Micro Flashcards

1
Q

Transformation vs conjugation (homologous vs nonhomologous recombo) vs transduction vs transposition

A

Integrating foreign genetic material from environment into host genome of bacterial cell vs bacterial mating/sexual reproduction that involves conjugation bridge made of sex pili and it transfers Fertility (F) factor unidirectionally from donor male (F+) to recipient female (F-) (transfer b/w 2 closely related DNA sequences vs transfer b/w 2 not-alike DNA sequences) vs a virus/vector that transfers genetic material into bacterium aka bacteriophage infection vs transfer of DNA by a transposon; transfer plasmid-to-plasmid or plasmid-to-genome

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2
Q

outcomes of genetic transfer

A
  • No change
  • Loss of gene activity – if new DNA interrupts a chromosomal gene
  • Enhanced gene function – if new DNA turns on a promoter or turns off a repressor
  • New gene activity – if new DNA encodes a gene that was not previously in the bacterium and if new gene can be expressed in functional form
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3
Q

definitive host vs intermediate host vs reservoir vs vector

A

host in which a parasite = sexually mature –> sexual reproduction vs host required for completion of parasite life cycle, but parasite = sexually immature –> undergo asexual reproduction vs host that harbors an infection that can be transmitted to humans; generally have asymptomatic or minimal disease vs organisms (often arthropods) that transmit parasite; often are also intermediate hosts

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4
Q

how can parasites evade immune response?

A

change stages, change host, intracellular escape (hide from immune response), ag variation (change coat/shed it), molecular mimicry (look like host)

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5
Q

sxs of hookworm dz

A

Itching and rash at site of larval entry, anemia and protein deficiency

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6
Q

sxs of ascariasis. how is it transmitted?

A

intestinal blockage; if extraintestinal infxn –> pneumonitis, eosinophilic asthma-like response (basically trigger parasite immune response). ingest eggs

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7
Q

location of Onchocerca volvulus

A

Africa, Central and South America

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8
Q

sxs of Onchocerciasis or River Blindness

A

painless skin nodules, blindness; both from inflamm response to dying larvae

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9
Q

which nematode has Tissue tropism?

A

Toxocara canis; from intestines throughout body via blood, but most disease associated with liver or eye infection

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10
Q

3 dx of toxocara canis that all must meet

A

Clinical signs
Exposure to puppies or kittens or history of pica
Lab findings (including eosinophilia) and serology using serum or vitreous humor

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11
Q

Taenia solium: cysticercosis vs neurocysticercosis vs taeniasis

A

“bumps” under skin that may be tender vs variety of neurologic symptoms from headache to sz vs GI disease; tapeworm lodges in sm. intestine
Generally asymptomatic apart from detection of proglottids in feces (can be large enough to be detected by eye)

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12
Q

Diphyllobothrium latum can have migrating proglottids. What can happen?

A

cause intestinal obstruction and cholangitis

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13
Q

Hymenolepis nana (dwarf tapeworm)

A

found in young children w/ heavy infxn, can present w/ itchy anus or HA. dx: eggs in stool; misdx: E. vermicularis (pinworm)

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14
Q

Dipylidium caninum

A

from swallowing infected flea. asymptomatic. dx: detection of proglottids on perianal region, in stool, in diapers, on floor coverings or furniture; are mobile when passed, so often mistaken for fly larvae (maggots) or a grain of rice

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15
Q

Fasciolopsis buski –> Fasciolopsiasis

A

from human and swine reservoirs, from raw or undercooked aquatic plants bearing cysts. asymptomatic. dx: presence of adult flukes or eggs in feces or vomit

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16
Q

Fasciola hepatica –> Fascioliasis

A

snails = intermediate host, ruminants = more definitive host; from ingestion of raw freshwater plants. tissue tropism: liver & bile ducts. has 2 stages: 1) Acute phase – larval fluke migrates from intestines to liver –> inflamm, tissue destruction, toxic/allergic rxns, non-specific symptoms of abdominal pain, N/V, hepatomegaly, fever). Labs = elevated eos and transaminase levels; 2) Chronic phase – months to yrs after infection; inflammation and intermittent blockage of bile ducts or gallbladder (cholangitis, cholecystitis); pancreas = inflamed. dx: Eggs in stool or drainage/aspiration of duodenal or biliary tissue; Pseudofascioliasis – eggs in stool d/t recent ingestion of sheep or beef liver that contained eggs

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17
Q

Which trematode has immunoevasion by adults?

