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Bateman - Phase 2a COPY > Microbiology > Flashcards

Microbiology Flashcards

1
Q

What are protozoa?

A

Single-celled eukaryotic organisms (definitive nucleus).

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2
Q

What is a protozoa’s main biological role?

A

Consumers of bacteria, algae, microfungi.

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3
Q

What are protozoa’s eaten by?

A

Invertebrates.

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4
Q

How to protozoa’s eat food?

A

Phagocytosis and then digest it in intracellular vacuoles

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5
Q

What are the FIVE major groups of protozoa’s?

A 
Flaggelates.
Amoebae.
Sporozoan.
Cilliates.
Microsporidia.
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6
Q

What are Mastigophora?

A

Mastigophora is a division of single-celled protozoans..
Flagellum as main locomotory organelle.
Usually reproduce by binary fission.

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7
Q

What are the different types of mastigophora and where are they found?

A 
Intestinal flagellates:
	Giardia lamblia.
	Haemoflagellates:
	Trypanosoma spp.
	Other body sites:
	Trichomonas vaginalis.
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8
Q

What is the case study of a person infected with Giardia lamblia? What is the treatment?

A

7-day business trip to Delhi 2-months ago
Loose stools – last day of stay in India
Ongoing offensive diarrhoea daily since return to UK
Flatulence, abdominal cramps.
Metronidazole, tinidazole.

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9
Q

What is the case study of a person infected with Trypanosmoa spp?

A 
Bitten on arm by insect: lesion developed 2 weeks later → Self-resolved
2 years later: fever, lethargy, myalgia
Weight loss ++
Personality change
Irritability
Increasing daytime somnolence
Coma
Blood film & CSF.
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10
Q

What does sarcodina mean?

A

Sarcodina (Amoebae)

- Move by means of flowing cytoplasm & production of pseudopodia.

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11
Q

What is an example of a sarcodina organism?

A

Entamoeba histolytica.

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12
Q

What is the case study of a person infected with amoebiasis?

A

2-month visit to rural Botswana
Bloody diarrhoea: stool – treated with metronidazole
On return to UK – Increasing Right Upper Quadrant Pain
CT: Liver abscess = Amoebic Liver Abscess.

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13
Q

What are the characteristics of Sporozoans?

A

Apicomplexa (Sporozoans)

- No locomotory extensions
- All species parasitic
- Most intracellular parasites
- Reproduce by multiple fission
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14
Q

What are some examples of Sporozoans?

A

order Haemosporida: Malaria Plasmodium spp.
subclass Coccidia: Cryptosporidium spp.
Toxoplasma gondii
Cyclospora cayetanensis.

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15
Q

What is the case study of Cryptosporidiosis?

A

1 week of watery diarrhoea, no blood but abdominal pain and now vomiting
Given IV fluids and antiemetic
Stool microscopy. DFA

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16
Q

What is the case study of Toxoplasmosis?

A

Recent HIV +ve diagnosis: CD4 count 70
2-week history of progressive left sided weakness
Headaches, visual disturbance.

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17
Q

What are the characteristics of Ciliophora (Ciliates)?

A

Very large group

- Cilia that beat rhythmically at some stage in lifecycle
- 2 types of nuclei (macronucleus & micronucleus).
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18
Q

What is an example of a ciliate and what does it cause?

A

Balantidium coli
Causes:
Severe diarrhoea +/- ulceration of colon.

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19
Q

What are the characteristics of Microsporidia?

A

Very small

- Production of resistant spores
- Unique polar filament: coiled inside spore
- Little known about human disease: diarrhoea in immunocompromised.
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20
Q

What is an example of a microsporidia?

A

Enterocytozoon bieneusi.

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21
Q

What protozoa causes malaria?

A

Plasmodia spp.

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22
Q

What are the five species that cause it?

A 
P. falciparum
P. ovale
P. vivax
P. malariae
(P. knowlesi).
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23
Q

How is malaria transmitted?

A

Transmitted by bite of female Anopheles mosquitoes.

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24
Q

Why is malaria becoming an increasing problem?

A

Increasing resistance of parasite to anti-malarials
Increased resistance of mosquito to insectides
Ecological & climate changes
Increased travel to endemic areas.

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25
Q

How is malaria spread?

