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IASM > MICROBIOLOGY - bacti, fungi, parasites (IAS46-49, 53) > Flashcards

MICROBIOLOGY - bacti, fungi, parasites (IAS46-49, 53) Flashcards

1
Q

Rank: bacteria, prions, viruses, protozoa, parasites, fungi in terms of descending size

A

parasites > protozoa > fungi > bacteria > viruses > prions

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2
Q

Reservoir of pathogen meaning?

A

Habitat of a microorganism for their growth

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3
Q

Port of exit of pathogens in organisms?

A

Feces, secretions

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4
Q

Where do:
cytosolic
intravesicular
extracellular pathogens (and toxins) invade respectively

A

Any cell

Macrophages

B cells

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5
Q

Define microbial virulence - what are the characteristics of a virulent organism

A

Capacity of microbe to cause disease in host

characteristics: low infective dose, high attack rate, high fatality rate

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6
Q

Define virulence factors

A

facilitate microbial attachment, invasion, multiplication or host defence evasion

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7
Q

3 methods of pathogenic mechanisms? Elaborate on their mechanisms

A

Direct cytolysis - due to intracellular replication in bacteria or toxin secretion (no of bacteria plateaus eventually)

Immunopathological damage - immune system damages hosts themselves due to molecular mimicry or upregulated inflammation

oncogenesis - integration of viral genome into host chromosome (eg EBV, HBV) or due to chronic inflammation (H. pylori)

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8
Q

Koch’s postulate?

A

Microbe must be present in ALL disease cases

microbe must be isolated from diseased hosts and grown in culture

should cause disease when introduced to healthy organism

Microbe must be recovered from experimentally infected host

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9
Q

What is the bacterial cell wall made of? Its structure?

Outer wall in what kind of bacteria? What components does it have?

The LPS structure and its function?

A

Peptidoglycan - made of glucan chains of alternating NAG and NAM, glucan chains joined by short peptides on NAM

Gram-negative bacteria, outer wall increases antibiotic resistance

components: lipoproteins, lipids, proteins, polysaccharides, lipopolysaccharides

LPS structure: O-polysaccharide, core polysaccharide and lipid A

O-polysaccharide as the antigen

Lipid A responsible for endotoxin properties - CD14 causes endocytosis, TLR4 responsible for triggering inflammation (Transcriptional response (cytokine expression & NLR-mediated canonical inflammasome activation)

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10
Q

What does the cytoplasm contain?

Plasmid function?

A

Cytoplasm - contains nucleoid + plasmids + ribosomes (30s and 50s subunits)

Plasmid may contain antibiotic resistant genes

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11
Q

Functions of capsule?

Functions of pili?

Structure of endospore? Its function and clinical implications?

A

Virulence factor for adhesion, antiphagocytic function

Virulence factor for adhesion, sex pili for exchange of plasmids

Outermost to innermost: exosporium > spore coat > spore cortex > inner membrane > spore cytoplasm containing nucleoid

Function: metabolically inert, dormant, highly resistant to heat/radiation/chemicals (so an issue with contamination/sterilization and disinfection/ infection control)

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12
Q

Bacteria phases of growth? Define generation time

A

1) lag phase - no change in bacti numbers as bacteria is adapting to new environment

2) log phase - bacteria numbers grow exponentially

3) stationary phase - bacteria numbers cannot increase because not enough nutrients/too much waste accumulated)

Generation time refers to the time needed for bacteria to double in amount in log phase, usually 30min

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13
Q

The 3 methods of genetic transformation of bacteria?

A

1) conjugation - exchange of plasmids between bacteria by sex pili’

2) transduction - bacteriophages infect bacteria, viral toxin gene incorporated into bacterial genome

3) Point mutation, changes antigenicity, virulence, transmissibility, antimicrobial susceptibility

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14
Q

Compare: intracellular bacteria and extracellular bacteria in terms of place of growth, growth opportunities, environmental conditions

A

Intracellular bacteria: grow within host cells, protected from host defense mechanisms

Extracellular bacteria: grow outside of host cells with more growth opportunities BUT harsher environmental conditions (eg have to face host immune system)

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15
Q

Gram stain process? Its principle? Appearance of gram +ve and gram -ve bacteria?

