73
Q

What symptoms are caused by balantidium coli infection?

A

Most people infected with Balantidium coli experience no symptoms. Immunocompromised patients may experience more severe signs and symptoms: persistent diarrhoea, dysentery, abdominal pain, weight loss, nausea, and vomiting. If left untreated, perforation of the colon can occur. Diagnosed with stool examination.

74
Q

What is the most common water-borne protozoal infection?

A

Giardiasis by Giardia lamblia

75
Q

What are the symptoms of giardiasis?

A

presents with diarrhoea, greasy stools which float, abdominal cramps and dehydration. However, most people do not present with any symptoms.

76
Q

List the important flagellates

A
  • Giardia lambda
  • Trichomonas vaginallis
  • Trypanosoma
  • Leishmania
77
Q

How is trichomonas vaginallis spread?

A

Sex

78
Q

What organism is responsible for the most curable non-viral STI in the UK?

A

Trichomonas vaginallis

79
Q

What disease and symptoms are produced by trichomonas vaginallis?

A

Up to 50% of people are asymptomatic. Women with symptoms experience vaginal discharge, vulval itching, dysuria, or offensive odour. Occasionally the presenting complaint is low abdominal discomfort or vulval ulceration. Men can also experience discharge and/or dysuruia.

80
Q

How is trichomoniasis diagnosed?

A

Diagnosis of Trichomoniasis is done by microscopy and/or a trichomonas rapid test.

81
Q

Which parasite can enhance HIV transmission?

A

Trichonomas vaginallis

82
Q

How is the Trypanosoma protozoa spread?

A

Transmitted by tsetse flies

83
Q

What disease and symptoms are caused by the Trypanosoma protozoa?

A

Infection can lead to a febrile illness with lymphadenopathy and ultimately invades the nervous system leading to alterations in consciousness causing the fatal disease of sleeping sickness.

84
Q

How is Leishmania spread?

A

Leishmania is a genus of protozoa transmitted by sand flies found in warm parts of the world (mainly the old world).

85
Q

What are the three presentation types of Leishmaniasis?

A

visceral, cutaneous and mucocutaneous.

86
Q

What are the symptoms of visceral leishmaniasis?

A

Visceral leishmaniasis is the most severe form, fatal if left untreated, characterised by irregular fever, weight loss, swelling of liver and spleen and anaemia.

87
Q

What are the symptoms of cutaneous leishmaniasis?

A

Cutaneous leishmaniasis presents with skin lesions on exposed body parts, often self-healing. However, can create serious disability and scars.

88
Q

What are the symptoms of mucocutaneous leishmaniasis?

A

Mucocutaneous leishmaniasis is disfiguring, destroying mucous membranes.

89
Q

List the important nematodes

A
  • Ascaris lumbricoides
  • Hookworms
  • Filaria such as Wuchereia bancrofti
  • Strongyloides
90
Q

Describe the infection caused by Ascaris lumbricoides

A

Infection with Ascaris is called ascariasis and usually produces no symptoms. However, infection with a large number of worms may cause abdominal pain or intestinal obstruction. Because adults feed on the contents of the small intestine, ascariasis can lead to malnourishment in individuals (especially children).

91
Q

Describe the symptoms caused by hookworms

A

Hookworms [such as Ancylostoma duodenale] can produce iron deficiency anaemia caused by blood loss at the site of intestinal attachment. This is the most common symptom of hookworm infection, accompanied by cardiac complication. Gastrointestinal and nutritional symptoms can also occur, as can local skin manifestations.

92
Q

Describe the symptoms caused by Filaria

A
  • Wuchereria bancrofti can cause lymphatic filariasis (elephantiasis)
  • Loa Loa worm can cause cutaneous filariasis
93
Q

Describe the symptoms caused by strongyloides

A

Strongyloides is an important worm infestation because the eggs produced by the adults can hatch within the host and invade human tissue leading to severe illness especially when the host is immunocompromised. It is cause of diarrhoeal illness in the tropics.