A 
Infection acquired during feeding from infected human
Infected for life
Life span of female 3 - 4 weeks
Night-biting (dusk – dawn)
Mainly bites indoors
Lifecycle depends on water.
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26
Q

What happens with malaria inside the host?

A

Plasmodia lifecycle has stages in human and mosquito host
Within human: Exo-erthrocytic & endo-erythrocytic stages
Critical to understanding pathogenesis, clinical features & spread of malaria
Variation in lifecycle between different Plasmodia spp. results in different clinical manifestations.

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27
Q

What are the different stages of malaria inside the host?

A

Liver cell stage.
Human blood stage.
Mosquito stages.

28
Q

What happens in the liver stage?

A

Liver cell.
Infected liver cell.
Schionzt
Ruptured Schionzt.

29
Q

What happens in P.ovale and P. vivax?

A

Liver stage in P. ovale & P. vivax has additional Hypnozoite stage.
Lie dormant and cause late relapse by reactivating months later.
Important: Not eradicated by most conventional anti-malarial treatments.

30
Q

What happens in the human blood stage?

A
  1. Immature trophozoite.
    Mature trophozoite.
    Schizont.
    Ruptured Schizont.

2.Immature trophozoite.
Gametocyte.
Mosquito ingests gametocyte.

31
Q

What happens in the mosquito stage?

A

microgamete enters macrogamete.
ookinete.
oocyst.
ruptured oocyst. releases sporozoites.

32
Q

What is released into the blood stream in malaria?

A

Merozoites released into blood stream
Occurs every 72 hours in P. malariae & 48 hours in others.
Symptomatic malaria: Fever, haemolysis etc.
Merozoites either re-infect RBCs or develop into sexual stage .

33
Q

What are the clinical features of Malaria?

A 
Very varied
FEVER almost invariable
Other common:
Chills & sweats
Headache
Myalgia
Fatigue
Nausea & vomiting
Diarrhoea
These acute symptoms common to all 4 species
Anaemia
Jaundice
Hepatosplenomegaly
‘Black water fever’.
34
Q

What is the pathogenesis of Malaria?

A

Parasite matures in RBCs → ‘knobs’ on RBC surface
Bind to receptors on endothelial cells in capillaries & venules
Bind to non-infected RBCs = ‘Rosetting’

35
Q

What are the clinical features of Malaria in adults?

A 
Coma
ARDS
Hypoglycaemia (pregnant women esp. susceptible)
Renal failure
Hypovolaemia, microvascular blockade
SHOCK
Can be secondary to bacterial sepsis
Cytokine release (e.g. TNF-α)
36
Q

What are the clinical features of Malaria in children?

A 
Non-specific: stop crying, playing, eating
Tachypnoea (& acidaemia)
Anaemia (peak 1 – 2 years)
Haemolysis 
Poor marrow production
Hypoglycaemia
Hyperinsulinism (also caused by Quinine rx)
Starvation
Glucose utilised by parasite.
37
Q

What are some non-specific features of a diagnosis of Malaria?

A

Anaemia.
Low platelets.
Hyperbilirubinaemia.
Mildly raised transaminases (ALT, AST).

38
Q

What are some methods to diagnose Malaria?

A

Thick & thin films
Light microscopy
3 separate films (different times) required to rule out completely
1st smear may be +ve in 95% cases.

39
Q

What is identified on the thin film in diagnosis of Malaria?

A

Species.

40
Q

How do you treat complicated falciparum malaria?

A

IV ARTESUNATE or IV QUININE.

41
Q

How do you treat uncomplicated falciparum malaria?

A 
PO Riamet (Artemether Lumefantrine) or
PO Quinine + Doxycycline as 2nd agent for early stage.
42
Q

How do you treat non-falciparum malaria?

A

PO Chloroquine.

43
Q

How do you treat P. vivax & ovale malaria?

A

Primaquine for hypnozoite clearance (check G6PD/pregnancy status).

44
Q

What is the only way you can see a virus?

A

By electron microscopy.

45
Q

Where do viruses only grow?

A

Inside cells.

46
Q

What do viruses have that is unique in their structure?

A

No cell wall structure but have an outer lipid protein coat surrounded in some viruses with a lipid coat.

47
Q

What are the stages of virus replication?

A
  1. ATTACHMENT
  2. CELL ENTRY
  3. INTERACTION
  4. REPLICATION
  5. ASSEMBLY
  6. RELEASE
48
Q

What gets released into the host cells cytoplasm?

