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Medicine Phase 2a > Microbiology - Part 2 (Fungi, Protozoa etc) > Flashcards

Microbiology - Part 2 (Fungi, Protozoa etc) Flashcards

1
Q

Why are fungi eukaryotic

A

Have a nuclear membrane

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2
Q

What is meant by fungi being heterotrophic

A

Get nutrients from what they are living on

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3
Q

How do fungi move/spread

A

By means of growth or spore release

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4
Q

Describe cell wall of fungi

A

Chitinous cell wall

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5
Q

Define yeast

A

Small single celled organisms that divide bu budding

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6
Q

What do moulds form from

A

Multicellular hyphae and spores

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7
Q

What are Dimorphic fungi

A

Fungi that exist as both yeasts and moulds, switching between the two when conditions suit

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8
Q

Give example of dimorphic fungi

A

Coccidioides immitis

  • grow as mould at ambient temperature
  • convert to yeast at body temperature after inhalation
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9
Q

Can fungi effect humans

A

Only a few fungal forms can actually infect humans.
Fungi have an inability to grow at 37 degrees
Fungi also can’t evade the adaptive/innate immune response

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10
Q

Describe the burden of fungal disease

A

Large as most people will have had at least one in lifetime e.g. nappy rash, tine pedis (athletes foot), fungal asthma
However life-threatening fungal infection is RARE in healthy hosts

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11
Q

What patients can suffer Invasive/life threatening fungal diseases

A

Immunocomprimised hosts
Post-surgical patients
(Healthy hosts)

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12
Q

What fungal infections are immuno-comprimised hosts at risk of?

A

Candida line infections
Pneumocystis
Invasive aspergillosis

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13
Q

What fungal infections are post-surgical patients at risk of?

A

Intra-abdominal infections

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14
Q

What fungal infections are healthy hosts at risk of?

A

Fungal asthma

Travel associated fungal infections e.g. dimorphic fungi

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15
Q

What is the aim of antimicrobial drug therapy?

A

To achieve inhibitory levels of agent at the site of infection without host cell toxicity

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16
Q

Why is selective toxicity harder to be achieved for fungi than bacteria

A

Fungi are eukaryotic and so more similar to human cells (and harder to differentiate)

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17
Q

What increases selective toxicity

A

Target does not exist in humans
Target is significantly different to human analogue
Drug is concentrated in organism cell with respect to humans
Organism has an increased permeability to the compound [used to target and treat it]

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18
Q

Give example of drug that targets fungal nucleus

A

Flucytosine

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19
Q

Give example of drug that targets fungal cells wall

A

Echinocandins

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20
Q

What does fungal cell wall contain

A

Mannoproteins
B 1,3-glucan
B 1,6-glucan
Chitin

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21
Q

What does fungal plasma membrane contain

A

Ergosterol

not cholesterol like in humans

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22
Q

Give examples of drugs that target fungal plasma membranes

A

Amphotericin
Azoles
Terbinafine

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23
Q

Define Amphoteric

A

A compound that is able to act as a base and an acid

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24
Q

What class of compounds does Amphotericin B belong to

A

Polyenes

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25
Q

What is meant by polyenes being a fungicidal

A

Cause pore formation in ergosterol containing membranes

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26
Q

Why is Amphotericin B more selective for fungi than human cells?

A

As has 10 times lower affinity for cholesterol in mammalian membranes than ergosterol

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27
Q

Although Amphotericin B is more specific for fungi, what toxicity can it still cause to humans?

A

Nephrotoxicity (dose dependent and usually reversible)
Distal Renal Tubular Acidosis (hypokalaemia)
Can cause hyperkalaemia if infused rapidly resulting in cellular damage
Also causes infusion related chills/rigors/hypotension and acute anaphylactoid reactions

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28
Q

What class of compounds does Terbinafine belong to

A

Allylamines

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29
Q

How does Terbinafine work?

