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FoM - principles of disease > bacteria, virus, parasite, fungi > Flashcards

bacteria, virus, parasite, fungi Flashcards

1
Q

what are the 3 domains of life?

A

bacteria - prokaryote
archaea - prokaryote
Eucarya - eukaryote

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2
Q

what is the difference between sterile and non-sterile sites? give examples:

A

Sterile sites i.e. contain no microorganisms
Brain
Heart
Liver
Kidney

Non-sterile sites i.e. contain microbiomes
Mouth
Oesophagus
Lungs
Stomach
Intestine

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3
Q

what are the common specimen types of different bacterial cultures?

A

Mid stream specimen of urine (MSSU) – urinary tract infection.

Sputum – lower respiratory tract infection.

Throat swab – tonsillitis/pharyngitis.

Swabs – wound infection, genital tract infection.

Faeces – infectious diarrhoea.

Blood culture – septicaemia (sepsis).

Cerebrospinal fluid (CSF) – meningitis.

Aspirate of pus – abscess. (drainage of abscess)

Bone – osteomyelitis.

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4
Q

what is the role of microscopy in diagnosing bacterial infections where you don’t have to stain them?

A

1- to see white blood cells (in urine, CSF)

Lymphocytes in CSF → Viral meningitis
Polymorphs in CSF → Bacterial meningitis

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5
Q

what is the role of microscopy in diagnosing bacterial infections where you have to stain them?

A

to see parasites (in faeces)

Different parasites can be recognised according to size

  • Gram stain - to visualise bacteria and yeasts/fungi
  • Special stains
  • Ziehl-Neelsen stain or auramine stain for Mycobacteria
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6
Q

why is light microscopy not used to identify viruses?

A
  • Viruses are not visible in light microscopy
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7
Q

How do you interpret the results after culturing organisms and performing susceptibility tests?

A

i.e. the measurement of the susceptibility of bacteria to antibiotics

1- Knowledge of commensal flora
e.g. if you got a wound swab from the skin you should know the normal skin flora.

2- Knowledge of common pathogens
e.g. common pathogens in a site on the body

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8
Q

what is healthcare-associated infection?

A

infections that occur in a healthcare setting (such as a hospital) that a patient didn’t have before they came in.

ONSET - 48H

HIC - Most common bacteria:
* Staphylococcus aureus bacteraemia
* Clostridium difficile infection

HIC - Most common virus:
* Norovirus

HIC - Multi-drug resistant organisms:
* e.g. MRSA, VRE, ESBL, CPE

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9
Q

How are viruses detected from clinical samples?

A

Molecular methods i.e. real-time/multiplex PCR

PCR → only detects sections of viral RNA/DNA

Antigen detection

Serology to detect antibodies and determine immunity

Two classes of antibodies:
IgM → occurs initially at the start of viral infection
IgG → comes later & confers long-term immunity

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10
Q

what are the components that make up a bacteria’s surface?

A

Cytoplasmic membrane - is a very thin, elastic and semi-permeable membrane around the bacterial cell contents.

Cell wall - is a permeable, rigid wall, covering bacteria, it gives the cell strength and shape.

Outer membrane - a component of the Gram-negative cell wall.

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10
Q

what are the diagnostic principles in parasitology?

A

Microscopy of different life cycle stages e.g.
* parasites, cysts and ova in faeces
* blood films for malaria

Culture is rarely possible for parasites, mostly for bacteria.

Serology is sometimes useful & important for reference laboratories.

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11
Q

What is the appearance of the gram stain under light microscopy of gram-negative/ positive?

A

Gram Positive → Purple

Gram Negative → Red/Pink

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11
Q

what are the characteristics of the gram-positive/ negative cell wall?

A

Gram-positive cell wall contains a thick Peptidoglycan layer.

gram-negative cell wall contains a thin Peptidoglycan layer and an Outer membrane

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11
Q

what is the cell wall? what do antibiotics do to the cell wall?

A

made of peptidoglycans, it is strong and relatively rigid & maintains its shape.

Antibiotics interfere with the construction of cell wall peptidoglycans i.e. penicillin
→ penicillin binds to proteins on the cell wall to inhibit cell wall synthesis

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12
Q

what are the 3 bacterial shapes?

