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Y2B1 - GIT 📕 > Microbiology 🦠 > Flashcards

Microbiology 🦠 Flashcards

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1
Q

Bacterial causes of GIT infections

A

● Periodontitis and dental caries
Alpha hemolytic Streptococci (Strept. mutans)

● Gastritis and peptic ulcer
Helicobacter pylori

●Diarrhea
Campylobacter , E. coli , Salmonella, Shigella, Vibrio, Yersinia, Cl. difficile, ……

● Food poisoning
Salmonella group, Cl. perfrengens, Vibrio parahaemolyticus, Exotoxins of: (Staph. aureus, Cl. botulinum, Bacillus cereus)

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2
Q

Distribution and diseases related to Helicobacter pylori

A

H. pylori is found worldwide and is associated with chronic superficial gastritis, gastric or duodenal ulcers and gastric carcinoma.

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3
Q

what is the morphology of helicobacter?

A

Non sporulating Gram-negative curved rods, motile with multipolar flagellae.

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4
Q

diagnosis of helicobacter

A

A. Invasive tests:
- Specimen
- direct smear
- culture
- others (Rapid Urease test - DNA probe and PCR)

B. Noninvasive diagnostic tests:
- Urea breath test
- Direct detection of H. pylori antigen in the stool.

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5
Q

specimen (Helicobacter diagnosis)

A

gastric biopsy

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6
Q

direct smear (Helicobacter diagnosis)

A
  • stained with Gram or Giemsa stain to show the morphology.
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7
Q

culture of gastric biopsies (Helicobacter diagnosis)

A
  • Microaerophilic
  • Grow on nonselective media, as chocolate agar, or antibiotic-containing selective media as Skirrow’s medium and incubate for 2 - 5 days.
  • Colonies can be identified by Gram stained film and by biochemical reactions urease, oxidase and catalase positive (3 +ve).
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8
Q

what is urea breath test? And what is the function of rapid urease test?

A

■Urea breath test: radio-labeled CO2 is detected in the breath after feeding labeled urea.

■ For direct detection of urease in gastric biopsy.

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9
Q

DNA probe & PCR (Helicobacter diagnosis)

A

for identification of H. pylori in gastric biopsy.

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10
Q

what are the most important species of cambylobacter?

A

The most important human species are C. jejuni and C. coli.

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11
Q

what is considered among the most common causes of enterocolitis in children?

A

C. jejuni is among the commonest cause of enterocoloitis especially in children.

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12
Q

what is the morphology of campylobacter?

A

Curved, (seagull) Gram negative bacilli, motile with single polar flagellum. They do not form spores.

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13
Q

wet smear from stool (Campylobacter diagnosis)

A

Examined by dark-field or phase-contrast microscopy for darting motility.

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14
Q

direct smear (Campylobacter diagnosis)

A

to detect morphology.

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15
Q

culture (Campylobacter diagnosis)

A
  • Microaerophilic (grow best in presence of 5% oxygen) and 10% CO2
  • selective media: are blood-based and antibiotics-containing media are used for their isolation from stools such as Skirrow’s medium and Campy blood agar optimal temperature for growth is 42°C for C. jejuni.
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16
Q

PCR (Campylobacter diagnosis)

A

for rapid detection, culture confirmation and for typing.

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17
Q

what causes infection by C. jejuni?

A

It is an important cause of diarrhea in children and young adults. The reservoir is gastrointestinal tract of animals and human infection results from the ingestion of contaminated water, milk or undercooked foods.

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18
Q

what are the virulence factors of C. jejuni?

A
  • Endotoxin of LPS.
  • Cytopathic extracellular toxins
  • Enterotoxins.
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19
Q

what are examples of medically important vibrios?

A

● V. cholerae: the agent of cholera.

● V. parahaemolyticus: transmitted by ingestion of raw sea-food and results in diarrhea, which is not severe as cholera.

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20
Q

what is the mode of transmission of vibrios (cholera)?

A

Ingestion of contaminated water or food.

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21
Q

what are the hosts of cholera?

A

Humans are the only natural host.

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22
Q

what is the pathogenesis of cholera?