A

Causes reversible inhibition of squalene epoxidase (an enzyme required for growth of the fungi).
Inhibits ergosterol biosynthesis.
Distributed extensively to poorly perfused sites such as skin and nail beds.

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30
Q

What is the bioavailability of Terinafine?

A

It is well absorbed by undergoes extensive first pass metabolism
Therefore bioavailability is 45%

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31
Q

What fungi is Terinafine mainly used against?

A

Candida and Aspergillus

Superficial infections including onychomycosis

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32
Q

What are side effects of Terinafine?

A

Well-tolerated but results in:
Taste disturbance
Deranged liver function tests (LFT)
Does also result in increased CYP450 metabolism (by multiple enzymes and is minimally inhibitory)

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33
Q

What class of drugs is Caspofungin, Anidulafungin and Micafungin from?

A

Echinocandin

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34
Q

How do Echinocandins work?

A

Inhibit formation of cell wall by inhibiting B-1,3-glucan synthase, preventing formation of glucan

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35
Q

Give examples of fungi resistant to Echinocandins and why

A 
Some fungi don't have large amounts of glucan (1,3B) in their cell wall so are intrinsically resistant e.g.:
Crytococcus
Zygomycetes
Trichosporon
(Limited activity against Scedosporium)
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36
Q

What are potential side effects of Echinocandins

A 
Limited drug toxicity:
Rare type-1 hypersensitivity
Hepatotoxicity
Hypokalaemia 
(but has few drug interactions)
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37
Q

What are uses of echinocandins?

A

Systemic disease

Activity against mould but not yeast forms of dimorphics

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38
Q

Why are echinocandins only given IV

A

poor oral bioavailability

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39
Q

How do Azoles work?

A

Inhibit ergosterol biosynthesis

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40
Q

What class of drugs would you use for superficial infections (including onychomycosis)

A

Allylamines e.g. Terbinafine

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41
Q

Give examples of Echinocandins

A

Caspofungin
Anidulafungin
Micafungin

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42
Q

Give examples of Azoles

A 
Clotrimazole
Miconazole
Ketonazole
Fluconazole
etc
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43
Q

Mechanism os Azoles

A

Inhibit ergosterol biosynthesis

Dose dependent inhibitors of 14a-sterol demethylase (important intermediate in pathway of cholesterol and ergosterol production)

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44
Q

Give adverse effects of Azoles (relatively safe tho)

A

Transaminitis

GI side effects (more so with Itraconazole e.g. nausea, abdominal pain, diarrhoea, rare life threatening liver failure)

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45
Q

Which Azoles have more pormenant drug interactions and with what

A

Itraconacole (potent CYP3A4 inhibitor)
Interactions with statins, steroids, (same as fluconazole)

Fluconazole (hydrophilic and excreted unchanged)
Less significant interactions with Warfarin, Calcineurin inhibitors, Anxiolytics

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46
Q

Pyrimidine Class:

Give example, mechanism and uses

A

5-fluorocytosine
Inhibits DNA and RNA synthesis
Systemic disease

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47
Q

Grisan class:

Give example, mechanism, uses

A

Griseofulvin
Inhibits microtubule assembly
Topical disease

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48
Q

What is onychomycosis

A

fungal infection of the nail caused by dermatophyte moulds

treatment limited and low success rate

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49
Q

Describe pathogenesis of Pneumocystis

A

Infection of healthy people is frequent and occurs early in life.
Disease develops with moderate-severe immuno-comprimisation (Especially those of HIV, transplant and steroids)
Patient has hypoxia worse than is suggested in chest X-ray

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50
Q

Treatment of pneumocystis

A

Co-trimoxazole, Clindamycin, Pentamidine, Trimetrexate

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51
Q

Give examples of Mycobacteria

A 
M. tuberculosis - TB/Tuberculosis
M. leprae - Leprosy
M. avian complex (MAC) - Disseminated infections in AIDS or patients with chronic lung disease
M. kansasii - Chronic lung infection
M. marinum - Fish tank granuloma
M.ulcerans - Buruli ulcer
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52
Q

Why is it difficult for antibiotics to Taggert the division phase of mycobacteria?