A

Schistosoma spp; secrete substances that resemble host proteins, coating themselves

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18
Q

Schistosomiasis/bilharziasis (4)

A
  • Katayma’s fever – occurs with egg production. Rash and itchy skin 1-2 days after infection, then cough, fever, abd. pain, diarrhea 1-2 months later
  • Tissue-specific manifestations as infection continues, have tissue fibrosis and granulomatous lesions around eggs
  • Many symptoms are immune-mediated – fibrosis (reduced organ function), granulomas, immune-complex formation, hypersensitivity (to eggs)
  • Hepatosplenomegaly and cirrhosis associated with chronic infection
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19
Q

how to dx schistosomiasis/bilharziasis?

A

eggs in stool or urine, serology by EIA possible using serum

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20
Q

giant roundworm vs pinworm vs hookworm vs tapeworm

A

Ascaris lumbricoides vs Enterobius vs Anklystoma duodenale, Necator americanus vs cestodes (carnival)

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21
Q

what does it mean for fungi to be systemic?

A

can spread to other organs

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22
Q

transmission, sxs, tx of histoplasmosis

A

bat/bird feces, environment to person; pulm dz but depends on intensity of exposure and immunologic status of host; tx depends on patients’ immune competence (Most resolve with supportive care and no antifungal)

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23
Q

how to dx coccidiodes?

A

Several serologic tests available (skin test common)

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24
Q

what does paracoccidiodes look like at 37 degrees C?

A

six or more blastoconidia connected to parent cell called “mariner’s” or “pilot-wheel”

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25
Q

how to distinguish aspergillus vs mucor?

A

acute angle hyphae vs right angle hyphae

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26
Q

sxs of Pneumocystosis/PCP

A

ground glass on CXR, exudate w/ plasma cells, hypoxia

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27
Q

which opportunistic and systemic fungus produce biofilms?

A

candida albicans

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28
Q

is candida spp endo or exogenous infxn?

A

mainly endo but can be exo from room contaminated equip or person to person

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29
Q

sxs of candida spp

A

Cutaneous infections occur in areas where skin surfaces occlude and are moist (i.e. armpits, groin, in between toes) and underneath toe/fingernails; Hematogenous candidiasis results in seeding of Candida into deeper tissues like the heart, eyes, bones/joints, and brain

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30
Q

how to dx vs tx candida spp?

A

Skin scraping and KOH, Culture to ID species level for later antifungal treatment choice, CHROMagar allows detection of mixed species of Candida vs Antifungal resistance and biofilm formation complicate treatment,
Remove nidus of infection to increase treatment success, Prevention is preferable to treatment (Avoid broad spectrum antimicrobials, meticulous catheter care, rigorous adherence to infection-control precautions, better hygiene practices)

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31
Q

why is candida auris rising?

A
  • Often multidrug resistant (some resistant to all antifungal classes)
  • Difficult to identify and can be misidentified leading to inappropriate management
  • Causes healthcare outbreaks (Spreads easily between hospitalized patients and nursing home residents)
  • 30-60% mortality in patients with C. auris (however, it is typically a secondary infection)
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32
Q

2 causative agents of cryptococcus?

A

C. gattii and C. neoformans

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33
Q

how to dx cryptococcus?

A
  • Microscopy of CSF by gram stain or India ink or other stains show encapsulated budding yeasts
  • Direct detection of the capsular polysaccharide antigen (CrAg) in serum or CSF (Doesn’t differentiate C. gattii from C. neoformans –> use CGB agar to differentiate: yellow = neoformans, blue = gatti)
34
Q

C. gattii causes parenchymal lesions known as?

A

cryptococcomas

35
Q

sxs of mucor and rhyzopus/mucormycosis

A

-Pulmonary – presents like pulmonary aspergillosis
Fungi can invade into pulmonary vessels (angioinvasion) causing infarction, embolism and thrombosis
-Hemorrhage with hemoptysis (can be fatal)
-Associated with cancer patients on chemotherapy and organ or stem cell transplant recipients (neutropenic)
-Gastrointestinal – can lead to hemorrhage and/or perforation; more common in children and young infants
-Cutaneous – most common form in immunocompetent individuals; can also result from hematogenous dissemination
-Disseminated – infection spreads and involves the brain

36
Q

how is malasezzi furfur transmitted? where does it infect?

A

direct contact, not in environ or animal. No immune response to keratinized surfaces –> infxn is chronic and persistent

37
Q

how are dermatophytes transmitted?

A

Geophilic – environment to humans or animals
Zoophilic –animals to humans
Geophilic/zoophilic are inflammatory and respond well to therapy
Anthropophilic –from person-to-person
Chronic, relatively non-inflammatory, difficult to cure

38
Q

tinea = subq infxn. what does this mean?