A
  • V. cholera penetrates the mucus layer covering of intestinal mucosa by secretion of neuraminidase and proteases and adhere to the mucosal cell by fimbriae and outer proteins where they subsequently produce enterotoxin which causes extensive fluid and electrolyte loss that causes → dehydration, hypokalemia, metabolic acidosis and anuria.
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23
Q

what is the clinical picture of cholera?

A

watery diarrhea with flakes of mucus and epithelial cells (rice-water stool).

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24
Q

laboratory diagnosis of first case of cholera in non-endemic area

A
  1. specimen
  2. Direct examination of the feces
  3. culture
  4. Colonies examination
  5. PCR
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25
Q

specimens for examination of cholera

A

mucus flecks from rice water stools.

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26
Q

direct examination of feces (Cholera examination)

A
  • Wet smear to detect rapidly motile bacteria by dark-field microscope.
  • Gram stained film to show morpology Comma-shaped, curved Gram negative bacilli, motile by a single polar flagellum. It is non sporing, non capsulated.
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27
Q

culture (Cholera examination)

A
  • V. cholera is highly aerobic.

●Media:
- Grow on simple media.
- Inoculation of sample on alkaline peptone water then subculture from the surface pellicle after 6-8 hrs on TCBS (thiosulphate citrate bile sucrose).
- On TCBS medium, they give yellow colonies as they ferment sucrose.

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28
Q

colony identification (Cholera examination)

A

●Gram stained film (mention morphology).

●Biochemical reactions:
- Cholera-red reaction:positive.
- Oxidase positive
- Indole positive.
- Sugar fermentation; glucose, maltose, mannite and sucrose with production of acid only.

●Agglutination with V. cholera O1 polyvalent antiserum.

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29
Q

PCR (Cholera examination)

A

to detect cholera toxin gene.

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30
Q

how is cholera diagnosed during an epidemic?

A
  • Cases can be diagnosed by microscopic examination of stools for comma shaped bacilli with characteristic motility which can be immobilized by specific antisera.
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31
Q

what are the causative organisms of food-borne infections?

A
  1. salmonella
  2. shigella
  3. vibrio species
  4. brucella
  5. staph aureus
  6. clostridia
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32
Q

compare between the morphology of salmonella & shigella

A
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33
Q

culture of salmonella and shigella

A
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34
Q

what are the media used for culture of salmonella & shigella?

A

Enrichment broth medium:
- Selenite or tetrathionate broth before agar inoculation of stool sample.

Selective media:
- Salmonella Shigella (SS) agar & Xylose-Lysine-Deoxycholate (XLD) agar

Macconkey’s agar& DA (Deoxycholate citrate agar) “indicator media”
- Pale yelow colonies as they are non lactose fermenters

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35
Q

what are the virulence factors for salmonella?

A
  1. Endotoxin, Exotoxin, enterotoxin
  2. The (VI) antigen plays a role in the pathogenesis of typhoid
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36
Q

what are the virulence factors for shigella?

A

(Shiga toxin)

Type: exotoxin = Cytotoxin

Action:
1. Inhibits protein synthesis of mammalian cells
2. Enterotoxic & neurotoxic properties.

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37
Q

what does salmonella cause?

A
  1. Food Poisoning (acute gastroenteritis)
  2. Typhoid & Paratyphoid fever (Enteric fever) “more severe”
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38
Q

which type of salmonella causes food poisoning (acute gastroenteritis)?

A

S. typhimurium & S. enteritidis

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39
Q

what is the mode of transmission of salmonela causing food poisoning?

A

Transmitted from contaminated food (poultry meat or dairy products)

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40
Q

what is the pathogenesis of infection with salmonella causing food poisoning?

A

The organisms Invade the enteric epithelium but no system infection.

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41
Q

what is the IP of salmonella causing food poisoning?

A

12-48 hours after ingestion of contaminated food.

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42
Q

what is the clinical picture of infection with salmonella causing food poisining?

A

diarrhea, vomiting & fever that last 2-5 days

“diarrhea, Vomiting and fever after nearly a day after ingesting chicken or milk —-> suspect salmonella infection”

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43
Q

what is the cause of typhoid & paratyphoid fever?

A
  • Typhoid fever caused by S.typhi & is Strictly human disease
  • Paratyphoid fever is caused by S.paratyphi A or B or C.
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44
Q

what is the method of transmission of salmonella causing typhoid & paratyphoid fever?

A

Transmitted from human reservoir by contaminated water or food.