A

Slow growth means it’s difficult for antibiotics to target division phase

M. tuberculosis generation time 15-20 hours (compared to 1 hour for common bacterial pathogens)

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53
Q

Describe microbiology of mycobacteria

A 
Aerobic
Resistance to staining by acid and alcohol
May cause meningitis (TB meningitis)
Can withstand phagolysosome killing
Non-spore forming
Non-motile Bacilli
High content of high molecular weight lipid in cell wall
Slow growing
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54
Q

What are key components of the cell wall?

A

Mycololic acids and liporabinomannan - make strong waxy cell wall that is hard for immune system to target/damage

Weakly gram-positive or colourless (difficult to stain mycobacteria due to thick cell wall)

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55
Q

Who discovered TB

A

Robert Koch

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56
Q

*State what Koch postulated

A

Bacteria should be found in all people with disease
Bacteria should be isolated from the infected lesions in people with the disease
A pure culture inoculated into a susceptible person should produce symptoms of the disease
The same bacteria should be isolated from the intentionally infected individual

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57
Q

What makes mycobacteria resistant to gram stain?

A

High lipid content with mycolic acids in call wall

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58
Q

What stain can be used to test for mycobacteria?

A

Ziehl-Neelsen stain

Pink/Red (positive for acid-fast)

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59
Q

What can be used to detect/analysis nucleic acid in mycobacteria

A

Polymerase Chain Reaction (PCR)
Amplifies nucleic acid
rapid diagnosis in TB endemic countries

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60
Q

Describe immunology of mycobacterial disease

A

Mycobacteria are acid-fast bacilli that are phagocytosed by macrophages and placed in macrophage’s phagolysosome.
Bacteria has adapted to intracellular environment, aims to withstand phagolysosomal killing and escape to cytosol with presence of thick waxy cell wall.
Microbicidal molecules used by host to kill mycobacterium.
Acidifaction aids digestion and degradation by proteases of the mycobacteria - results in antigens to present to T cells.
CD4 T cells generate interferon gamma which helps activate intracellular killing in macrophage
IL-12 release by macrophages further stimulates generation of T helper cells and thus interferon gamma release
Granulomas arise in a response to try and contain and possibly starve the mycobacteria over time

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61
Q

What allows mycobacteria to withstand phagolysosomal killing

A

Thick waxy cell wall

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62
Q

What is function of IL-12 in mycobacterial immunology

A

Released by macrophages

Further stimulates the generation of T-helper cells and interferon gamma release

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63
Q

What is result win genetic defect in interferon gamma or IL-12 receptors or elements of their signalling pathways? (mycobacterial immunology)

A

Susceptibility to mycobacterial infection

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64
Q

How do CD4 T-cells help activate intracellular killing by macrophages

A

Generation of interferon gamma

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65
Q

What is done to try and contain mycobacteria

A 
Granulomas formed to try and contain mycobacteria
Macrophages become epithelioid cells and some macrophages fuse with each other to form giant multinucleate cells "Langerhans giant cells"
T cells (incl cytotoxic CD8 T-cells) infiltrate granuloma
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66
Q

What happens to tissue infected by mycobacteria in granuloma formation

A

Central tissue may necroses and form a caveating granuloma

Granuloma prevents nutrients from entering thereby starving bacteria

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67
Q

What is equivalent of caveating granuloma in lung

A

Central tissue necrose

Formation of a CAVITY

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68
Q

What happens to TB in granuloma

A

TB will go into a dormant sate inside granuloma

Can be reactivated at some point in the future

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69
Q

The highly immunogenic nature of mycobacterial lipid stimulate T-cell responses, how long after exposure to M.tuberculosis

A

3-9 weeks

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70
Q

What are positive T-cell responses to M.tuberculosis exposure

A

Macrophage killing of mycobacteria
Containment of infection
Formation of tissue granuloma

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71
Q

What are negative T-cell responses to M.tuberculosis exposure

A

Hypersensitivity reactions (type 4) with skin lesions, eye lesions and swelling of joints

72
Q

How can we measure reactivity in IGRAs

A

Reactivity can be measured in Tuberculin Skin Test (of IGRA) where intramural injection of purified protein derivatives induce skin swelling and redness.