A

Spherical e.g. cocci

Rod-shaped e.g. bacilli

Spiral & corkscrew

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13
Q

what are peptidoglycans?

A

they are N-acetylglucosamine acid and N-acetylmuramic acid molecules linked alternately in a chain, with short peptides forming cross-links.

found on the cell wall

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14
Q

what is the lipopolysaccharide outer membrane?

A

It’s a structure that is only present in Gram-negative bacteria. It protects peptidoglycans from bile salts and lysozymes.

It blocks many antibiotics from getting into the bacterial cell.

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15
Q

what is lipid A?

A

one of the components of Lipopolysaccharide that forms endotoxin.

When endotoxin is released into the bloodstream, it may give rise to endotoxic shock

It is a clinical state characterised by fever and low blood pressure

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16
Q

what are 2 types of capsules?

A

There are two types of capsules (polysaccharide layer):

  • Rigid capsule → prevent phagocytosis
  • Slimy capsule → forms biofilms and microcolonies
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17
Q

what is a flagellum? what are the 4 different types?

A

a long thin filament twisted spirally in an open regular waveform.

Provides motility to bacteria to move to an optimal environment

1- A-Monotrichous → one flagellum from one side

2- B-Lophotrichous → flagella from one side

3- C-Amphitrichous → flagella from both sides

4- D-Peritrichous → flagella all over

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18
Q

what are fimbriae?

A

they are short filaments that are far more numerous than flagella.

Important in mediating adhesion between bacterial cells and host cells.

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19
Q

Describe how bacteria replicates:

A

A bacterial cell has a single chromosome with no nucleus.

It replicates by binary fission to produce two daughter cells.

It may contain Plasmids which are DNA structures that replicate independently of the chromosome.

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20
Q

how does genetic variation occur in bacteria?

A

Genetic variation in bacteria occurs through:

1- Spontaneous mutation in the chromosome

2- Transfer of DNA through Plasmids

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21
Q

what is bacterial conjugation?

A

it’s a mechanism of gene transfer that requires direct contact between donor and recipient cells.

Steps:

F pilus forms a pathway between Donor cell F+ and Recipient cell F- through a receptor.

A single strand of the Plasmid enters the Recipient cell F-

Then synthesizes a complementary plasmid to the one in Donor cell F+

F- becomes F+

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22
Q

what are bacteriophages?

A

a type of virus that infects bacteria.

All of them are composed of a nucleic acid molecule that’s surronded by a protein structure.

It hijacks the cell machinery and makes it produce viral components until it bursts through lysis

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22
Q

what is sporulation?

A

is a highly resistant process whereby dormant bacteria are formed.

This process preserves the genetic material of bacteria when conditions are lethal and inhospitable.

Each normal (vegetative) cell forms one spore (dormant)

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22
Q

what are ribosomes? how are the divided?

A

they are structures in the bacterial cell cytoplasm, they consist of RNA and associated proteins.

Their role is to synthesize proteins.

They are divided into subunits, measured by the unit Svedberg.

70S ribosomes → made up of large (50S) and small (30S) subunits

30S subunit → made up of (16S) subunit - which is used for bacterial identification

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22
Q

how do you detect and culture bacteria from a patient? 4 steps

A

1- Get a specimen from a patient

2- Staining to determine whether it’s gram-positive or gram-negative infection to select the appropriate antibody

3- Incubation of a small amount of specimen onto agar plates at 37 C

4- Formation of bacterial colonies

Use a light microscope with an oil immersion lens (x1000) & staining to see the bacteria

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23
Q

what are the 2 bacteria classifications?

A

1- Phenotypically → i.e. relating to observable physical properties
e.g.

  • Gram stain (gram + & gram -)
  • Growth requirements
    (aerobic & anaerobic & microaerophilic)
  • Serologic
  • Mass spectrometry (protein profiling)

2- Genotypically → i.e. relating to DNA (used more in modern times)
e.g.

  • Ribosomal RNA sequence analysis
  • Whole genome sequencing
24
Q

what is a parasite? how are they classified?