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45
Q

what is the source of infection with salmonella causing typhoid & paratyphoid fever?

A

Case or carrier.

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46
Q

what is the pathogenesis of typhoid?

A
  • Bacteria penetrate intestinal mucosa –> multiply in mesenteric lymph nodes —> pass into blood stream causing septicemia within the first week
  • The organism lodge in the gall bladder & shed Into the intestine for weeks.
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47
Q

salmonella carriage

A

About 5% of clinically cured patients remain carriers for months or years.

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48
Q

laboratory diagnosis of salmonella case

A
  1. sample
  2. Direct film
  3. culture “the most specific”
  4. biochemical reactions
  5. serodiagnosis
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49
Q

sample for diagnosis of salmonella

A

1st week —> blood Culture or clot culture
2nd week —> feces by stool culture.
3rd week —> urine by urine culture.

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50
Q

what are the biochemical reactions used for detection of salmonella?

A

Film: Stained by Gram for characteristic morphology

Biochemical reaction:
1. Ferment glucose, mannitol, & maltose with acid & gas.
2. Lactose is not fermented.
3. H2S produced from thiosulfate.

Slide agglutination test: Using ‘O’ & ‘H’ antisera against salmonella

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51
Q

serodiagnosis for detection of salmonella

A

Widal tube agglutination test

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52
Q

what is widal tube agglutination test?

A

The patent’s serum is tested for its tires of antibodies against O,H & Vi antigens.

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53
Q

what is the diagnostic titre for salmonella in Egypt?

A

In Egypt, the diagnostic titre is 80 or more.

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54
Q

charachters of H & O antigens of salmonella

A

O Antibody appears early & disappears early
H antibody appears late & disappears late.

  • So:
    1. if O titre higher than H titre –> Eary infecton
    2. if H titre higher than O titre –> late infection
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55
Q

how are carriers of salmonella diagnosed?

A
  • Isolation of the organism from urine or feces & If negative from bile or duodenal aspirate.
  • Anti-Vi antibodies in a titre of more than 1:10 is suggestive of chronic typhoid carrier
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56
Q

what is the method of infection with shigella?

A

Fecal-Oral route as Ingestion of contaminated food & water.

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57
Q

what is the pathogenesis of bacillary dysentery (shigellosis)?

A

Bacterias multiply in large intestine, penetrate epithelial cells & multiply intercellular causing tissue destruction

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58
Q

what is the clinical picture of infection with shigella?

A

Abdominal pain, cramps, diarrhea, fever, vomiting & blood, pus or mucous in stool after 12-50 h of exposure

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59
Q

laboratory diagnosis of shigella

A
  1. sample
  2. direct film
  3. culture
  4. identification of colonies
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60
Q

sample for shigella diagnosis

A

stool which contains mucus and blood

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61
Q

how are colonies of shigella detected?

A

Film: stained by gram for charachteristic morphology

biochemical Reactions

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62
Q

biochemical reactions of shigella

A
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63
Q

what is the mode of transmission of Brucella?

A

Consuming contaminated milk or milk products (zoonosis) no human to human transmission.

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64
Q

pathogenesis of brucella

A
  • Brucellae enter through the gut.
  • They localize in the reticuloendothelial system (the lymph nodes, liver, spleen, and bone marrow).
  • Brucellae are facultative intracellular parasites, multiply in
    monocyte macrophage cells of reticuloendothelial system     (spleen, liver, bone marrow, lymph nodes and kidneys) forming granulomas in these organs.
  • Release of brucella from granulomas causes recurrent bacteraemia and recurrence of fever and chills (symptoms recur and recede at about 10 day intervals).
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65
Q

what are the types of clostridia?

this bacteria is hard to diagnose and treat

A
  • C. perfringens
  • C. botulinum “more viulence”
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66
Q

what is the mode of transmission of C. perfringens?

A

Reheated meat dishes containing spores of the organism or enterotoxins

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67
Q

pathogenesis of C. perfringens

A
  • Spores vegetate, clostridia multiply producing toxins
  • Enterotoxin form an active pore that enhances calcium influx, causing cell death.
  • This cell death results in intestinal damage that causes fluid and electrolyte loss, Leading to diarrhea and abdominal colic.
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68
Q

what is the mode of transmission of C. botulinum?