A

Crystal purple > iodine (forms complex with crystal violet) > alcohol (to decolorize Gram-negative bacteria) > safranin (counterstain to stain gram-negative bacteria)

Principle: the thin peptidoglycan wall of Gram-negative bacteria means these bacteria cannot retain the Gram stain well

+ve: purple, -ve: pink

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16
Q

How to classify bacti?

A

Check sid ppt for quick revision

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17
Q

Staphylococcus - catalase positive or negative? Oxygen requirement?

A

Positive, facultatively anaerobic

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18
Q

S. aureus - coagulase +ve or -ve? Colony morphology?

Describe the 2 types of coagulase test

A

Positive, golden-yellow colonies, in clusters

slide coagulase test - Binding to fibrinogen; the fibrin deposited on the surface inhibits phagocytosis

Tube coagulase test - Activation of prothrombin to initiate clot formation in plasma

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19
Q

The 4 aims of virulence factors in S. aureus? For each aim list the virulence factors and their specific functions

A

Evasion of host defence mechanisms:
catalase, coagulase prevent clot formation,
protein A: helps avoid opsonization and induces B cell death (it acts as toxin to trigger B cell apoptosis)

Adherence to host cell: teichoic acid

Invasion into host cells: protease, lipases, DNAses, hyaluronidase (breakdown of hyaluronic acid)

Toxins: a-hemolysin damages blood cell, toxic shock syndrome toxin (TSS toxin causes TSS)

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20
Q

Epidemiology of S. aureus (its reservoir) and mode of transmission?

A

Humans act as reservoir, transmitted by direct contact

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21
Q

2 categories of diseases that S. aureus can cause? Name examples for each category

A

Pyogenic -
skin, soft tissues (folliculitis, furuncles, carbuncles)
bone/joints: osteomyelitis, septic arthritis
infection of wounds, surgical sites,
pneumonia

toxin-mediated:
TSS (toxic shock syndrome)/scalded skin
food poisoning

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22
Q

S. aureus antibiotic resistance types?

A

90% methicillin resistant but MRSA (methicillin-resistant) occurs, VRSA also occurs, mostly penicillin resistant

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23
Q

S. epidermidis and S. saprophyticus - coagulase positive or negative, and what diseases they cause?

A

Coagulase negative

epidermidis: infections with prosthesis
saprophyticus: acute cystitis in young women

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24
Q

Strep and enterococci - catalase positive or negative? Oxygen requirement?

Strep pneumoniae - hemolysis pattern and the pattern’s appearance?

Strep pyogenes, agalactiae - hemolysis pattern and its appearance? Lancefield group?

Enterococci hemolysis pattern and appearance? Lancefield group?

A

NEGATIVE, facultatively anaerobic

pneumoniae: a-hemolytic with greenish discoloration of blood agar

pyogenes/agalactiae: b-hemolytic, complete clearing of agar

pyogenes: Lancefield A, agalactiae: Lancefield B

enterococci: gamma-hemolytic, lancefield D

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25
Q

Diseases S. pneumoniae can cause? what antibiotic can it be resistant to? Does it have capsule?

A

Pneumonia, meningitis, otitis media, sinusitis, septicemia, penicillin

HAS CAPSULE, THICK POLYSACCHARIDE CAPSULE

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26
Q

Diseases S. pyogenes and agalactiae can cause?

A

Pyogenes: skin/soft tissue disease, SCARLET FEVER, RHEUMATIC FEVER, TSS

agalactiae: neonatal sepsis

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27
Q

Diseases enterococci can cause? Name 3

what antibiotic is enterococci especially resistant to?