A

an organism that lives in or on another organism (host) and derives its nutrients at the expense of this host.

They are classified by:

  • Cellular structure
  • Life cycle - complex stages

An organism which acts as an intermediate host for a parasite is known as a Vector

25
Q

what are the 3 classifications of parasites? give 3 examples of each:

A

Protozoa → malaria & amoebae & flagellates

  • Helminths (worms) → roundworms & tapeworms & flukes
  • Ectoparasites (outside of body) → lice & ticks & mites
26
Q

what are protozoa? how do they replicate?

A

Protozoa are microscopic, single-celled organisms, that can be free-living or parasitic.

They can multiply in humans and they transmit through two routes:

1- Live in a human’s intestine → faecal-oral route

2- Live in the blood or tissue of humans → insect vector

27
Q

what is malaria?

A

Malaria is a protozoan infection, the most common cause of death by parasitic infection globally, usually found in the tropics and subtropics.

It is a mosquito-borne preventable disease caused by a parasite called Plasmodium

Vector → Anopheles mosquito (female)

non-specific symptoms i.e. fever, chills, headache, sore throat

Blood films → parasitaemia

27
Q

what is amoebic dysentery?

A

a protozoan infection that causes bloody diarrhoea.

It is caused by an invasion of Entamoeba histolytica in the gut wall.

Contraction of infection - through ingestion of faecal matter through contaminated food

i.e. Faecal-oral route

Clinical relevance:

  • Intestinal and extra-intestinal infections
  • Liver abscess in late disease
28
Q

what are helminths? how do we diagnose?

A

To diagnose we look into stool samples of patients and check for worm eggs

Most are transmitted through the faecal-oral route but use an intermediate vector

Common in resource-poor / hygiene-poor areas

1- Nematodes → Roundworms

2- Cestodes → Tapeworms

3- Trematodes → Flatworms

29
Q

describe nematodes (roundworms)

A

Enterobiasis (pinworm/threadworm) → 1cm, threadlike, very common in children

Causes anal itch

Diagnosis → sellotape on perianal region and check for eggs under a microscope

Treatment → anti-helminth tablets kill adult worms

[2] Ascaris lumbricoides/Ascaris Infection → 15-35 cm, largest nematode.

Often asymptomatic, may cause failure to thrive in children / blocking the small intestine & bile duct

→ Bowel obstruction

30
Q

what are cestodes?

A

Cestodes are long, segmented tapeworms. e.g.

[1] Taenia saginata (beef)

[2] Taenia solium (pork)

Can migrate to the brain from the gut and make cysts causing → Neurocysticercosis

[3] Echinococcus

  • carried by dogs, wolves, foxes (intermediate host)
  • ## humans ingest eggs in dog faeces → eggs hatch and form cysts in the liver.

Eating larval cysts}} (intermediate host) that are found in raw or undercooked meat.

Adult tapeworms in humans (definitive host) → eggs excreted through human stool

Animals, e.g. pigs/cows, eat grass with human stool and the cycle continues.

The life cycle of worms can only keep going if animals are eating grass-containing eggs
i.e. poor sanitation/hygiene

31
Q

what are trematodes?

A

Different species cause human infection in various body sites
i.e. Blood, Lung, Liver, Pancreas, Intestines

[1] Schistosomiasis, has three types:

  • S. haematobium (bladder)
  • S. mansoni (intestinal)
  • S. japonicum (intestinal)
  • endemic in tropical areas i.e. 200 million people affected annually
  • Acquired by swimming in infected freshwater - development in snails (intermediate host)
  • Swimmer’s itch is a common sign
  • Can lead to liver failure & bladder cancer if untreated
32
Q

what are ectoparasites?

A

they are parasites that live outside the body.

Usually insects with six legs or arachnids with eight legs.

33
Q

how is malaria diagnosed?

A

Through blood microscopy

Thick and thin blood films under a microscope

Severity of malaria → number of red blood cells infected by Plasmodium parasites

We can then determine which type of treatment to use.

34
Q

what diagnostic principles in parasitology?