94
Q

What is the most common cause of acquired epilepsy in the world?

A

Taenia solium

95
Q

How are taenia transmitted?

A

Taenia (also known as tapeworms) can come from uncooked from pork (T. solium or T. asiatica) or from beef (T. saginata).

96
Q

What are the symptoms of taeniasis?

A
  • Tapeworms can cause digestive problems such as abdominal pain, loss of appetite, weight loss and upset stomach.
  • Taeniasis from T. saginata usually presents with more symptoms, as the size of the worm is larger.
  • Taenia solium often causes epilepsy
97
Q

List the important flukes

A

Schistosoma

98
Q

What are the symptoms of schistosomiasis?

A
  • Within two months, schistosomiasis presents with fever, chills, cough, and muscle aches.
  • Children who are repeatedly infected can develop anaemia, malnutrition, and learning difficulties.
  • After years of infection, the parasite can also damage the liver, intestine, lungs, and bladder.
99
Q

Name two ectoparasites, explain the symptoms they cause, and how they are diagnosed.

A
  • Sarcoptes scabei causes itching due to dermatitis. Diagnosed by the appearance of a rash and presence of burrows.
  • Lice may be asymptomatic or cause tickling feeling, itching, allergic reaction
100
Q

List the different species of relevant lice

A
  • Pediculus humans capitis
  • Pediculus humans corporis
  • Pthirus pubis
101
Q

How does the innate immune system have a direct and facilitative role in the clearance of fungal infection?

A

Direct role through the anti-fungal effector cells.
It also has a facilitative role through the production of pro-inflammatory cytokines and chemokines, and antigen presentation.

102
Q

Why does response to fungal infection change over time?

A

Each distinct growth form of a fungus is called a morphotype. As the morphotype of the fungus changes, the innate response varies.

103
Q

What are the anti-fungal roles of the three major anti-fungal immune effector cells?

A
  • Neutrophils are involved in the phagocytosis of opsonised (by both complement and antibodies) and unopsonised fungi. They are also involved in the oxidative killing of fungi as well as produce cytokines to help with the response.
  • Macrophages are also involved in the phagocytosis of opsonised and unopsonised fungi. They have a key role in granuloma formation and in the release of pro-inflammatory cytokines in order to maintain latency of response. Macrophages also act as antigen presenting cells.
  • The main role of the dendritic cell is in antigen presentation, and therefore in Th1/2 polarisation. They can also phagocytose and kill fungi as well as produce cytokines.
104
Q

Describe the oxidative killing of fungi by neutrophils

A

The NADPH oxidase enzyme complex is a multi-subunit enzyme complex which mediates the ‘respiratory burst’. During phagocytosis, oxygen consumption is increased through the activity of NADPH-oxidase generating superoxide anion and hydrogen peroxide . These metabolites give rise to yet other reactive oxygen species that are strongly anti-microbial, but which may also cause tissue damage and apoptosis.

105
Q

What fungi is vulnerable to death by respiratory burst?

A

Candida albicans

106
Q

Describe the non-oxidative killing of fungi by neutrophils

A

Neutrophils can also produce NETs (Neutrophil Extracellular Traps) which are extracellular fibres derived from chromatin and coated with granule proteins.

107
Q

What fungi is vulnerable to NETs produced by neutrophils?

A

Aspergillus fumigatus

108
Q

True/False: NETs require ROS

A

True, NETs require ROI-mediated signalling cascades.

109
Q

What fungi are vulnerable to death by macrophage phagocytosis?

A

Aspergillus fumigatus

110
Q

What fungi can survive after macrophage phagocytosis and how?

A
  • Cryptococcus neoformans may survive in the phagolysosome before escape.
  • Candida albicans experiences nutrient starvation inside the macrophage phagolysosome, prompting germination and escape.
111
Q

How does the innate immune system detect the presence of fungal cells?