A
  • Infect skin, nails or in/on hair shaft – ectothrix, endothrix, favic
  • Tropism for keratinized tissue, secrete keratinases that can degrade cutaneous tissue but DO NOT invade deeper into the subcutaneous tissue
  • Risks included weakened immune system, public showers, locker rooms, sharing personal items i.e., hairbrushes, clothing, hats
39
Q

how is sporothrix schenkii transmitted?

A
  • Spore enters body by direct inoculation/small break in the skin
  • Spore can be inhaled to cause pulmonary disease
  • Can become disseminated; seen in people with compromised immune response (HIV, COPD, diabetes, alcoholism)
40
Q

sxs of sporothrix schenkii (lymphocutaneous sporotrichosis)

A
  • Cutaneous: small painless nodular lesions that grows and often becomes ulcerated and are slow to heal
  • Pulmonary: cough, dyspnea (shortness of breath), chest pain, fever
  • Disseminated: can spread by lymphatic system, signs depends on tissue infected
41
Q

what is Chromoblastomycosis?

A

caused by Fonsecaea pedrosoi. Dematiaceous (naturally pigmented) molds
In situ, Medlar bodies or copper penny bodies that are chestnut brown (melanin), thick-walled cells w/ septa
Transmitted from environ to person
dx: skin scrapings, KOH prep, microscopy
tx: extremely difficult! Cryo- or heat therapy
Squamous cell carcinomas can occur within chronic lesions

42
Q

Hortaea werneckii (tinea nigra)

A

branched septate brown hyphae. transmitted by inoculation of contaminated material into a break in the skin; not infectious –> can’t go person to person. sx: pigmented (gray to black) macule(s), no scaling or invasion of hair follicles, patches are non-inflammatory. dx: skin scrapings (KOH), confirm with culture. tx: topical azole

43
Q

Epidermophyton vs microsporum vs trichophyton

A

Macroconidia: Smooth-walled, borne in clusters of two or three; microconidia: absent; hair invasion: none vs Macroconidia: Numerous, large, thick and rough-walled; microconidia: rare; hair invasion: ectothrix vs Macroconidia: Smooth-walled, rare; microconidia: numerous, spherical teardrop or peg shaped; hair invasion: endothrix

44
Q

Koch’s postulates

A

microbe must be found in all orgs that are sufferring the dz and not in healthy orgs, microbe must be isolated from dzed org and be grown in pure cx, that cx should cause the exact dz when inoculated to healthy host, microbe should be reisolated and grown in cx and be identical to orig microbe

45
Q

Koch’s postulates supports Germ Theory but has limitations:

A

not all microbes can be grown in lab, not all microbes cause same dz to everyone equally, some microbes can cause diff dz’s, one dz can by caused by mult microbes

46
Q

Coccobacillus vs Vibrio vs Fusiform bacillus

A

an oval coccus vs curved, comma-shaped rod vs rod with tapered ends

47
Q

examples of DNA viruses

A

Hepadnaviridae, Herpesviridae, Adenoviridae, Parvoviridae, Poxviridae, Papillomaviridae, Polyomaviridae. 2x stranded x/ Parvoviridae

48
Q

examples of pos sense ssRNA viruses

A

retrovirus, togavirus, flavivirus, coronavirus, hepevirus, calcivirus, picornavirus. Retroviridae = dsRNA –> double layered capsid

49
Q

characteristics of RNA viruses

A

All neg sense are enveloped and have helical capsid

All non-enveloped have icosahedral capsid

50
Q

how does virus enter host cell?

A

viral attachment protein binds to protein or carb of specific receptor; binding has no energy or temp requirement. VAP on naked viruses = part of capsid structure, on enveloped viruses = inserted into viral envelope. some viruses need coreceptor w/ host cell

51
Q

parasite development: Cysts vs Oocysts vs Sporulated cysts vs Ova vs Larvae

A

parasite develops a thick cell wall to protect against harsh environment or in nutrient-poor environment vs fertilized oocyte that is encysted (thick cell wall) and excreted into the environment vs after excretion, ova develop into sporozoites while encysted vs fertilized vs intermediate stage between ova and adult

52
Q

parasite structure: Tegument vs Proglottids

A

tough exterior surface found on most helminths vs individual segments of tapeworms

53
Q

parasitic movement: Flagella and cilia vs Pseudopodia

A

inserted into cell membrane vs cytoplasmic extension, integral to cell membrane, in protozoa

54
Q

fungi: mold vs yeast

A

generally multicellular, replicating by fission and hyphae formation; filamentous/wooly/hairy; saprobic phase vs generally single cell that replicates by budding; buds = blastoconidia, germ tubes = pseudohyphae; parasitic phase

55
Q

fungi cell wall

A

rigid, contains chitin and beta glucan; has ergosterol instead of chol

56
Q

fungi: mycelia vs conidia

A

mat-like structures formed by many hyphae vs asexual reproductive structures produced by aerial hyphae –> airborne dissemination

57
Q

what are some fungi dimorphic?