A

Catheter-associated urinary tract infection, biliary sepsis, polymicrobial intra-abdominal/biliary infections

cephalosporins

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28
Q

Does Bacillus form spores? oxygen requirement?

diseases bacillus species can cause? 2 species + 1 disease each

A

Spore forming, aerobic

bacillus anthracis: anthrax

bacillus cereus: food poisoning

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29
Q

Listeria monocytogenes diseases? How is the disease transmitted? Form spores?

A

neonatal meningitis, invasive listeriosis in immunocompromised adults or elderly (>60), foodborne (esp milk, chicken)

No spores

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30
Q

Corynebacterium diptheriae disease? Disease morphology?

Morphology of the bacteria? Any spores?

A

Diptheria, Sore throat with an adherent grey pseudo-membrane in the oropharynx (white throat)

V/L - shaped, “chinese character appearance” No spores

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31
Q

Nocardia morphology? Besides gram stain how can it be stained, and its stained appearance?

Disease it causes? Any spores?

A

Branched filaments, can be stained by modified Ziehl-Neelsen stain, pink color so acid fast

Nocardiosis (granulomatous infection) (pulmonary, CNS, cutaneous)
No spores

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32
Q

Mycobacterium: acid fast or not? Any spores?

Which disease can mycobacterium cause? and the species causing it?

What agar used to culture mycobacterium and Nocardia? What media is it?

Method of transmission?

A

Acid fast (pink stain), no spores

M. tuberculosis (tuberculosis)

Lowenstein-Jensen agar - selective media (has nutrients to promote growth of desired organism BUT antimicrobials to inhibit growth of others)

AIRBORNE

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33
Q

Clostridium oxygen requirement? Diseases some clostridium species can cause? Form spores?

A

ANAEROBIC, FORMS SPORES

C. botulinum: botulism

C. tetani: tetanus

C. perfringens: gas gangrene, intra-abdominal/pelvic sepsis, food poisoning

C. difficile: pseudomembranous colitis

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34
Q

Neisseria morphology and oxygen requirement? Oxidase + or -?

A

Diplococci, AEROBIC (most are aerobic unless specified), oxidase positive

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35
Q

Neisseria gonorrhoeae epidemiology? Reservoir and mode of transmission?

A

Humans as reservoir, transmission by sexual and mucosal contact

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36
Q

N. gonorrhoeae diseases? How to diagnose N. gonorrhoeae

What type of media (supportive/selective/enrichment/differential) is the agar used to test

A

Urethritis in men (PUS FORMED)
urogenital infection in women,
extragenital infection (pharyngitis, rectum proctitis)
disseminated infection (infective endocarditis, septic arthritis, meningitis)

GONOCOCCAL OPTHALMIA NEONATORUM (infection of newborn baby)

Thayer-Martin agar (selective media)

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37
Q

N. meningitidis epidemiology?

A

Human reservoir, transmission by respiratory droplets, direct mucosal contact

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38
Q

Virulence factors of N. meningitidis?

A

Polysaccharide capsule (for attachment) - ONLY IN N. meningitidis

Pili/fimbriae (attachment)

lipooligosaccharide - for endotoxin (trigger immune response) - CD14 for endocytosis, TLR4 for triggering transcriptional response (cytokine expression & NLR-mediated canonical inflammasome activation)

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39
Q

Diseases N. meningitidis can cause?

A

MENINGITIS, septicemia

◆ purulent conjunctivitis
◆ meningococcal pneumonia
◆ purpura fulminans

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40
Q

Vaccine types against N. meningitidis?

A

polysaccharide vaccine; quadrivalent conjugate vaccine; serogroup B protein-based vaccine

41
Q

Enterobacterales aerobic requirement? Normal habitat?

A

Facultatively anaerobic, human and animal large bowel

42
Q

Enterobacterales antigen?

A

KOH -

K antigen: capsule antigen
O antigen: somatic LPS (the O polysaccharide)
H antigen: flagellar antigen

43
Q

General diseases Enterobacterales can cause?