73
Q

Describe IGRAs

A

Interferon Gamma Release Assays
Use antigens specific to M.tuberculosis e.g. ESAT-60 and CFP10 to distinguish between this and BCG vaccine or environmental mycobacteria.
IGRAs demonstrate exposure to M.tuberculsosis but NOT ACTIVE INFECTION

74
Q

State the principles of mycobacteria treatment

A
  • Slowly replicating bacteria so need prolonged treatment - 6 months of antimicrobials
  • There are different populations of mycobacteria in particular locations intracellularly and extracellularly or in environments of differing pH
  • Resistance may emerge on treatment so use multi-drug combinations to ensure target all populations and mutants
  • Compliance is essential; directly observed treatment used for many patient groups to ensure success
75
Q

*Give examples of anti-tuberculous drugs in standard therapy of mycobacteria

A

Isoniazid (INH)
Rifampicin (RIF)
Pyrazinamide (PZA)
Ethambutol (ETH) for 2 months

Isoniazid and Rifampicin for further 4 months

76
Q

What is given for mycobacteria (anti-tuberculous drugs) if resistance develops to standard therapy

A

Fluroquinolones
Injectable agents including Streptomycin, Cyclosporine, Capreomycin
Prothionamide

77
Q

Give examples of side effects from anti-tuberculous drugs

A

Hepatotoxicity - Isoniazid, Rifampicin, Pyrazinamide
Peripheral neuropathy with isoniazid - give vitamin B6 to protect against this
Optic neuritis - ethambutol

78
Q

What is given to protect against peripheral neuropathy from Isoniazid

A

Vitamin B6

79
Q

What is a primary complex

A

Granuloma
Lymphatics
Lymph nodes

80
Q

*Describe Primary Tuberculosis

A

Bacilli settle in apex (top part near shoulders) and granuloma forms
Bacilli taken in lymphatics to hilarious lymph nodes
In apex of lungs there is more air and less blood supply so fewer white cells to fight off infection
Primary complex can form

81
Q

Why does tuberculosis proliferate more in apex of lung

A

More air and less blood supply so fewer defending white cells to fight off infection

82
Q

Describe Latent tuberculosis

A

Cell-mediated immune (CMI) response from T-cells
Primary infection is contained but CMI persists
No clinical disease (normal chest X-ray)
Detectable CMI to TB on tuberculin skin test of IGRA

83
Q

What chest X-ray would you see in latent tuberculosis

A

Normal chest X-ray

84
Q

Describe Pulmonary Tuberculosis infection

A

Could occur immediately following primary disease (post-primary) or after latent reactivation
Cell-mediated immune response from T-cells
Necrosis in lesion
Caseous material coughed up leaving cavity
TB may spread in lung causing other lesions
CMI and caseation in lesion results in cavity

85
Q

(How and) where does TB spread beyond the lungs

A

Bacilli can spread from apex to hilar lymph nodes and then elsewhere causing:

  • TB meningitis
  • Miliary TB
  • Pleural TB
  • Bone and joint TB
  • Genitourinary TB
86
Q

*What is military TB

A

widespread dissemination and tiny spotted lesions all over lungs and elsewhere

87
Q

In worm infection, what is the Pre-Patent Period?

A

Interval between infection and the appearance of eggs in the stool

88
Q

Describe features of worm-related disease

A

Rare in UK (usually cases are imported).
Adult worms can NOT replicate inside body, so if can’t get out it will eventually die.
Although they can usually produce innumerable larvae or eggs, total worm burden can NOT increase without constant re-exposure to infection.

