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E&E Exam 3 > Microbiology > Flashcards

Microbiology Flashcards

This includes bacteriology and virology.

1
Q

What is colonization resistance?

A

(Bacteria must adhere to a target cell to produce disease and if that cell has already adhered to a say resident bacteria, the pathogenic bacteria cannot bind)

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2
Q

(T/F) The receptors in the GI tract for fimbriae and carbohydrates are often specific for non-pathogenic bacteria.

A

(T)

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3
Q

What is the major defense in the small intestines against pathogenic bacteria?

A

(Peristalsis → sweeps non-adherent bacteria away)

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4
Q

What is the major defense in the large intestines against pathogenic bacteria?

A

(Specific physicochemical properties → low redox potential and fatty acids)

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5
Q

Which three cells sense and sample the intestinal contents, communicate with other immune cells, and have toll-like and NOD-like receptors to sense microbes?

A

(Epithelial, M, and dendritic cells)

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6
Q

How does the use of antimicrobial therapy put a patient at risk for GI tract infections?

A

(Decrease colonization resistance)

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7
Q

How does a change in diet put a patient at risk for GI tract infections? Two answers.

A

(Can cause a change in bacterial flora and can change gut motility)

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8
Q

What are the two routes of infection for large inoculums of pathogenic bacteria?

A

(Feco-oral route and ascending from the lower GI tract)

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9
Q

What effect do enterotoxins have on their target cell?

A

(Disruption of fluid and electrolyte regulation of the target cell)

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10
Q

What effect do cytotoxins have on their target cell?

A

(Damage and kill target cell → associated with invasion)

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11
Q

What are the three bacteria that have been shown to commonly cause GIT infection in calves?

A

(E. coli, Salmonella, and C. perfringens)

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12
Q

What are the three bacteria that have been shown to commonly cause GIT infection in adult cattle?

A

(Salmonella, Clostridium spp., and Mycobacterium avium ssp. paratuberculosis)

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13
Q

What is the causative agent of neonatal colibacillosis? Be specific.

A

(Enterotoxigenic E. coli)

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14
Q

What are the two virulence factors that the special strains of E. coli have that allow them to cause diarrhea?

A

(Fimbriae and enterotoxin)

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15
Q

(T/F) After bacteria causing neonatal colibacillosis attach to their target cells, they then invade those cells to cause further damage.

A

(F, do not invade)

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16
Q

What does it mean that the enterotoxins that enterotoxigenic E. coli produce are cytotonic?

A

(They do not damage enterocytes, they instead change cell morphology without killing the cell so they do not induce inflammation)

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17
Q

How do enterotoxigenic E. coli cause diarrhea if their enterotoxins do not damage target cells?

A

(By blocking the absorption of electrolytes, leads to electrolyte accumulation in the GIT and water efflux to follow → watery/hypersecretory diarrhea)

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18
Q

What is the most important aspect of therapy for ETEC infections?

A

(Tx of diarrhea → replace fluids and electrolytes)

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19
Q

Which species is most commonly affected by diarrhea induced by infection with Campylobacter spp.?

A

(Humans)

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20
Q

Why can Salmonella spp. GIT infections cause hemorrhage and deposition of fibrin in addition to hypersecretory diarrhea whereas ETEC do not?

A

(Salmonella has cytotoxins and endotoxins in addition to enterotoxins, the resulting inflammation also plays a role in hypersecretory diarrhea, ETEC only has enterotoxin)

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21
Q

The infection of what cells is imperative to an animal becoming a carrier for Salmonella?

A

(Macrophages)

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22
Q

(T/F) Salmonella is not a GIT normal flora.

A

(T)

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23
Q

(T/F) Clostridium perfringens is a GIT normal flora.

A

(T)

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24
Q

C. perfringens type D is associated with enterotoxemia/enteropathies (choose one) and so you will mostly see systemic/enteric (choose one) signs. (

A

Enterotoxemia, systemic signs)

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25
Q

C. perfringens types A, B, C, and E are associated with enterotoxemia/enteropathies (choose one) and so you will mostly see systemic/enteric (choose one) signs.