A

GI infections: gastroenteritis, dysentery
extra-intestinal infections: UTI, respiratory tract infections, bacteremia, meningitis, intra-abdominal sepsis

44
Q

Diseases E. coli can cause?

A

ETEC (enterotoxigenic E. coli): Traveller’s diarrhea,
STEC: (shiga toxin-producing E. coli) hemorrhagic colitis, hemolytic uraemic syndrome

45
Q

What color are E. coli colonies on CHROMID agar

A

Red

46
Q

Klebsiella morphology on agar (reasons for this look?) and diseases it can cause (name 2) and risk factors

Is it a lactose fermenter (if yes specifically which type)

A

Mucus look because of capsule formation

Diseases: community pneumonia, abcess formation

Risk factor: elderly, alcoholics, those with underlying diseases

Yes - mucoid lactose fermenter

47
Q

What diseases does Salmonella cause? (there are 2 types of salmonella- classify by this categorization)

What disease does Shigella cause? Function of shiga toxin?

How to determine whether a person may have salmonella/shigella (what agar)

A

Salmonella typhi: eg S. enterica - typhoid fever, paratyphoid fever

Non-typhi salmonella: gastroenteritis

Shigella: dysentery,

Shiga toxin: Inhibits eukaryotic protein synthesis, eventually leading to host cell death

MacConkey agar - clear colonies then XLD agar: black colonies (if E. coli gold colonies)

48
Q

Vibrionaceae: Morphology, oxidase + or -, reservoir?

A

Curved bacilli, oxidase +ve, found in water bodies (freshwater and seawater)

49
Q

General diseases Vibrios can cause?

A

GI tract infection, Severe systemic infections, e.g., skin and soft tissue infections (rare)

50
Q

Vibrio cholerae disease - symptom as well? Is it fatal and why

A

Cholera - rice water stool, rapidly fatal because of rapid dehydration

51
Q

How does cholera toxin work

A

increases intracellular cAMP at intestinal epithelium -> inhibits sodium and chloride absorption -> increases chloride and water secretion

52
Q

What diseases do V. parahaemolyticus and V. vulnificus cause

how to differentiate V. cholerae and non-cholera vibrios

A

parahaemolyticus: gastroenteritis
vulnificus: skin infection

TCBS agar - for V. cholerae only, agar turns yellow

53
Q

Non-fermenters: oxygen requirement? Are they antibiotic resistant?

A

STRICTLY aerobic, VERY antibiotic resistant

54
Q

P. aeruginosa morphology? Oxidase + or -?

A

Metallic green appearance, fruity smell, oxidase positive

55
Q

P. aeruginosa disease?

A

Hospital-acquired infections, fatal in neutropenic septicemia

56
Q

Acinetobacter and Burkholderia diseases?

A

Acinetobacter: For A. baumannii nosocomial infections
B. pseudomallei: melioidosis

57
Q

Haemophilus influenzae factors that require blood or blood components for its growth?

A

X factor, V factor (XAVI)

X factor: haemin
V factor: NAD or NADP

58
Q

Diseases caused by H. influenzae? (rod or cocci?)

A

Meningitis, pneumonia, sinusitis, otitis media (basically same as S. pneumoniae). gram -ve rod

59
Q

Does H. influenzae have capsule? If yes, how many types of capsules and which type causes most invasive diseases in children and infants?

A

Yes - 6 capsule types, type b

60
Q

What vaccine is available against H. influenzae

A

Polysaccharide conjugate vaccine (against capsular polysaccharide type B)

61
Q

Legionella disease and Bordetella disease?

Which agar to culture Bordetella

A

Legionella pneumophila: Legionnaire’s disease
Bordetella pertussis: pertussis (whooping cough)

Bordet-Gengou agar

62
Q

2 types of strict anaerobes, gram-negative bacilli?