89
Q

What % of the world are affected by Ascarius lumbricoides

A

25%

90
Q

What are Ascarious Lumbricoides?

A

Large roundworm

Found world wide, mainly in tropics

91
Q

What are 3 groups of worm?

A

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

92
Q

Give examples of different types of Nematodes

A

Intestinal
Larva migrans
Tissue (filaria)

93
Q

Give examples of different places where you’d find Trematodes

A

Blood
Liver
Lung
Intestinal

94
Q

What are different types of Trematodes

A

Non-invasive

Invasive

95
Q

Describe how Intestinal Nematodes spread

A

Soil-transmitted varieties
All are transmitted from human to human via eggs or larvae
Egg/Larvae is not usually infectious when first passed and has to undergo a period of development in the soil.
Faecal-Oral spread therefore**

96
Q

Ascarious Lumbricoides - what are effects on adults (or worms generally)?

A

Often asymptomatic
Mainly mechanical issues (intestinal obstruction, biliary/pancreatic duct obstruction, appendicitis)
Malnutrition
Disrupt surgical anastomoses (connection between vessels) after intra-abdominal surgery

97
Q

What is Loeffler’s Syndrome (worms)?

A

Associates with larval migration through lungs

Occurs 10 to 14 days after infection commenced

98
Q

What are symptoms of Loeffler’s syndrome?

A 
Cough
Fever
CXR infiltrates
Wheeze
Eosinophilia
99
Q

What are treatment options for Ascarious Lumbricoides

A

Piperazine
Pyrantel
Mebendazole
Levasimole

100
Q

Give 2 examples of Hookworm

A

Ancyclostoma duodenale
Necator americanus
(small white worm 1 cm long, life expectancy 1-5 years)

101
Q

What is the most common cause of iron-deficiency anaemia?

A

Hookworm

102
Q

*How would you diagnose hookworm

A

stool microscopy for eggs

103
Q

Give treatment for hookworm

A

Iron supplements:
Pyrantel
Mebendazole

104
Q

**What is the only common helminth infection in the UK?

A

Enterobius vermicularis

Pinworm (or threadworm)

105
Q

Describe life cycle of Enterobius vermicularis

A
  • Adult is resident in the large bowel.
  • The female adult emerges from the anus at night to lay eggs on the perineum.
  • The eggs, which become infectious after 4 hours, are ingested by the next host.
  • There is no tissue migratory phase
106
Q

Describe clinical presentation of pinworm/ Enterobius vermicularis

A 
Pruritis ani
Appendicitis
Vaginal penetration (endometritis, salpingitis, infertility)
(Paranasal sinuses?)
Commonly affects whole families
107
Q

**Describe diagnosis of Enterobius vermicularis

A

Microscopy of sellotape strip from perianal region

108
Q

**Describe treatment of Enterobius vermicularis

A

Mebendazole
Piperazine
Pyrantel (treat whole family)

109
Q

*Give examples of different Schistosomiasis

A

Schistosoma haematobium
Schistosoma mansoni
Schistosoma japonicum
(adult fluke approx 12cm long)

110
Q

Give examples of Tissue Nematodes (the filaria)

A

Wuchereria bancroftii (elephantiasis)
Brugia malayi
Loa loa
Onchocerca volvulus

111
Q

Give examples of Tapeworms

A 
Taenia saginatum (beef tapeworm)
Pok tapeworm (can cause neurocysticercosis)
Echinococcus granulosus (dog tapeworm)
Echinococcus multilocularis (artic fox ")
Diphyllobothrium latum (fish tapeworm)
112
Q

What is Katayama fever?

A

An initial immune-complex mediated illness 2-4 weeks after exposure (schistosomiasis)

113
Q

Describe pathology to worm/egg on surface

A

T-cell mediated immune response to worm/egg surface leading to cytokine release
IL-12 can suppress egg-induced pathology (mediated by interferon gamma)
Granuloma develops
Fibrosis if egg laying continues

114
Q

Where can you get flukes?