A

one phase to increase infectivity, one stage to grow and disseminate in host

58
Q

fungal asexual sporulation: sporangia vs conidia

A

asexual spores contained within a sporangia vs asexual spores with no containment

59
Q

ectoparasite vs endoparasite vs protozoa

A

vectors vs metazoa (helminths) vs protozoa

60
Q

bacterial replication: sporulation vs germination

A

metabolically inactive (vegetative or dormant); bacteria under stress; 1 chrm = surrounded by dehydrated cortex w/ keratin-like protein coat + dipicolinic acid vs metabolically active with triggers of mechanical stress, changes in environment (e.g., pH, water), or presence of specific nutrients (e.g., alanine)

61
Q

Quorum sensing vs Pathogenicity islands vs Operons

A

process in which each bacterium in microenvironment produces a specific small molecule, and when enough bacteria (i.e., a quorum) are producing the factor, the behavior of all bacteria in the group changes in some way to benefit ALL bacteria; ex: biofilm production vs group of genes controlled by a single promoter that function together to generate a specific virulence mechanism; very often a type III secretion system vs group of genes with shared functions that are grouped together in a DNA sequence; a means to coordinate gene expression

62
Q

describe transcpxn vs transln in pos sense viruses

A

viral RDRP makes neg template from pos mRNA –> RDRP makes more pos mRNA from neg template. ex: picorna, noro, toga, flavi, corona

63
Q

describe transcpxn vs transln in neg sense viruses

A

newly transcribed pos mRNA in viral particle –> RDRP makes neg mRNA from pos template. ex: rhabdo, paramyxo, orthomyxo, bunya, filo

64
Q

transcpxn & transln of retroviruses

A

positive sense RNA genome = converted to complementary DNA (cDNA) via RNA-dependent DNA polymerase (reverse transcriptase (RT)) w/in virus –> cDNA = transported into the nucleus –> cDNA = integrated into the host cell DNA => provirus –> host DNA-dependent RNA polymerase transcribes the viral DNA sequence into mRNA –> full-length positive sense RNA progeny genomes

65
Q

describe DNA virus replication

A
  1. attachment/absorption: VAP binds to specific host receptor
  2. penetration: virus uses energy and/or temp to penetrate capsid into cell
  3. uncoating:
    - non-enveloped capsid releases genome into cyto/nuc => virioplexis
    - enveloped virus does membrane fusion w/ VAP
    - non/enveloped virus can do receptor-mediated endocytosis
  4. replication: using host transcpxn/sln to replicate viral DNA
  5. assembly: progeny virions made
  6. release: progeny virions released and kills cell –> can infect new cells
66
Q

how can viruses alter cell metab vs directly dmg cell?

A

o DNA viruses inhibit cellular DNA synthesis.
o RNA viruses shut down synthesis of host RNA.
o Production of viral proteins interfere with production of host proteins.
o Viral genes or proteins can override growth regulatory signals in host cell.
vs
o Lysis as progeny virions = released
o Compromised membrane integrity due to membrane loss as progeny viruses bud from host cell
o Toxicity of newly synthesized viral proteins –> cytopathic effect/cytopathicity/cytopathogenesis

67
Q

is mutation rate high or low for DNA vs RNA polymerase?

A

low vs high b/c no proofreading

68
Q

selection vs antigenic drift vs antigenic shift

A

favored development of particular virions (ones that have high virulence) vs minor changes in genetic sequence d/t random point mutations –> little effect on dz severity vs major changes d/t genetic reassortment –> significant effect on disease severity

69
Q

2 mechanism for exchanging viral genetic info: recombination vs reassortment

A

sequence similarity between two distinct genetic elements –> can create new genotypic virions or a provirus vs single cell is infected with 2 genetically distinct viruses –> mix gene segments

70
Q

lytic vs non-lytic infxn

A

mature virions = fully formed inside the cell –> cell lysis triggered –> release progeny virions
vs
o Exocytosis – viral proteins inserted in ER membrane –> assembled capsids enter ER and progress through Golgi –> transported to cell surface in vesicles “pinched off” from Golgi –> vesicles fuse with cell membrane –> expel virus
o Budding – viral glycoproteins = inserted into cell membrane –> viral capsids form at the cell surface –> extrude from the cell membrane –> pinches off and seals –> release progeny virions