A

By direct ingestion of botulinum toxin in a contaminated food (especially home canned).

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69
Q

pathogenesis of C. botulinum

A
  • Incubation period: 18-36 hours
  • Neurotoxin acts specifically on cholinergic nerves by preventing the release of acetyl choline at the synapses and at the neuromuscular junctions causing flaccid paralysis.
  • Neurologic features: blurred vision, inability to swallow, difficulty in speech, respiratory paralysis and death.
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70
Q

diagnosis of Brucella

A
  • Specimen
  • Microscopic examination of direct film
  • blood culture
  • serology
  • Brucellin ID skin test
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71
Q

specimens for diagnosis of Brucella

A

Blood, biopsy of lymph node, spleen, liver and bone marrow.

blood sample is taken when the case has fever

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72
Q

direct film of Brucella

A
  • Gram staining is not useful to show the organisms in clinical specimens as they are intaracellular
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73
Q

blood culture of brucella

A

(Need to be obtained early in disease):

  • Incubated 3-4 weeks with 5-10 % CO2 at 37°C on enriched media.
  • Blood agar and trypticase soya agar are media of choice.
  • Identification of cultures by Gram stained film for morphology (Gram negative cocco bacilli; non-spore-forming non-motile, non capsulated) and slide agglutination with specific antiserum
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74
Q

what are the media used to grow Brucella?

A

Blood agar and trypticase soya agar

75
Q

serology of Brucella

A
  • brucella agglutination test :
    ➢ slide or tube agglutination test
    ➢ detect serum antibodies against brucella (diagn. Tire : 160 or rising)
  • ELISA to differentiate between specific IgM and IgG
76
Q

laboratory diagnosis of C. perfringens

A
  • Specimens
  • Biochemical reactions
77
Q

Specimens & culture for diagnosis of C. perfringens

A
78
Q

biochemical reactions of C. perfringens

A
  • C. perfringens ferments glucose, lactose, maltose and sucrose producing large amounts of gases and acids.
  • It produces stormy clot in litmus milk.
79
Q

what is laboratory diagnos of C. botulinum based on?

A
  • Based on clinical presentation.
  • Demonstrating toxin in the food, patient’s feces , serum, or vomitus.
80
Q

what are the causes of viral gastroenteritis?

A
  • Rotavirus
  • Norovirus (Norwalk virus)
  • Adenoviruses
  • Astroviruses
  • Enteroviruses:
    1. Poliovirus
    2. Echovirus
81
Q

what is the family of Rotavirus?

A

Reoviridae family

82
Q

what is the morphology of Rotavirus?

A

Envelope: Non-enveloped.

Capsid: icosahedral particles (with a double layered capsid).

Size: 60-80 nm in diameter.

Shape: It appears as (wheel) shape by electron microscope.

83
Q

what is the type of genome of Rotavirus?

A

Double stranded RNA.

84
Q

what is the number of segments of Rotavirus genome?

A

segmented (11 segment).

85
Q

what does the genomic segments of Rotavirus encode for?

A
  • Structural VP proteins
  • Non-structural NSP proteins
86
Q

Structural VP proteins of rotavirus

A

(VP 1 , VP 2 , VP 3 , VP 4 ,(VP 5 + VP 8 ), VP 6 and VP 7)

  • VP 7 and VP 4: structural proteins of the outer capsid.
  • VP 6: the inner capsid.
87
Q

Non-structural NSP proteins of rotavirus

A

(NSP1, NSP2, NSP3, NSP4and NSP5)

  • NSP 4: has enterotoxin like activity and can induce diarrhea in mice
88
Q

what is the method of transmission of rotavirus?

A

Feco-oral route

89
Q

incidence of infection with Rotavirus

A

Common in children between the age of 6 months and 2 years.

90
Q

what is the incubation period of Rotavirus?

A

1-4 days

91
Q

what is the pathogenesis of Rotavirus?

A
  1. The virus infects the mature enterocytes on the tips of small intestine villi, lead to villous epithelium atrophy.
  2. Compensatory repopulation of the epithelium by immature secretor crypt cells.
  3. Decrease of villous epithelium absorption, impairment of sodium and glucose absorption.
  4. Increase in intestinal water and electrolyte secretion.
92
Q

what is the clinical picture of Rotavirus?