A

(Enteropathies, enteric signs)

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26
Q

Enteritis/dysentery induced by infection of Clostridium perfringens is typically associated with young/middle/old aged animals (choose one).

A

(Young)

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27
Q

Clostridium perfringens bacteria produce endotoxins/exotoxins (choose one) to cause mild to severe diarrhea and dysentery.

A

(Exotoxins)

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28
Q

Since Clostridium perfringens is a normal flora, it can be hard to diagnose, what are the tests of choice for the diagnosis of C. perfringens as the causative agent of diarrhea/dysentery in an affected animal?

A

(ELISA → used for detection of toxin and PCR → used for detection of enterotoxigenic strains of bacteria; a combination of both is best overall for diagnosis)

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29
Q

Brachyspira hyodysenteriae is a gram-negative/positive (choose one) spirochaete that is an obligate/facultative (choose one) anaerobe that is highly motile.

A

(Gram-negative, obligate anaerobe)

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30
Q

What is the major reserve for B. hyodysenteriae?

A

(Asymptomatic pig carriers)

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31
Q

What disease is caused by M. avium ssp. paratuberculosis that is characterized by progressive persistent, granulomatous enteritis and severe, chronic diarrhea leading to emaciation and death?

A

(Johne’s disease)

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32
Q

With Johne’s dz, the affected portions of the GIT are thickened and sclerotic due to infiltration with what cell type?

A

(Macrophages)

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33
Q

Why can Lawsonia intracellularis not be cultured?

A

(They are obligate intracellular parasites)

34
Q

What are the two syndromes that can be caused by Lawsonia intracellularis infections in pigs?

A

(Porcine proliferative enteropathy or proliferative hemorrhagic enteropathy)

35
Q

How does overeating allow C. perfringens type D to migrate from the large intestine to the small intestine where it multiplies and causes disease?

A

(Overeating leads to gut stasis and acidosis)

36
Q

What exotoxin is produced by C. perfringens type D?

A

(Epsilon prototoxin)

37
Q

Why does C. perfringens type D not cause disease in the large intestine but it does when it migrates into the small intestine?

A

(Epsilon prototoxin needs to be activated by trypsin to be absorbed into circulation and cause dz, trypsin is only present in the small intestine so when it migrates there, you get dz)

38
Q

Why do animals infected with C. perfringens type D show signs of neurologic disease?

A

(Epsilon toxin causes increased capillary permeability which leads to brain edema and eventual necrosis)

39
Q

What is the causative agent of edema disease of pigs?

A

(Shiga toxin E. coli)

40
Q

What test can be used to identify the exotoxin and pili of the STEC that causes edema disease of pigs for a definitive diagnosis?

A

(PCR)

41
Q

What clinical signs result from the release of cytokines and vasoactive amines that can occur non-specifically in response to a viral infection?

A

(Fever and depression)

42
Q

Epitheliotropic viruses cause what clinical signs?

A

(Diarrhea and ulcers)

43
Q

Endotheliotropic viruses cause what clinical signs?

A

(Hemorrhage, edema, ischemia/necrosis)

44
Q

Since you know that parvovirus affects only rapidly dividing cells, where along the microvilli epithelium do you think they affect?

A

(Crypts since that is where the rapidly dividing cells are located)

45
Q

Rotavirus is a DS RNA non-enveloped virus that replicates in what cell and where within that cell?

A

(Replicates in the cytoplasm of mature enterocytes)

46
Q

How does rotavirus cause diarrhea?

A

(Stimulates the enteric nervous system which triggers the cells in the crypts to secrete water into the lumen)

47
Q

Are antigen or antibody tests best for diagnosing rotavirus?

A

(Antigen)

48
Q

What tissues/cell types does coronavirus have a tropism for? Two answers.

A

(Respiratory and intestinal epithelium)

49
Q

What is the highly contagious alphacoronavirus that causes vomiting and diarrhea in pigs by severely blunting and fusing the intestinal villi and has a high neonatal mortality?

A

(Transmissible gastroenteritis virus)

50
Q

Is there a vaccine for transmissible gastroenteritis virus?

A

(Yes)

51
Q

What is the difference between TGE and porcine epidemic diarrhea virus?