A

A number of cell wall components of the fungi act as PAMPs, detected by PRRs (Pattern Recognition Receptors). TLRs (Toll-like Receptors) are one of the activators of innate and adaptive immunity to fungi. Dectin-1 is a major fungal pattern recognition receptor (PRR) which not only senses fungi at the cell surface but it’s also responsible for the internalisation of fungi.

112
Q

How are fungi opsonised by the innate immune system?

A

Opsonisation is done by pentraxin 3 and mannose-binding lectin, allowing phagocytes to more easily recognise the pathogens.

113
Q

What adaptive immune system cells are involved in fungal clearance?

A

This mainly involves the generation of antigen-specific T-helper, CD8+ T-cells and Treg cells and B-cells. This response specifically targets the pathogen and induces memory cells that prevent subsequent infection.

114
Q

What aspect of immunity needs to be impaired for mucosal candida infection?

A

Impaired cell mediated immunity

115
Q

What aspect of immunity needs to be impaired for disseminated candida infection?

A
  • Impaired mucosa, breach of epithelial barrier,
  • neutropenia,
  • chronic granulomatous disorder
116
Q

What aspect of immunity needs to be impaired for Aspergillus infection?

A
  • Neutropenia
  • high dose corticosteroids
  • chronic granulomatous disorder
117
Q

What aspect of immunity needs to be impaired for Cryptococcus infection?

A
  • Impaired cell mediated immunity

- high dose corticosteroids

118
Q

What leaves a person with increased susceptibility to fungal infections?

A
  • Immunosuppression
  • Surgery
  • Hereditary immune impairments
119
Q

Give examples of three hereditary conditions that affects our response to fungi

A
  • Human Dectin-1 deficiency leads to mucocutaneous fungal infections. It also leads to impaired macrophage binding to Candida albicans and increase susceptibility to Aspergillosis
  • Human CARD9 deficiency. A functional CARD9 is needed for TNF-a production in response to β-Glucan stimulation. It is also required for Th17 differentiation in humans.
  • Plasminogen alleles – defects can lead to increased susceptibility to Aspergillus fumigatus as plasminogen binds directly to that fungus.
120
Q

What are the classes of fungi based on what damage-response continuum shape they create?

A
  • Class 1 pathogens cause damage in hosts in hosts with a weak immune response or in the setting of a normal host response. The curve plotted host-response against damage, would show as the host response increases, damage to the host decreases. Such organisms include Candida albicans and Cyrtpococcus neoformans.
  • Class 2 pathogens cause damage at the extremes of both weak and strong immune responses. At low immune responses it is the pathogen that directly causes the damage, while at high immune responses, the pathogen causes the damage through the toxic immune response.
121
Q

What are the shapes bacteria can take?

A

The main shapes are cocci, bacilli and spirochete

122
Q

List important bacterial virulence factors

A
  • Diverse secretion systems
  • Flagella (important in movement and attachment)
  • Pili (important in adherence factors)
  • Capsules (can protect against phagocytosis)
  • Endospores (metabolically dormant forms of bacteria)
  • Biofilms (organised aggregates of bacteria embedded in a polysaccharide matrix, making it antibiotic resistant)
123
Q

What bacteria have capsules?

A

Streptococcus pneumoniae

124
Q

What bacteria can exist as endospores?

A

Bacillus and Clostridium species

125
Q

What bacteria can form biofilms?

A

Pseudomonas aeruginosa and Staphylococcus epidermidis

126
Q

What type of exotoxins can be produced by bacteria?

A
  • Neurotoxins
  • Enterotoxins
  • Pyrogenic exotoxins (by release of cytokines)
  • Tissue invasive exotoxins
127
Q

Give examples of neurotoxins produced by bacteria

A
  • tetanus

- botulinum

128
Q

How doe enterotoxins cause disease?