A

(Main cause of severe diarrhea in children under 5 years of age)

  • Acute Watery non-bloody diarrhea (< 14 days)
  • (three or more loose or watery stools in a 24 hour period)
  • Vomiting
  • Fever
  • Abdominal pain.
  • If not treated: dehydration, acidosis and shock and death may occur
93
Q

diagnosis of rotavirus

A
94
Q

treatment of Rotavirus

A
  • Rehydration, either oral or intravenous.
  • Replacement of fluid and restoration of electrolyte balance.
  • In high childhood mortality, zinc supplementation has been shown to reduce the duration and severity of diarrhea and prevent subsequent diarrheal episodes.
  • No special antiviral treatment exists.
  • No antimicrobial treatment for rotavirus is recommended unless bacterial cause of diarrhea such as Shigella dysentery is found.
95
Q

prevention and control of Rotavirus

A

General measures: Good hygiene, handwashing and cleanliness of food.

Specific measures: Live attenuated oral vaccine is now available. (mention the vaccines)

96
Q

what is the main cause of severe gastroenteritis in children under 5 years?

A

Rotavirus

97
Q

what is the family of Noroviruses (Norwalk Virus)?

A

Caliciviridae

98
Q

type of genome of Noroviruses (Norwalk Virus)

A

Single-stranded RNA, linear.

99
Q

what is the morphology of Noroviruses (Norwalk Virus)?

A
  • non-enveloped.
  • Icosahedral with (32 cup-like depressions, Calyx ) on capsid surface.
100
Q

what is the method of transmission of Noroviruses (Norwalk Virus)?

A

feco-oral route

101
Q

diagnosis of Noroviruses (Norwalk Virus)

A

Stool samples collected during the first few days of illness are examined as follows:

  • Demonstration of the virus particle in stools by Electron microscopy.
  • Detection of virus genome by Reverse transcriptase PCR.
  • Antibody responses can be detected by ELISA immunoassays.
  • Infection by the Norwalk virus induces a specific IgG, IgA and IgM serum antibody response,
  • Most patients are resistant to reinfection for 4-6 months.
102
Q

what is the incubation period of Noroviruses (Norwalk Virus)?

A

24–48 hours.

103
Q

what is the second most common cause of viral gastroenteritis?

A

Noroviruses (Norwalk Virus)

104
Q

does Noroviruses (Norwalk Virus) have rapid or slow onset?

A

onset is rapid

105
Q

what are the symptoms of Noroviruses (Norwalk Virus)?

A
  • Diarrhea
  • Nausea
  • Vomiting
  • Low grade fever
  • abdominal cramps
  • headache
  • malaise
106
Q

For how long may viral shedding of Noroviruses persist?

A

Viral shedding may persist for as long as 1 month.

107
Q

what is the most common complication of Noroviruses (Norwalk Virus)?

A

Dehydration is the most common complication in young and elderly individuals.

108
Q

treatment of Noroviruses (Norwalk Virus)

A

Replacement of fluids and restoration of electrolyte.

109
Q

control of Noroviruses (Norwalk Virus)

A

Neither specific antiviral agents nor vaccines are available for treating Noroviruses.

110
Q

what are examples of Enteroviruses?

A
  1. Poliovirus
  2. Echoviruses
111
Q

what is the morphology of Poliovirus?

A

Size: Small (30 nm)

Genome: single-stranded RNA

Capsid: Icosahedral capsid Antigenically 3 types can be distinguished.

112
Q

what is the type of genome of Poliovirus?

A

single-stranded RNA

113
Q

what is the method of transmission of Poliovirus?

A

feco-oral route

114
Q

pathogenesis of Poliovirus

A
  • After ingestion of the virus, there is local multiplication in the oropharynx and associated lymph nodes. also, in the gut mucosa and regional lymph nodes.
  • Virus is produced and released into the gut (and throat initially) and can be isolated from the throat or stool for some weeks following the incubation period.
  • Viraemia follows, and the patient may experience a fever about a week after exposure.
  • Most infections are asymptomatic, although transient febrile illness in some patients.
  • Occasionally (1/100 – 1/1000 of cases) the viraemia may lead to CNS involvement and paralysis due to permanent damage to the AHC ( anterior horn column ) neurons of spinal cord .
  • About 1% of people infected with the most virulent strains experience paralysis.
  • Death is usually due to resp.failure by paralysis of the intercostal muscles and diaphragm
115
Q

what causes death in advanced cases of infection with Poliovirus?