A

Diagnostic principles in Parasitology: (deep)

[1] Definitive diagnosis → identify parasites in host tissue or faeces/urine

[2] Blood microscopy e.g. thick and thin blood films for malaria

[3] Stool microscopy is used to find enteric pathogens

e.g. Ova, cysts and parasites

[4] Helminth infection

  • Eosinophilia → (high eosinophil levels)
  • Elevated IgE → (high IgE levels to fight parasitic infections)

[5] Indirect testing (antibody & antigen testing)

  • Serology → immune testing
  • Rapid diagnostic tests
34
Q

what is a fungus?

A

a chemo-organotrophic eukaryote that lacks chlorophyll and forms spores.

Cell wall → contains polysaccharides, often chitin or glucan, and it absorbs nutrients.

Membrane → contains ergosterol - major sterol

Classification is based on morphology

can infect plants and animals

35
Q

what are the 3 main groups of the fungal kingdom?

A

Basidiomycetes

Ascomycetes

Zygomycetes

36
Q

what are dermatophyte fungi?

A

cause skin infections

one main virulence factor - an enzyme that degrades and utilizes keratin as a nutrient source.

Diseases caused by these fungi - tinea, which are named according to the region they infect in the body.

Causative agents:
Epidermophyton - Microsporum - Trichophyton

37
Q

describe the Malassezia species:

A

they are frequent colonisers and part of the normal skin microbiota, usually found in sebum-rich areas like the scalp and chest.

Their absence might be an indication of disease. but in certain conditions, they can cause superficial infections in immunocompromised individuals.

38
Q

what are 3 host factors that contribute to the pathogenicity of fungal infections?

A

1- Favorable micro-environments e.g. (warm, moist areas) encourage the growth of fungi on skin and mucous membranes

2- Broad-spectrum antibacterial agents
reduce competition for epithelial colonization sites in the gut

3- Immunosuppression of all types
create a window of opportunity for fungal invasion

39
Q

what forms can immunosuppression of host defences come in?

A

Iatrogenic: ‘illness caused by medical examination or treatment’
- Steroids

  • Anti-cancer chemotherapy
  • Solid-organ transplantation

Disease processes:
- AIDS

  • Leukaemia
  • Endocrinopathies
40
Q

what are candida infections (candidiasis, candidosis)?

A

fungal infections caused by yeasts

C. Albicans can form hyphae (filamentous form of growth) → pleomorphic fungus

Clinical diseases:

  • Superficial → mouth, vagina, penis, skin, nails
  • Deep-seated → disseminated infections in immunocompromised hosts
41
Q

describe the dissemination (spreading) of candida species

A

1- Bacteria in competition with Candida in the gut.

2- Antibacterial added → bacteria ↓

3- Candida overgrowth & might get access to epithelium.

4- Surgical insult → Candidia gets into the bloodstream & forms a biofilm on the catheter surface.

5- It then becomes resistant to anti-fungal treatments.

42
Q

what is chronic mucocutaneous candida infection?

A

a type of candida infection that arises in individuals with an unusual combination of endocrine and immune dysfunction.

(autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy - APECED)

43
Q

what is apergillosis?

A

an infection caused by a type of fungus called Aspergillus

Causative species:

Aspergillus fumigatus
Aspergillus flavus
Aspergillus nidulans (in CGD patients)
Aspergillus lentulus
other species on rare occasions

Types of disease:

simple asthma

asthma with eosinophilia

aspergilloma
(fungal ball in lungs - Farmer’s lung)

invasive bronchopulmonary aspergillosis
(associated with haematological malignancy - hyphae filaments penetrating lung tissue)

disseminated aspergillosis

Route of infection:

  • inhalation of conidia (spores)
44
Q

how is Aspergillus fumigatus transmitted?

A

transmitted to humans through inhalation of conidia, which germinate to hyphae (the main mode of vegetative growth) in the lung tissue.

It is angioinvasive i.e. invades the walls of blood vessels

45
Q

what is cryptococcosis?

A

an infection caused by a type of fungus called cryptococcus

Main causative species: (yeasts with a thick extracellular capsule)

Cryptococcus neoformans

Cryptococcus gattii

Human diseases:

pulmonary cryptococcosis

meningitis (particularly in AIDS patients) → 1/2 million deaths each year

disseminated infection in severely compromised hosts

46
Q

considering the damage response curve, why is it bad to have very weak immunity?