A 
Blood
Liver
Lung
Bowel
(they all have a snail as an intermediate host)
115
Q

**Define Protozoa

A

Single-celled eukaryotic organisms with a definitive nucleus

116
Q

What is main biological role of protozoa

A

Consumers of bacteria, algae and microfungi

117
Q

Give examples of different protozoa

A 
Mastigophora (flagellates)
Sarcodina (Amoebae)
Apicomplexa (Sporozoans)
Ciliophora (Ciliates)
Microsporidia
118
Q

What is main locomotory organelle of Mastigophora (flagellates)

A

Flagellum

Usually reproduce by binary fission

119
Q

Give examples of Mastigophora (flagellates)

A

Giardia lamblia (Intestinal flagellates)
Trypanosoma spp. (Haemoflagellates)
Trichomonas Vaginalis

120
Q

Describe symptoms of Gardia lambia

A

Flatulence
Abdominal cramps
(Intestinal flagellates)

121
Q

Describe clinical presentation of African Trypanosomiasis

A

Lesion develops 2 weeks after getting bitten on arm by insect
2 years later fever, lethargy and myalgia
Excessive weight loss; Personality change; Irritability; Coma; Increased daytime tiredness

122
Q

How does Sarcodina (Amoebae) move

A

By means of flowing cytoplasm and production of pseudopodia

123
Q

Give example of Sarcodina (Amoebae)

A

Entamoeba histolytica

124
Q

Describe presentation of amoebasis

A

Bloody diarrhoea upon abroad visit (e.g. rural Botswana)
UK return get increasing right upper quadrant pain
Liver abscess seen on CT

125
Q

Describe features of Apicomplexa (Sporozoans)

A

No locomotory extensions
All species are parasitic (most are intracellular)
Reproduce by multiple fission

126
Q

Give exampled of Apicomplexa (Sporozoans)

A

Plasmodium spp.
Cryptosporidium spp.
Toxoplasma gondii

127
Q

Which Apicomplexa (Sporozoans) protozoa causes Malaria

A

Plasmodium spp.

128
Q

Describe presentation of toxoplasmosis

A

Recent HIV positive diagnosis (low CD4)
2-week history of progressive left sided weakness
Headaches and Visual Disturbances
Commonly presents when people are immunosuppressed (chemo or HIV/AIDS)

129
Q

Describe features of Ciliophora (Ciliates)

A

Have cilia that beat rhythmically at some stage in lifecycle
2 nuclei types (micronucleus and micronucleus)
Very large group

130
Q

Give example of Ciliophora (Ciliates)

A

(Protozoa)
Balantidium coli - presents in those who are immunocompromised
(causes severe diarrhoea and/or ulceration of colon)

131
Q

Describe features of Microsporidia

A

Very small
Production of resistant spores
Causes diarrhoea in immunocompromised

132
Q

Give example of Microsporidia

A

Enterocytozoon bieneusi

133
Q

*What 4 species of Protozoa cause malaria and what is most common?

A

Plasmodia falciparum (most common)
P. ovale
P. vivax
P. malariae

134
Q

How is malaria transmitted?

A

Bite of Female Anopheles Mosquito

135
Q

How many cases per year are there of Malaria

A

300-500 million cases per year (80% Africa)

136
Q

How many deaths per year are there of Malaria

A

700,000 to 2.7 mil deaths a year

137
Q

Why in there increasing incidence of malaria

A
  • Increasing resistance of parasite to antimalarials
  • Increased resistance of mosquito to insecticides
  • Ecological & climate changes - means mosquitoes can be found in more countries
  • Increased travel to endemic areas
138
Q

Describe the vector by which malaria spreads

A

Female Anopheles mosquito - mainly bites at night
Worldwide distribution
Infection is acquired during feeding from infected human
Lifespan of female mosquito is 3-4 weeks
Mosquito is infected for life

139
Q

True or False:

Variation in lifecycle between different Plasmodia spp. results in different clinical manifestations

A

True

140
Q

Describe the parasitology of malaria

A

Female anopheles mosquito becomes infected after taking a blood meal with gametocytes (sexual form of malarial parasite).
Developmental cycle in mosquito usually takes 7-20 days (depends on temperature), culminating in the migration of infective sporozoites to insect’s salivary glands.
Sporozoites are inoculated into a new human host, which are rapidly taken up by liver (if not destroyed by the immune system).
Sporozoites multiply in hepatocytes as merozoites - this is the pre-erythrocytic sporogeny.
After afew days , infected hepatocytes rupture, releasing merozoites into the blood where they’re taken up by erythrocytes.
In erythrocytes, parasites again multiply changing from merozoites to trophozoites to schizont and finally appearing as 8-24 new malarials.
Erythrocyte ruptures, releasing merozoites to infect further cells.

141
Q

When do sporozoites become in hepatocytes (if not destroyed by immune system)

A

Merozoites

Pre-erythrocytic sporogeny

142
Q

In malaria parasitology, what bacteria can have parasites that remain dormant in liver as hypnozoites?

A

P. vivax
P. ovale

These may reactivate at any time causing relapsing infection (therefore ask 2 year travel history to counter this)

143
Q

What are hypnozoites?

A

Dormant merozoites (parasite from sporozoites) in liver.

Due to dormancy, these will not be eradicated by anti-malarials

144
Q

Summarise the stages of malaria parasite in body

A 
Sporozoites
Merozoites (liver)
Trophozoites (erythrocyte)
Schizonts (erythrocyte)
Merozoites
145
Q

What is the cycle of malaria parasite in body called

A

Erythrocytic schizogony

146
Q

How long does Erythrocytic schizogony cycle take for each malaria species

A

48 hours in P. falciparum, P. vivax and P. ovale

72 hours in P. malariae

147
Q

What can merozoites develop into

A

Trophozoites

some into Gametocytes

148
Q

What cells are mainly targeted by P.vivax and P.ovale

A

Reticulocytes

Young erythrocytes

149
Q

What cells are mainly targeted by P.malariae

A

Older cells

150
Q

Which malaria causing species will parasitise any stage of erythrocyte

A

P.falciparum

151
Q

Describe pathogenesis of malaria

A

Relates to anaemia, cytokine release and widespread organ damage in P.falciparum

152
Q

How does P.falciparum cause widespread organ damage

A

Impaired microcirculation
Red cells contain Schizonts that adhere to lining of capillaries in brain, kidneys, gut, liver and other organs.
Schizonts can also cause rupture, releasing toxins and stimulating further cytokine release.

153
Q

What causes anaemia in malaria?

A

Haemolysis of infected red cells
Haemolysis of non-infected red cells (Blackwater fever - dark urine)
Splenomegaly
Folate depletion

154
Q

What is normal incubation period for someone with malaria

A

10-21 days

155
Q

Describe clinical features of malaria (common to all 4 species)

A 
Fever is common (not always present)
Chills and sweats
Headache
Myalgia
Fatigue
Nausea and vomiting
Diarrhoea
156
Q

What is myalgia?

A

pain in muscle or group of muscles

157
Q

What less common symptoms would you see in adult patient with malaria

A 
Coma
ARDS (adult resp distress syndrome)
Anaemia
Jaunice
Hepato-splenomegaly
Hypoglycaemia (parasites eat up glucose)
Blackwater fever
Renal failure
Shock from bacterial sepsis
158
Q

What less common symptoms would you see in child patient with malaria

A 
Tachypnoea (rapid breathing)
Anaemia
Hypoglycaemia
Cerebral malaria
Raised intracranial pressure
CONVULSIONS (60-80%) 
(rule out meningitis)
Non specifc e.g. crying, eating etc
159
Q