A

Death is usually due to resp.failure by paralysis of the intercostal muscles and diaphragm

116
Q

what are the clinical forms of infection with Poliovirus?

A
  1. Abortive poliomyelitis
  2. Non paralytic poliomyelitis (Aseptic meningitis)
  3. Paralytic poliomyelitis
  4. Progressive post-poliomyelitis muscle atrophy.
117
Q

diagnosis of poliovirus

A
118
Q

vaccines for rotavirus

A

Rota Teq® (RV5): is given in 3 doses at ages 2 months, 4 months, and 6 months

Rotarix® (RV1): is given in 2 doses at ages 2 months and 4 months

119
Q

compare between polio vaccines

A
120
Q

what are the advantages of Live attenuated virus (Sabin vaccine)?

A
  1. Easy administration (oral drops).
  2. Good immunity “local” including IgA in the gut.
  3. It is also cheap to prepare and may spread to the community giving wider range of vaccination.
121
Q

what are the disadvantages of Live attenuated virus (Sabin vaccine)?

A
  1. Other wild enteroviruses present in gut may also interfere.
  2. It is very important to maintain ‘cold chain’ when storing and distributing vaccine.
  3. It cannot used in Immunocompromised patients.
122
Q

what are the advantages of Inactivated whole virus (Salk vaccine)?

A
  1. Stable.
  2. Safe and can be used in immuno-compromised.
123
Q

what are the disadvantages of Inactivated whole virus (Salk vaccine)?

A
  1. It Is given IV, so it is Difficult to administer.
  2. Gives no local immunity.
  3. Much antigen is required which makes the vaccine expensive.
124
Q

what is the number of Enteric Cytopathic Human Orphan viruses (echovirus) serotypes?

A

32 serotypes.

125
Q

echovirus is a common cause of infantile diarrhea

A

..

126
Q

what are echoviruses associated with?

A
  • Aseptic meningitis.
  • Rashes are most common in young children.
127
Q

when should infection with echovirus considered?

A
  • It’s impossible to diagnose an echovirus infection clinically.
  • However, echovirus infection must be considered in the following epidemic situations:
    1. summer outbreaks of aseptic meningitis.
    2. summer epidemics of a febrile illness with rash especially in young children.
128
Q

what is the method of transmission of Echovirus?

A

feco-oral route.

129
Q

what does Echovirus mainly infect?

A

infects young children mainly.

130
Q

diagnosis of Echovirus

A
131
Q

what family does Adenovirus belong to?

A

Adenoviridae

132
Q

what is the morphology of Adenoviruses?

A
  • 70 nm in diameter.
  • Double stranded DNA, icosahedral.
  • Non-enveloped virus
133
Q

what is the nature of Adenoviruses genome?

A

Double stranded DNA

134
Q

what is the number of Adenoviruses serotypes? and what serotypes cause infantile gastroenteritis?

A
  • There are 51 human serotypes.
  • Serotypes 40 and 41 have been etiologically associated with infantile gastroenteritis.
135
Q

what is the method of transmisson of Adenoviruses?

A

feco-oral route.

136
Q

pathogenesis of Adenoviruses

A
  • Adenoviruses replicate in intestial epithelium after ingestion.
  • It causes gastroenteritis and intussusception in infants but usually produce subclinical infections rather than overt symptoms.
137
Q

diagnosis of Adenoviruses

A
138
Q

treatment of Adenoviruses

A

Replacement of fluids and restoration of electrolyte balance.

139
Q

control of Adenoviruses

A

Neither specific antiviral agents nor vaccines are available for treating adenovirus.

140
Q

what family do Astroviruses belong to?

A

Astroviridae
(The name stems from the Greek Astron, meaning star)

141
Q

what is the morphology of Astroviruses?

A

Size: 28 nm

Genome: single stranded, positive sense RNA.

Shape: It appears as small round viruses with an appearance like that of a five- or six pointed star by direct visualization with electron microscopy.

142
Q

what is the nature of genome of Astroviruses?

A

single stranded, positive sense RNA.