A

They act on the GI tract to cause diarrhoea. They inhibit NaCl reabsorption, activate NaCl secretion or kill intestinal epithelial cells.

129
Q

What is the difference between the enterotoxins that cause infectious diarrhoea and those that cause food poisoning?

A
  • Infectious diarrhoea occurs when bacteria colonise and bind to the GI tract, continuously releasing their enterotoxin locally.
  • Food poisoning occurs when bacteria grow in food, releasing the enterotoxin into the food. The digested toxin is ingested resulting in symptoms.
130
Q

What bacteria cause infectious diarrhoea?

A
  • Vibrio cholerae
  • Escherichia coli
  • Shigella dysenteriae
  • Campylobacter jejuni
131
Q

What bacteria cause food poisoning?

A

Bacillus cereus or Staphylcoccus aureus

132
Q

What bacteria release pyrogenic exotoxins?

A

Staphylcoccus aureus and Streptococcus pyogenes.

133
Q

What is a endotoxin?

A

Endotoxins are toxins only produced by Gram+ bacteria as they are the lipid A moiety of LPS outer membrane and are shed in steady amounts from living bacteria.

134
Q

Define outbreak

A

An outbreak is a greater-than-normal or greater-than-expected number of individuals infected or diagnosed with a particular inflection in a given period of time, and/or a particular place.

135
Q

What are the features of the E.coli strain that caused the 2001 outbreak?

A
  • entero-aggregative and thus causing gastroenteritis
  • shiva-toxin producing and thus causing haemolytic-ureic syndrome
  • making it a EAHEC strain
136
Q

What are the symptoms of haemolytic-uraemic syndrome?

A
  • acute renal failure
  • haemolytic anaemia
  • thrombocytopenia
137
Q

How does shiva-toxin produce toxicity?

A

shiga-toxin inhibits protein synthesis in eukaryotic cells, as well as affecting the microflora of the gut.

138
Q

What are e.coli strains that produce shiga-toxin called?

A

EHEC (enterohaemorragic e.coli)

139
Q

What are e.coli strains that have aggregative adherence fimbriae called?

A

EAEC (enteroaggregative E.coli)

140
Q

How can we tell that an infection is caused by an outbreak strain?

A

PCR

141
Q

How can an outbreak be identified?

A
  • surveillance

- timely reporting systems

142
Q

What are the most popular six categories of communicate diseases in Europe?

A
  • Respiratory Disease
  • Sexually Transmitted Infections
  • Food and Waterborne Diseases
  • Emerging and Vector-Borne Disease
  • Vaccine Preventable Diseases
143
Q

List the bacteria that cause respiratory diseases

A
  • Legionella Pneumophillia

- Mycobacterium tuberculosis

144
Q

List the bacteria that cause STIs

A
  • Treponema pallidum
  • Chlamydia trachomatis
  • Neisseria Gonorrhaeae
145
Q

List the bacteria that cause food and waterborne diseases

A
  • Bacillus anthracis
  • Vibrio cholera
  • Literia monocytogenes
  • Shigella dysenteriae
  • Salmonella species
  • Escherichia coli
  • Campylobacter jejuni
146
Q

List the emerging and vector-borne bacteria

A
  • Yersinia pestitis

- Coxiella burnetti

147
Q

List the vaccine preventable bacteria

A
  • Corynebacterium diphtheriae
  • Haemophillus influenza
  • Neisseria meningitidis
  • Streptococcus pneumoniae
  • Bordatella pertussis
  • Clostridium tetani
148
Q

How does legionella pneumophillia cause disease?

A

Causes legionnaires’ disease through infecting and growing in alveolar macrophages.

Important virulence factor is the type IV secretion system which allows secretion of effector proteins that allow replication in a LCV (Legionella containing vacuole) in the host cell.

149
Q

How does mycobacterium tuberculosis cause disease?