Describe clinical features specific to P.vivax or P.ovale

A

Relatively mild illness
(P.vivax can occasionally cause severe disease)
Slow developing anaemia
May be tender hepatosplenomegaly
Spontaneous recovery usually within 2-6 weeks
HYPNOZOITES in liver can cause relapse for many years after infection
(Repeated infections can lead to chronic ill health)

160
Q

Describe clinical features specific to P.malariae

A

Relatively mild illness but tends to run a more chronic course
Parasitaemia (parasites in blood) may persist for years with or without symptoms
Nephrotic syndrome and Glomerulonephritis in children

161
Q

Describe clinical features specific to P. falciparum

A

Around 75% of cases
Unlikely to present more than 3 moths after exposure.
Causes vast majority of deaths.
Blackwater fever resulting from widespread intravascular haemolysis
High parasitaemia
Cerebral malaria - diminished consciousness, confusion and convulsions progressing to coma and death
Rapid deterioration in patients

162
Q

What causes cerebral malaria symptoms of diminished consciousness, confusion and convulsions in P.falciparum infection

A 
Hypoxia to brain
Reduced brain
perfusion caused by
schizonts adhering to the
endothelial cells of
capillaries
163
Q

True or False:
Malaria should be in the differential diagnosis of ANYONE who presents with FEBRILE ILLNESS in, or having recently left a malarious area

A

True

164
Q

Give non-specific symptoms of malaria

A

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

165
Q

What physical tests can be used to diagnose malaria

A

Thick and Thin films
(Done at least 12 hours apart to check for presence of parasite)

3 separate films should be examined before malaria is declared unlikely

166
Q

Describe how thick and thin films are used in malaria diagnosis

A

Thick film:
Sensitive but low resolution (difficult to interpret the parasite but have a higher yield).
Tells you is malaria is present.

Thin film:
Identify morphological features and quantification of
parasitaemia.
Tells you type and parasite count, above 2% = severe.
Identification of species on thin film - trophozoite most
commonly used.

167
Q

Describe treatment of complicated falciparum malaria

A 
IV Artesunate
IV Quinine (but can cause hypoglycaemia)
168
Q

Describe treatment of uncomplicated falciparum malaria

A

Oral Riamet
Oral Quinine
(add doxycycline as 2nd agent to treat undiscovered/ untreated malaria)

169
Q

Describe treatment of non-falciparum malaria

A

Oral Chloroquine

170
Q

While oral chloroquine is used in treatment of non falciparum malaria, describe treatment of P.vivax & P.ovale malaria

A

PRIMAQUINE for hypnozoite clearance

Not suitable for those with G6PD deficiency and pregnancy status

171
Q

Describe types of genetic immunity to malaria

A

Sickle cell trait protects you
Glucose-6-phosphate dehydrogenase deficiency (G6PD) - enzyme that is essential for assuring the normal life span for red blood cells, deficiency results in the sudden destruction of red blood cells and can lead to haemolytic anaemia - malaria parasites CANNOT SURVIVE in these red
cells

172
Q

Describe acquired immunity in malaria

A

Recurrent infection can result in semi-immunity but lost if not reinfected after a couple years
Maternal transmission of antibodies across placenta (diminishes over time)

173
Q 
Which pair is correct?
Pityriasis versicolor = bacterium
Ringworm = helminth
Aspergillus fumigatus = mycobacterium
Falciparum malariae = fungal
Giardia lamblia = protozoal
A

Giardia lamblia = protozoal

Pityriasis versicolor is fungal
Aspergillus fumigatus is fungal
Falciparum malariae is parasitic protozoal
Ringworm is caused by various fungi, not helminths

174
Q

Mycobacteria. Which is not a feature?

a) Resistance to destaining by acid and alcohol
b) Cell wall contains lipoarabinomannan
c) They only divide every 20 hours
d) They cannot withstand phagolysosomal killing
e) May cause meningitis

A

d) They cannot withstand phagolysosomal killing

175
Q

What causes ringworm?

A 
Various fungi
(NOT a helminth)

Medicine Phase 2a (22 decks)

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