143
Q

pathogenesis of Astroviruses

A
  • It causes diarrhea mainly in small children and the elderly which suggested a reduction in antibodies in recent years.
144
Q

what family do Toroviruses & Coronavirus belong to?

A

Coronaviridae

145
Q

what is the nature of genome of Toroviruses?

A

Single-stranded RNA of positive sense

146
Q

what is the shape of Toroviruses?

A

helical symmetry.

147
Q

diseases caused by Toroviruses

A
  • They are associated with persistent and acute diarrhea in children.
  • Represent an important cause of Nosocomial Diarrhea.
148
Q

what is the nature of genome of Coronavirus?

A

composed of positive sense RNA.

149
Q

what is the shape of Coronavirus?

A

Helical symmetry and a spiculated envelope that gives them the appearance of a crown.

150
Q

what do Cytomegalovirus (CMV) and Epstein Barr virus (EBV) cause?

A

Diarrhea in patients with AIDS and transplant recipients.

151
Q

classification of viruses affecting the liver

A

1- Hepatitis viruses:
* Hepatitis viruses (A, B, C, D, E, G).

2- Viruses that may affect the liver during their course of illness:
* Yellow fever virus; EBV; CMV; HSV.

152
Q

what is the family of Hepatitis B Virus (HBV)?

A

HBV is the prototype member of the family Hepadnaviridae, which has 2 subfamilies.

153
Q

Number of people infected by Hepatitis B Virus (HBV)

A
  • About 350 million persons are chronically infected with HBV worldwide.
154
Q

morphology of Hepatitis B Virus (HBV)

A
  • Virions are 42 nm in diameter and possess a nucleocapsid or “core”, surrounded by an outer coat is termed “surface antigen” or HBsAg.
  • Core contains circular partially d/s DNA plus RNA- dependent DNA polymerase (reverse transcriptase).
155
Q

Mode of transmission of Hepatitis B Virus (HBV)

A
  • Infection results from inoculation with blood or serum, blood transfusions, contaminated dental or surgical instruments.
  • Transplants; IV drug abusers; sexually; from mother to child (trans-placental and breast milk).
156
Q

pathogenesis of Hepatitis B Virus (HBV)

A
  • The virus replicates in liver and virus particles, as well as excess viral surface protein, are shed in large amounts into the blood.
  • Viraemia is prolonged and the blood of infected individuals is highly infectious.
  • Incubation period: 2 - 5 months.
  • HBV tends to cause a more severe hepatitis than other hepatitis viruses.
  • Asymptomatic infections occur frequently.
157
Q

what is the incubation period of Hepatitis B Virus (HBV)?

A

2 - 5 months.

158
Q

which causes more severe hepatitis?

A

HBV tends to cause a more severe hepatitis than other hepatitis viruses.

159
Q

chronicity & oncogenecity of Hepatitis B Virus (HBV) In infants and children

A
  • 80–90% of infants infected during the first year of life and 30–50% of children infected before the age of 6 years develop chronic infections.
160
Q

chronicity & oncogenecity of Hepatitis B Virus (HBV) In adults

A
  • less than 5% of healthy persons who are infected as adults will develop chronic infections; and
  • 20–30% of adults who are chronically infected will develop cirrhosis and/or liver cancer.
161
Q

Laboratory diagnosis of Hepatitis B Virus (HBV)

A
  • Depends on detection of hepatitis markers which include:

A. Viral antigens Markers:
- Surface antigen (HBsAg)
- ‘‘e’’ antigen (HBeAg)

B. Antibody Markers:
- Surface antibody (anti-HBs)
- “e” antibody (anti-HBe)
- Anti core

162
Q

Surface antigen (HBsAg)

A
  • ts presence in serum indicates exposure to the virus.
  • It is the first Ag to appear and the last to disappear.
  • Chronic carriers are HBsAg-positive.
163
Q

e’ antigen (HBeAg)

A
  • its presence in serum indicates that a high level of viral replication.
  • It is a marker of severe illness and high infectivity.
164
Q

Surface antibody (anti-HBs)

A
  • t becomes detectable late in convalescence, and indicates immunity following infection.
  • It remains detectable for life and is not found in chronic carriers.
  • The only marker present in vaccinated persons
165
Q

“e” antibody (anti-HBe)

A
  • It becomes detectable as viral replication falls.
  • It indicates low infectivity in a carrier.
166
Q

Anti core

A
  • IgM: Rises early in infection and indicates recent infection.
  • IgG: Rises soon after IgM, and remains present for life in both chronic carriers as well as those who clear the infection.
  • Its presence indicates exposure to HBV.
167
Q

what is the role of PCR in diagnosis of HBV?