A

Causes tuberculosis. The bacterium can enter a dormant state, causing latent tuberculosis.

The Mycolic acid layer has an extra lipid layer which makes treatment more difficult. Treated with six months of Isonizid and Rifampicin.

150
Q

How does Chlamydia trachomatis cause disease?

A

It is an obligate intracellular pathogen (can only grow and divide within host cells, so cannot be cultured outside host cell.

It is the most frequent STI in Europe. It is also popular in other parts of the world where it is responsible for 3% of the worlds blindness.

151
Q

How does Neisseria Gonorrhoaea cause disease?

A

Causes gonorrhoea through establishing infection in the urogenital tract. The bacteria interact with non-ciliated epithelial cells.

Important virulence factors include pili to aid in adherence, and antigenic variation to escape detection and clearance by the immune system.

152
Q

What pathogen is responsible for the most common GI infection in Europe?

A

Campylobacter jejuni

153
Q

Define healthcare-associated infection

A

Healthcare-associated Infections (HAI) are infections that occurs >48h after exposure to healthcare.

154
Q

How many patients a year acquire health-care associated infection in the EU each year?

A

3.2 million

155
Q

What are the most frequent types of HAI?

A

surgical site infections, urinary tract infections, pneumonia, bloodstream infections and gastrointestinal infections.

156
Q

What are the three main reasons hospitals are a source of infection?

A
  1. Interventions performed, such as central lines, catheterisation, intubation, chemotherapy, prophylactic antibiotics, inappropriate prescribing and prosthetic material.
  2. Dissemination of infection by people moving from ward to ward.
  3. Concentration of people – hospitals have a large concentration of people, who also tend to be immunocompromised, increasing the chance of infection.
157
Q

List examples of common hospital infections caused by bacterial pathogens.

A 
Gram positive
• Enterococcus faecium 
• Staphylococcus aureus 
• Clostridium difficile 
Gram positive
• Acinetobacter baumanii 
• Pseudomonas aeruginosa 
• Enterobacteriacae such as E. coli, Klebisella pneumoniae, and Enterobacter species
158
Q

Describe the resistances of the ESCAPE pathogens

A
  • Enterococcus faecium (vancomycin resistant)
  • Staphylococcus aureus (methicillin resistant)
  • Clostridium difficile (can establish infection more easily if previous antibiotic treatment had wiped out normal gut flora)
  • Acinetobacter baumanii (highly drug resistant)
  • Pseudomonas aeruginosa (multi drug resistant)
  • Enterobacteriacae such as E. coli, Klebisella pneumoniae, and Enterobacter species (multi drug resistant)
159
Q

What is the most frequent cause of bacteraemia by a Gram- bacteria?

A

Pathogenic Escherichia coli

160
Q

What is the most frequent cause of community and hospital acquired UTI?

A

Pathogenic Escherichia coli

161
Q

What are E. coli usually resistant to?

A

cephalosporins

162
Q

What do bacteria that are resistant to cephalosprins express?

A

Most isolates that are resistant to cephalosporins express the extended

163
Q

What are bacteria that are usually resistant to cephalosporins usually sensitive to?

A

Carbapenems

164
Q

What enzyme gives bacteria resistance to carbapenems?

A

carbapenemase enzyme

165
Q

What infection does Klebsiella pneumoniae cause?

A

UTI and respiratory tract infections, particularly in immunocompromised patients.

166
Q

What is Klebsiella pneumonia usually resistant to?

A

ephalosporins, fluroquinolones, and aminoglycosides in Europe

Carbapenems in USA

167
Q

the most important cause of antimicrobial resistant infection worldwide

A

MRSA Methicillin Resistant Staphylococcus Aureus

168
Q

How is methicillin resistance produced?

A

by expression of additional penicillin-binding protein PBP2A has a low affinity for methicillin and can still function in he presence of the antibiotic.

Year 2 MCD 2 (5 decks)

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