A

results in invasion from pathogens and dissemination

Diseases:

Systemic candidosis

Acute invasive Aspergillosis

47
Q

considering the damage response curve, why is it bad to have very strong immunity?

A

results in a hyperinflammatory response
(damaged tissue)

Diseases:

Recurrent Candida vaginitis

Allergic bronchi pulmonary aspergillosis (ABPA)

Dermatophytosis

48
Q

what are the diagnostic methods of fungal infections?

A

Direct detection:

1 - Histopathology

Biopsy of lung tissue → A. fumigatus hyphae

Skin scraping treatment with KOH → visualise dermatophytes

Direct smear with Periodic Acid Shiff (PAS) staining → fungi

Vaginal smear with Calcofluor white stain → C. albicans hyphae

Culture organisms and use ChromAgar Candida → detect species based on colour

Germ tube test in serum → C. albicans form hyphal germ tubes

2 - High-res CT scans

Liver → Candida infection

Pulmonary → Aspergillosis

Other methods:

  • detection of circulating fungal antigens
  • detection of circulating antibodies to fungi
  • PCR for fungal DNA
  • Culture of fungus from a normally sterile site
  • MALDI-ToF Biotyping
49
Q

what are 4 antifungal treatments? state what they target, route of administration and mechanism of action

A

Azoles (Triazoles) and Allylamines → Target sterols

Route of administration→ oral & IV & topical

Mechanism of action → inhibit the production of ergosterol

[2] Echinocandins → Target wall

Route of administration → IV only

Mechanism of action → inhibit the production of glucan

[3] Polyenes → Target membrane

Route of administration → oral & IV & topical

Mechanism of action → bind to ergosterol to make pores in the membrane

[4] Flucytosine → Target DNA synthesis

50
Q

what are the 6 problems associated with antifungal treatments?

A

Spectrum of activity

Static or cidal

IV vs oral

Toxicity

Antifungal Resistance

Expensive Cost

51
Q

what are viruses? what are the 3 structures?

A

small (20-400 nm) non-cellular organisms; their genetic element cannot replicate independently of a living (host) cell.

Virion: extracellular form of a virus

  • Exists outside the host and facilitates transmission from one host cell to another
  • Contains nucleic acid genome surrounded by a protein coat and, in some cases, other layers of material

Structures:

[1] Icosahedral: 20 equilateral triangular faces, 12 vertices and 30 edges

[2] Helical: protein binds around DNA/RNA in a helical fashion

[3] Complex: neither of the above

52
Q

what are obligate intracellular pathogens?

A

they are pathogens that can only replicate inside host cells.

Most viruses have a specific host range and only infect specific host cell types, this is known as tissue tropism

53
Q

what is the taxonomy of viruses? what are 4 ways they’re classified?

A

Order → Family → Genus → Species

Virus families can be classified according to:

1- Virion shape/symmetry

2- Presence/absence of envelope

3- Genome structure

4- Mode of replication

54
Q

what is the virus transmission replication process?

A

Virus replication process:

1- Attachment to the host cell

2- Uncoating of envelope

3- Replication of Genomic nucleic acid in the nucleus

4- Nucleic acid + Proteins Insertion into membrane

5- Assembly of Virion

6- Release of Virion outside of cell

55
Q

what are the 4 consequences of viral infection?

A

[1] Clearance of virus}} i.e. with no, short or long-term immunity

* Hepatitis C (no lasting immunity)
* Measles (long-term immunity)

[2] Chronic infection

* HIV, hepatitis B, hepatitis C

[3] Latent infection:

* Herpes Virus

[4] Transformation i.e. long-term infection with altered cellular gene expression

* Epstein-Barr Virus, Human Papilloma Virus
56
Q
A

Mechanisms:

1- Modulation of {{c1::cell cycle control}} (driving cell proliferation)

2- Modulation of {{c1::apoptosis}} (prevention of programmed cell death)