A

(PEDV is associated with lower neonatal mortality otherwise clinical signs are similar)

52
Q

What season are bovine coronavirus (betacoronavirus 1) outbreaks usually associated with?

A

(Winter)

53
Q

Equine coronavirus (betacoronavirus 1) is usually self-limiting, acute, or chronic (choose one) and usually presents as fever, depression, lethargy, anorexia, and uncommonly, diarrhea.

A

(Self-limiting)

54
Q

Mutation of select strains of what virus results in feline infectious peritonitis virus emergence?

A

(Feline enteric coronavirus which is an alphacoronavirus 1)

55
Q

What cells does FIPV have a tropism for?

A

(Macrophages)

56
Q

Cats less than what age are the most susceptible to FIP?

A

(Cats less than 1 year of age)

57
Q

What type of inflammation occurs in all organs including the eye and brain in the dry form of FIP?

A

(Pyogranulomatous vasculitis)

58
Q

What type of inflammation occurs resultant of the wet form of FIP?

A

(Fibrinous pleuritis, peritonitis, and/or pericarditis)

59
Q

How can you tell the difference between a cat with lymphoma versus the dry form of FIP depositing pyogranulomatous lesions in the body?

A

(FIP tracks with blood vessels whereas lymphoma can be anywhere)

60
Q

What type of inclusion bodies does parvovirus (SS DNA virus) form?

A

(Intranuclear inclusion bodies)

61
Q

What is the key to limiting the transmission of parvovirus to healthy animals?

A

(Biosecurity)

62
Q

What other virus is canine parvovirus a host-range mutant of?

A

(Feline panleukopenia virus)

63
Q

Why does feline panleukopenia virus have a seasonal pattern?

A

(Because kittens are born in a seasonal pattern and FPL occurs primarily in weaned kittens after maternal antibodies wane)

64
Q

What two scenarios result from a transplacental infection of feline panleukopenia virus?

A

(Fetal death or cerebellar hypoplasia)

65
Q

What is the difference between the immune suppression caused by FPL versus canine parvovirus?

A

(FPL - panleukopenia (wow, very surprising), canine parvo - leukopenia)

66
Q

What are the two bovine viral diarrhea biotypes?

A

(Non-cytopathic and cytopathic)

67
Q

The most severe form of acute BVD is associated with which biotype of BVD?

A

(Noncytopathic)

68
Q

Which biotype of BVD can result in persistently infected animals?

A

(Noncytopathic)

69
Q

BVD vaccines are made using which BVD biotype?

A

(Cytopathic)

70
Q

If a fetus is infected with BVD at or less than 20 days of development, what results from that infection?

A

(Abortions and mummification)

71
Q

If a fetus is infected with noncytopathic BVD at or less than 150 days of development, what results?

A

(Persistently infected calf; can also get congenital defects/abortion at any point)

72
Q

What occurs when a BVD persistently infected animal is infected with a cytopathic BVD strain at any point in its life?

A

(BVD mucosal disease)

73
Q

Why are PI calves typically older, when they present with mucosal disease, than immunocompetent calves who get infected with BVD?

A

(B/c the most common way PI calves get BVD mucosal dz is there is a mutation of their noncytopathic virus to cytopathic which takes time)

74
Q

What is the causative agent of ‘cattle plague’ which presents with clinical signs including fever, anorexia, oculonasal discharge, ulcers in the mouth and on the tongue, and severe watery and bloody diarrhea?

A

(Rinderpest)

75
Q

BVD and Rinderpest have similar clinical signs, how can you tell the difference between them?

A

(Histologically, rinderpest caused the formation of syncytial cells while BVD does not)

76
Q

What is the canine morbillivirus?

A

(Distemper)

77
Q

How is canine distemper virus spread?

A

(Aerosol droplets)

78
Q

What are the two options for what follows an acute infection of canine distemper virus?

A

(Recovery and lifelong immunity or neurologic disease and death)

79
Q

Dogs with infectious canine hepatitis can shed the virus in their urine for what time frame after recovery?

A

(More than 6 months)

80
Q

What occurs in dogs after they recover from an acute infection of ICH?

A

(Immune complex glomerulonephritis)

E&E Exam 3 (8 decks)

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