What diseases are these 2 associated to

A

Oral flora (Fusobacterium)
Gut flora (Bacteroides)

■ diseases caused usually when out of normal habitat
■ mixed infections (with other bacteria); abscess formation; intra-abdominal infections; genital tract infections; head and neck infections

63
Q

Spirochaetes: name 2, which diseases do they cause

A

Treponema pallidum: causes syphilis (STD)
H. pylori (stomach ulcer), related to gastritis, adenocarcinoma of stomach

64
Q

Syphilis symptoms? Name 2

Can Treponema pallidum be cultured in vitro

A

Congenital infections, notched abnormal teeth

NO

65
Q

How can fungi be classified

A

Yeasts, molds, dimorphic fungi

66
Q

Fungi cell membrane components and which is most abundant

A

Glucan (60% and most abundant being beta-(1,3-) glucan), chitin (10%), 30% protein

67
Q

How do yeasts reproduce

A

Budding (spore forming)

68
Q

Candida epidemiology and the disease it causes? Name some risk factors (5)

A

Candida: commensals on skin, GI tract, female reproductive tract

Candidiasis

Risk factors: Immunocompromised, Broad spectrum antibodies, transplants, steroids, ICU, IV

69
Q

Candidiasis in immunocompetent and immunocompromised hosts?

A

Immunocompetent: vaginal thrush

Immunocompromised: symptoms more refractory (do not respond to treatment), oral thrush, systemic candidiasis eg in liver/spleen

70
Q

Candidiasis diagnostic methods?

A

Culture using Sabouraud agar, Gram stain (gram +ve), detection of antigen (Beta-d-glucan antigen)

71
Q

Treatment method for candidiasis?

A

Polyenes: Nystatin if topical (forms complex with ergosterol in cell membrane), amphotericin B when systemic infection

Azoles: eg Fluconazole to inhibit ergosterol synthesis

Echinocandins eg micafungin to inhibit cell wall synthesis

72
Q

Name 1 nucleoside analogue used to treat fungal infection

A

5-flucytosine

73
Q

Cryptococcus neoformans morphology under stain? What risk factors for C. neoformans?

Besides stain how can it be identified

A

WIth halo because of capsule when stained under India ink

Immunocompromised patients

Cultured or checked for capsular polysaccharide antigen

74
Q

Mould morphology?

A

multicellular, long filaments, reproduce by spores

75
Q

Aspergillus method of identification and disease? Risk factor?

A

Systemic infection, identified by galactomannan antigen, nucleic acid, culture

Risk factor: Immunocompromised (eg HIV/neutropenia/organ transplants/immunosuppressants/

76
Q

Dermatophyte species? What disease do dermatophytes cause

A

Trichophyton, Epidermophyton, Microsporum

Disease: tinea - aka ringworm (tinea pedis, tinea capitum, tinea unguium)

77
Q

Dimorphic fungi - name 1 example and its morphology at 37c and 25c

How can it be detected

Risk factors?

Symptoms?

A

Talaromyces marneffei - 37c yeast, 25c mold (mold has diffusible red pigment) on agar

Detected by patient antibodies

Immunocompromised patients

Multiple skin lesions with papules with central necrotic umbilication

78
Q

Fungi that cannot be cultured?

A

Pneumocystis jirovecii

79
Q

Define: Parasitism, parasite, host

A

Parasitism: any reciprocal association in which a species depends
upon another for its existence

parasite: the organism that derives all benefit from dependence upon another organism

host: the organism that harbors the parasite

80
Q

How can parasites be typified (in relation to host)

A

Level of dependence, time, physical relationship

Level of dependence: obligate (fully dependent) or facultative

time: temporary or permanent

physical relationship: endoparasite or ectoparasite

81
Q

Define definitive and intermediate host

A

Definitive host: Houses the parasite in active form
Intermediate host: houses intermediate form of parasite

82
Q

How to diagnose parasitic infection?

A

1)Demonstration of parasites in appropriate clinical specimens by direct microscopic examination, staining, or tissue sections.