A

The role of PCR in diagnosis of HBV infection should be limited to estimation of the virus load before, during and after treatment.

168
Q

prevention of HBV

A

1) Active Immunization
2) Passive Immunization

169
Q

method of Active immunization from HBV

A
  • Recombinant HBsAg vaccines produced in yeast have been available since 1986 and are now widely used.
  • The administration of three doses (0,1,6 months) induces protective levels of antibodies in 95% of vaccine recipients.
170
Q

Who is active immunization of HBV administrated to?

A
  • People at high risk of infection with HBV: Health care workers; sexual partners of chronic carrier and Infants of HBV carrier mothers.
  • Universal immunization of infants was introduced in Egypt since April 1995. Infants receive 3 doses at 0, 6, and 14 weeks of age.
171
Q

passive immunization of HBV

A
  • Hepatitis B immune globulin should be administered to non-immune individuals following single episode exposure to HBV-infected blood e.g. needle stick injuries.
172
Q

treatment of HBV

A

Combination therapy of both IFN-α-2A and Lamivudine gives good results.

173
Q

what are the most common viral infection?

A

In Egypt, most studies found that at least 12 - 15% of adult population have antibodies to HCV making it the most common viral infection and may be the most important health problem in Egypt

174
Q

morphology of Hepatitis C Virus (HCV)

A
  • HCV is a member of Flaviviridae. It is an enveloped virus with linear, ssRNA+ve genome.
  • The genome contains genes code for structural proteins (core, E1, E2), and nonstructural proteins (NS2, NS4A, NS4B, NS5A, NS5B and P7).
  • 6 main genotypes exist, each with several subtypes, based on sequence data. Genotype 4a is prevalent in Egypt.
175
Q

Mode of transmission of Hepatitis C Virus (HCV)

A
  • Parenteral route; Intravenous drug abusers; hemophiliacs and recipients of unscreened blood transfusions.
  • The possibility of sexual transmission? Vertical transmission?
  • Breast feeding does not appear to be a significant risk factor.
176
Q

pathogenesis of Hepatitis C Virus (HCV)

A
  • HCV infects primarily hepatocytes, but there is no evidence for a virus induced cytopathic effects on liver cells.
  • Death of hepatocytes is probably caused by immune attack by cytotoxic T cells.
177
Q

Chronicity & Pathogenecity of Hepatitis C Virus (HCV)

A
  • At least 4 of genome products (namely core, NS3, NS4A and NS5B) play roles in oncogenic pathways to cause HCC as following:
  1. Interaction and suppression of anti-oncoproteins (e.g. P21 and P53).
  2. Stimulation of production of cytokines as IL-10 (inhibits Cellular immunity), and IL-6 (inhibits innate immunity).
178
Q

Laboratory diagnosis of Hepatitis C Virus (HCV)

A

1) Serology
2) Viral genome detection

179
Q

serology of Hepatitis C Virus (HCV)

A
  • Reliable serological tests (e.g. ELISA) confirmation by a more specific test like RIBA (Recombinant Immune Blotting Assay) in low prevalence countries.
  • In Egypt we do not need confirmation of ELISA by RIBA but instead we go to do PCR.
180
Q

viral genome detection of Hepatitis C Virus (HCV)

A

PCR (quantitative and qualitative) detects viral genome in patient’s serum, in liver biopsy or in macrophages.

181
Q

prevention of Hepatitis C Virus (HCV)

A
  • No vaccine; Prevention of infection spread and health education are essential to minimize exposure
  • Health care workers in contact with body fluids should learn the principals of infection control.
182
Q

treatment of Hepatitis C Virus (HCV)

A
183
Q

what is the current regimen in Egypt for treatment of Hepatitis C Virus (HCV)?

A

The current regimen give in Egypt is combination of Sofosbuvir (Sovaldi) and Daclatasvir (Daklinza) for 12 to 24 weeks based on existence of cirrhosis.

Y2B1 - GIT 📕 (9 decks)

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