71
Q

what are prions? PrPC vs PrPSC. Process of virion replication

A

misfolded PROTEINS (no nucleic acid). natural form, 3 alpha helices, sensitive to proteinase K vs mutated form, beta pleated sheets, resistant to proteinase K. PrPC misfolds to PrPSC and enters brain (or random already mutated PrPSC enters brain ) –> PrPSC binds to PrPC –> PrPC becomes PrPSC –> undergoes conformational change in cyto and ER –> form fibrils –> fibrils break off and disseminate –> fibril formation at other sites

72
Q

what are defective particles or virions?

A

incomplete viral particles that are non infectious
o Lack some genetic information required for replication and infxn
o Partial or complete loss (empty viral capsids)
o Can function as “immune decoys” – e.g., influenza virus, hepatitis B virus (HBV)

73
Q

Polycistronic mRNA vs Monocistronic mRNA vs Polyprotein

A

Multiple proteins translated from a single mRNA – each with defined start and stop sites; proks and pos sense ssRNA viruses vs One protein per mRNA strand; euks vs One long protein translated from mRNA, then cleaved into separate proteins; usually functionally related

74
Q

cell media: Non-selective vs Enriched or complex vs Selective vs Differential

A

standard medium vs contains extra supplements to encourage growth vs allows some to grow, but suppresses growth of others vs growth of different organisms produce different effects based on microbe’s physiology

75
Q

Bacteriostatic drugs vs Bactericidal drugs

A

inhibit bacterial growth and reproduction by inhibiting RNA synthesis –> Delay bacteria until host immunity can kill vs directly kill bacteria by inhibiting cell wall or DNA synthesis –> Not dependent on host response –> more rapid effect

76
Q

Sterilization vs Disinfection

A

complete removal of all microbial organisms – vegetative, sporulated, pathogenic and commensal organisms; only on inanimate objects vs elimination of MOST pathogenic, vegetative microorganisms; on inanimate objects

77
Q

4 major ways to control/elim microbes: antisepsis, heat, radiation, and chemicals

A
  • Antisepsis – elimination of most pathogenic, vegetative microorganisms on animate objects; chemical treatments only
  • Heat – dry heat and wet heat (e.g., boiling). Most efficient form is autoclaving –> destroy all organisms, viruses, and spores, but may not denature prions
  • UV light – UV-A, UV-B, and UV-C causes thymine dimers to form –> mutations –> possible death
  • Ionizing radiation like X-rays and gamma rays
  • Chemicals that denature enzymes – challenges include generation of toxic waste that requires special disposal or incidental exposure to product (carcinogens); ex: Phenol derivatives (Lysol) and aldehydes (formalin), Chlorine and iodine, Heavy metals (mercury, silver, copper), Ethylene oxide
  • Chemicals that denature membranes like soap and alc
78
Q

Trichuris trichuria

A

Soil-transmitted (feces outside contaminate food)

  • Southern US
  • Symptoms: rectal prolapse (mucus and blood in stool)
  • Children can have long-term complications (anemia, neuro)
  • Diagnosis via polar plugs - ova in stool
79
Q

Brugia malayi

A
  • Vector: Aedes or Mansonia mosquito
  • Results in lymphatic filariasis (lymphedema, possible elephatiasis)
  • Diagnosis: blood smears with microfilariae - must collect between 10PM and 2AM
80
Q

antibacterial targets: cell wall biosynthesis vs protein synthesis vs nucleic acid synthesis vs cell membrane integrity vs virulence factor activity:

A

peptidoglycan synthesis and β-lactam antibiotics vs 30S ribosomal subunit and aminoglycosides –> Aminoglycosides bind 30S ribosomal subunit –> inhibit initiation and cause misreading of mRNA codon –> protein mutation; 50S ribosomal subunit and erythromycin –> Macrolides (e.g., erythromycin) bind 50S ribosomal subunit –> inhibit tRNA translocation –> prevent peptide bond formation b/w amino acids vs DNA gyrase makes cuts to relieve tension of DNA strand as it is unwound during replication; Quinolones (e.g., ciprofloxacin) bind DNA gyrase (topoisomerase II) and topo IV causing release of cut DNA – a fatal event
vs mycobacterial mycolic acid synthesis and isoniazid vs exotoxins and vaccine-induced antibodies

81
Q

T. brucei

A

transmitted by tsetse fly from Africa (East and West)