  1. Serology: detection of antigens or antibodies in blood or other body fluids.
  2. Culture of parasites (extremely uncommon): applicable only to a small number of parasites, mainly protozoa.
  3. Nucleic acid amplification (eg PCR)
83
Q

How to prevent parasite infection

A

Elimination: 1) of parasites in reservoir 2) of parasite vectors

Avoid exposure to parasite/vector

Chemoprophylaxis (eg antimalarial)

Vaccines (eg 2 vaccines available against malaria)

84
Q

Classify parasites based on physical relationship with hosts?

A

Endoparasites: Protozoa or helminth (trematode, cestode, nematode)

ectoparasite: arthropods

85
Q

Protozoa - how many cells? Classified into which 2 groups? For lumen dwelling further classify

GIVE EXAMPLES FOR ALL GROUPS

A

Unicellular

Lumen-dwelling or blood and tissue dwelling (extraluminal)

Lumen-dwelling:
in GI tract (eg Entamoeba histolytica) - Causes amoebic colitis/dysentery and amoebic liver abscess

in Genital tract: Trichomonas vaginalis (STI), Giardia lamblia

Extraluminal (blood/tissue): Toxoplasma gondii, Plasmodium

86
Q

Nematode morphology and classification? For each group give an example and properties of that example

A

Round worms

Classified into:
Intestinal nematodes, eg: Strongyloides stercoralis (asymptomatic in immunocompetent host, can lead to hyperinfection in immunocompromised host) (IF RUSH JUST REMEMBER THIS)

Blood and tissue nematodes, eg: Angiostrongylus cantonensis (associated with raw or undercooked snails/slugs/freshwater shrimp/land crabs - assoc. with meningitis)

Wuchereria bancrofti, Brugia malayi: Lymphatic filariasis

Enterobius vermicularis: perianal pruritusxz

87
Q

Trematode morphology? What hosts do they all need?

1 example of: Liver, Lung, Intestinal and Blood fluke, and what is it associated with

A

Flukes, leaf-shaped flatworms, freshwater snails

Clonorchis sinensis the liver fluke - associated with intake of undercooked freshwater fish, carcinogen associated with CHOLANGIOCARCINOMA

Lung fluke: Paragonimus, associated with eosinophilic pneumonia

Intestinal fluke; Fasciolopsis buski

Blood fluke: Schistostoma app.

88
Q

Cestode - morphology? Which 2 groups? Examples for each group?

A

Segmented adults - Taenia solium/saginata

Intestinal cestode (adult stage) - Taenia solium (ingesting larvae)
Tissue cestode - (larval stage) - Taenia solium (cysticercosis) - ingesting eggs of Taenia solium

89
Q

Ectoparasite examples?

Some vectors of parasites?

A

Fleas, scabies mite, maggots of flies

Mosquitoes, tsetse flies, fleas, lice, sandflies, blackflies, triatomine bugs

90
Q

5 main plasmodium species and their distribution? Which is most fatal? Which 2 species cause majority of human malaria cases?

A

Most fatal: P. falciparum

P. falciparum: tropics

P. malariae: sporadic

P. vivax: global

P. ovale: West Africa, some South Pacific islands, also found in other parts of the world sporadically.

P. knowlesi: Southeast Asia, esp Malaysia/Malaysian Borneo, simian malaria that sometimes causes human infection

P. vivax and P. falciparum cause most malaria cases

91
Q

Malaria transmission methods? Its vector?

A

Vector: FEMALE Anopheles mosquito

Blood transfusion and organ transplantation

Contaminated needles/medical instruments and medications

Vertical transmission: mother to unborn infant before or after delivery

92
Q

Plasmodium life cycle? In general

A

Infection

Pre-erythrocytic cycle

Erythrocytic cycle

Transmission to Anopheles

For P. vivax and ovale ONLY: Secondary schizogony in hepatocytes

93
Q

Each step in depth?