3- {{c1::Reactive oxygen species}} mediated damage

(some persistent viral infections can cause persistent inflammatory processes which lead to cancer via reactive oxygen species)

e.g. Virus & Cancer diseases

  • EBV: Burkitt’s lymphoma, Hodgkin’s lymphoma, nasopharyngeal carcinoma, post-transplant lymphoproliferative disease (PTLD)
  • Human herpes virus 8: Kaposi’s sarcoma, primary effusion lymphoma, Castleman’s disease
  • Human T-cell Lymphotropic Virus (HTLV): Adult T-cell leukaemia/lymphoma
  • Human Papillomavirus (HPV): cervical, anal, oropharyngeal cancers
  • Hepatitis B and Hepatitis C: hepatocellular carcinoma
56
Q

what is viral latency?

A

when a virus lies dormant (latent) in the cell after primary infection.

The full viral genome is retained in the host cell, but its expression is restricted, so that few viral antigens and no viral particles are produced.

This allows the reactivation of viral replication, which may or may not cause apparent disease.

Reactivation is more likely to occur in immunocompromised individuals.

Examples:

1- Herpes Simplex Virus

2- Varicella Zoster Virus

56
Q

what are the mechanisms of viral infections that can lead to cancer? give examples

A

1- Modulation of cell cycle control (driving cell proliferation)

2- Modulation of apoptosis (prevention of programmed cell death)

3- Reactive oxygen species-mediated damage

(some persistent viral infections can cause persistent inflammatory processes which lead to cancer via reactive oxygen species)

e.g. Virus & Cancer diseases

  • EBV: Burkitt’s lymphoma, Hodgkin’s lymphoma, nasopharyngeal carcinoma, post-transplant lymphoproliferative disease (PTLD)
  • Human herpes virus 8: Kaposi’s sarcoma, primary effusion lymphoma, Castleman’s disease
  • Human T-cell Lymphotropic Virus (HTLV): Adult T-cell leukaemia/lymphoma
  • Human Papillomavirus (HPV): cervical, anal, oropharyngeal cancers
  • Hepatitis B and Hepatitis C: hepatocellular carcinoma
57
Q

what are 3 detection methods of viruses?

A

[1] Whole organism - i.e. virus

→ electron microscopy

→ culture using light microscopy to see (uninfected/infected cells)

[2] Part of organism – e.g. antigen, nucleic acid

→ antigen detection

→ nucleic acid detection from the sample then amplify a region of the target organism genome

[3] Immune response to a pathogen – i.e. antibodies

→ antibody detection

- determines acute/recent infection

- determines prior infection/response to vaccination
58
Q

what can antivirals be used for?

A

[1] Prophylaxis

(to prevent infection)

[2] Pre-emptive therapy

(when evidence of infection/replication is detected, but before symptoms are apparent)

[3] Overt disease

[4] Suppressive therapy

(to keep viral replication below the rate that causes tissue damage in an asymptomatic infected patient)

58
Q

Why are antiviral drugs much more limited than antibiotics?

A

Because there are limited viral proteins that are potential targets for antiviral drugs

59
Q

what are 5 ways to prevent viral infections?

A

immunisation

  • Vaccination
  • Passive immunisation with immunoglobulin

Prophylactic treatment post-exposure

  • Post-exposure prophylaxis in HIV

Infection prevention and control (IPC) measures

  • Isolation of symptomatic patients
  • Personal protective equipment (PPE)
  • Safe use and disposal of sharps

Blood/tissue / organ screening

Antenatal screening - identifying those at high risk of a disorder for prenatal diagnosis

60
Q

what are 5 ways to eradicate viruses?

A
  • No animal reservoir or ability to amplify in the environment
  • clearly identifiable, with accurate diagnostic tool
  • No chronic carrier state
  • Efficient and practical intervention, e.g. vaccination
  • Political & social support

Examples: Smallpox (eradicated in 1979)

  • Measles
  • Polio
61
Q

All antiviral agents are virustatic (inhibit viral infection via a reversible extracellular mechanism), and none are virucidal (can kill viruses).

Only a minority of antiviral agents are used against infections because they commonly cause Toxicity to host cells which has nasty side effects.

A

FoM - principles of disease (28 decks)

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