A

Only the viral ‘core’ carrying the nucleic acid and some associated proteins acting as enzymes for replication and negation of intracellular host defence factors are freed into the host cell cytoplasm.

49
Q

Where can assembly of a virus take place?

A

Can occur in nucleus (e.g. herpesviruses); in cytoplasm (e.g. poliovirus); or at cell membrane (e.g. influenza virus).

50
Q

How do viruses cause disease?

A

A. Damage by direct destruction of host cells
B. Damage by modification of host cell structure or function.
physical modification.
functional modification.
C. Damage involving ‘over-reactivity’ of the host as a response to infection.
D. Damage through cell proliferation and cell immortalisation.
E. Evasion of both extracellular and intracellular host defences.
virus persistance.
virus variability.

51
Q

What is the pathogenesis of the rotavirus infection?

A

. Following ingestion, rotaviruses infect the epithelial cells of the small intestine, mainly the jejunum. (Rotaviruses are resistant to acid pH).

  1. Histologically, there is shortening and atrophy of the villi, flattening of the epithelial cells, and denuding of the microvilli, decreasing the surface area of the small intestine.
  2. This limits production of digestive enzymes such as the disaccharides, normally synthesized by cells of the brush border.
  3. The patient suffers malabsorptive state in which dietary nutrients such as sugars are not absorbed by the small intestine.
  4. This results in a hyperosmotic effect causing profuse diarrhoea.
52
Q

What is the chronic carrier state in Hep B?

A

Limited but sustained viral replication.
Natural hepatocyte regeneration.
Proliferation of hepatocytes due to the oncogenic
properties of HBV.
Liver cell destruction by CD8+ T cells (CTLs) that
recognise HBV proteins on the hepatocyte surface as
‘foreign’.
No clinical symptoms but HBV particles circulate in
the patient’s bloodstream.

53
Q

What are the mechanisms for viral evasion of host defences at the cellular level?

A

Persistence or latency.

Cell-to-cell spread.

54
Q

What are the mechanisms for viral evasion of host defences at the molecular or genetic level?

A

Antigenic variability.
Prevention of host cell apoptosis.
Down regulation of interferon and other intracellular host defence proteins.
Interference with host cell antigen processing pathways.

55
Q

What are the different mechanisms for viral variation and evasion of host defences?

A

Variation through formation of ‘quasi-species’.
Variation through gene re-assortment and mutation.
Variation through many stable serotypes.

56
Q

What are the different types of worms?

A

Nematodes (roundworms).
Trematodes (flatworms, flukes).
Cestodes (tapeworms).

57
Q

Where are nematodes found?

A

Intestinal
Larva migrans
Tissue (filaria).

58
Q

Where are trematodes found?

A

Blood
Liver
Lung
Intestinal.

59
Q

What are cestodes divided into?

A

non-invasive

invasive

60
Q

What is the pre-patent period?

A

The PRE-PATENT PERIOD is the interval between infection and the appearance of eggs in the stool.

61
Q

What do worms need to develop?

A

Adult worms cannot usually reproduce without a period of development outside the body.

62
Q

How are intestinal nematodes transmitted? What do they need to grow and become infectious?

A

All are transmitted from human to human via
eggs or larvae.

The egg or larva is not usually infectious when first passed and has to undergo a period of development in the soil.

Faecal-oral spread is therefore the order of the day.

63
Q

What are the key attributes of a pathogen?

A

Infectivity, the ability to become established in host, can involve adherence and immune escape.
Virulence, the ability to to cause disease once established.
Invasiveness, the capacity to penetrate mucosal surfaces to reach normally sterile sites.

64
Q

What are the key steps in pathogenicity?

A

Evade host defence and adhere.
Translocation and evasion.
Avoid opsonisation.
Leak out into blood stream.

65
Q

What does Microbiome describe?

A

‘Microbiome’ describes the totality of micro-organisms, their genetic elements and their environmental interactions in an environment. ‘Metagenomomics’ uses genetic approaches to describe the diversity of micro-organisms in an environment.

66
Q

What do viruses need to survive?

A

Need rapid cell entry
Free virus in blood stream easily neutralised
Infected cells destroyed.

Bateman - Phase 2a COPY (15 decks)

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