A

A) Infection:
1) Anopheles mosquito injects sporozoites into human bloodstream, 2) Sporozoites reach the hepatocytes within 30 min

B) Pre-erythrocytic cycle:
1）sporozoites infect hepatocytes,
2）asexually reproduce to produce merozoites within a schizont,
3）schizont ruptures to release more merozoites
4） merozoites released infect hepatocytes or invade circulating RBC

C) Erythrocytic cycle:
merozoites infect RBC, then:

1) Schizogony (make schizonts) - asexually reproduce to form more merozoites in schizont, schizont ruptures, releases merozoites to continue infecting

OR

2) Gametogony (make gametocytes) - formation of gametocytes (male is microgametocyte, female is macrogametocyte) within RBC, gametocytes taken up when female Anopheles mosquito takes a blood meal

D) Transmission by Anopheles:
1) Gametocytes mature, sexual reproduction to form zygote and oocyst

2) Sporogony: Sporozoite formation in oocyst, oocyst ruptures to release sporozoites, sporozoites migrate to salivary gland of mosquito

B chronogically)
Secondary schizogony (Vivax and ovale ONLY)
Hypnozoite formation:
Vivax and Ovale may stay in hepatocytes - form hypnozoite, persists for many years (so can have 2nd infection)

94
Q

Pathogenesis of malaria? the 5 stages?

A

3 + 2: 3 related to RBC, 2 inflammatory

1) Increased RBC destruction as:
RBCs lose deformability,
become infected by parasites (especially P. falciparum),
spleen becomes enlarged (splenomegaly) because of immune reaction to destroy more RBCs

2) Infected RBC cytoadherence to endothelium in P. falciparum infection - microvascular obstruction (think something like a clot)

3) RBC lysis - iron depletion, anemia, hemoglobinuria (blackwater fever - free hemoglobin excreted in urine, so urine becomes coca-cola colored)

4) Nephrotic syndrome - immune complexes deposit in kidneys during chronic P. malariae infection

5) Cytokine production during infection

95
Q

4 symptoms of malaria?

A

1) Paroxysms - Chills, rigor in the first 1-2 hours, then spiking fever in subsequent hours, then sweating and defervescence (body temperature decreases rapidly) - patients do not follow typical fever patterns

Fever patterns for malaria:
Vivax, Ovale, Falciparum: 48-hour cycle
Malariae: 72-hour cycle
Knowlesi: 24-hour cycle

2) Severe malaria - falciparum infection mostly, vivax occasionally
- end organ damage, eg cerebral malaria, severe anemia, renal failure, circulatory shock, hypoglycaemia

3) Relapse - recurrence of symptoms after COMPLETE initial clearing of parasitaemia due to reinvasion of bloodstream by hypnozoite (P. vivax and P. ovale)

4) Recrudescence: recurrence of symptoms because of incomplete clearing to very low levels of parasitaemia (but not fully cleared)

96
Q

Malaria diagnosis?

A

1) take history (travel location, prophylaxis, fever patterns but not useful clinically, blood/blood product transfusion etc)

2) Take specimens - peripheral blood anticoagulated with EDTA

3) Make thick and thin blood films with Giemsa, Wright or Field’s stains (1 single negative blood test DOES NOT rule out malaria)

4) Antigen testing or PCR

97
Q

Principles of malaria treatment? List some examples of medications as well

A

Suppressive therapy - chemoprophylaxis to prevent development of clinical syndromes, destroy asexual erythrocytic stages

Clinical cure: eliminate asexual erythrocytic forms during acute attack
Medication: Blood schizonticides, eg: Artemisinin based combination therapy (ACT), chloroquine, mefloquine, atovaquone-proguanil (many older drugs limited utility bc of drug resistance)

Radical cure: kill gametocytes and hypnozoites
Medication: tissue schizonticide, eg primaquine

98
Q

Methods of transmission of bacteria?

A

Most by contact - direct contact on mucosal surfaces or indirect contact on contaminated surfaces

N. meningitidis: droplet transmission

Mycobacterium TB: airborne

IASM (16 decks)

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