Microbiology

Question 1

What is colonization resistance?

Answer 1

(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)

Question 2

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

Answer 2

(T)

Question 3

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

Answer 3

(Peristalsis → sweeps non-adherent bacteria away)

Question 4

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

Answer 4

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

Question 5

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?

Answer 5

(Epithelial, M, and dendritic cells)

Question 6

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

Answer 6

(Decrease colonization resistance)

Question 7

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

Answer 7

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

Question 8

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

Answer 8

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

Question 9

What effect do enterotoxins have on their target cell?

Answer 9

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

Question 10

What effect do cytotoxins have on their target cell?

Answer 10

(Damage and kill target cell → associated with invasion)

Question 11

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

Answer 11

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

Question 12

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

Answer 12

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

Question 13

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

Answer 13

(Enterotoxigenic E. coli)

Question 14

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

Answer 14

(Fimbriae and enterotoxin)

Question 15

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

Answer 15

(F, do not invade)

Question 16

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

Answer 16

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

Question 17

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

Answer 17

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

Question 18

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

Answer 18

(Tx of diarrhea → replace fluids and electrolytes)

Question 19

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

Answer 19

(Humans)

Question 20

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

Answer 20

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

Question 21

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

Answer 21

(Macrophages)

Question 22

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

Answer 22

(T)

Question 23

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

Answer 23

(T)

Question 24

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

Answer 24

Enterotoxemia, systemic signs)

Question 25

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.

Answer 25

(Enteropathies, enteric signs)

Question 26

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

Answer 26

(Young)

Question 27

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

Answer 27

(Exotoxins)

Question 28

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?

Answer 28

(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)

Question 29

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

Answer 29

(Gram-negative, obligate anaerobe)

Question 30

What is the major reserve for B. hyodysenteriae?

Answer 30

(Asymptomatic pig carriers)

Question 31

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?

Answer 31

(Johne’s disease)

Question 32

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

Answer 32

(Macrophages)

Question 33

Why can Lawsonia intracellularis not be cultured?

Answer 33

(They are obligate intracellular parasites)

Question 34

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

Answer 34

(Porcine proliferative enteropathy or proliferative hemorrhagic enteropathy)

Question 35

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

Answer 35

(Overeating leads to gut stasis and acidosis)

Question 36

What exotoxin is produced by C. perfringens type D?

Answer 36

(Epsilon prototoxin)

Question 37

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

Answer 37

(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)

Question 38

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

Answer 38

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

Question 39

What is the causative agent of edema disease of pigs?

Answer 39

(Shiga toxin E. coli)

Question 40

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

Answer 40

(PCR)

Question 41

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

Answer 41

(Fever and depression)

Question 42

Epitheliotropic viruses cause what clinical signs?

Answer 42

(Diarrhea and ulcers)

Question 43

Endotheliotropic viruses cause what clinical signs?

Answer 43

(Hemorrhage, edema, ischemia/necrosis)

Question 44

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

Answer 44

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

Question 45

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

Answer 45

(Replicates in the cytoplasm of mature enterocytes)

Question 46

How does rotavirus cause diarrhea?

Answer 46

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

Question 47

Are antigen or antibody tests best for diagnosing rotavirus?

Answer 47

(Antigen)

Question 48

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

Answer 48

(Respiratory and intestinal epithelium)

Question 49

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?

Answer 49

(Transmissible gastroenteritis virus)

Question 50

Is there a vaccine for transmissible gastroenteritis virus?

Answer 50

(Yes)

Question 51

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

Answer 51

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

Question 52

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

Answer 52

(Winter)

Question 53

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

Answer 53

(Self-limiting)

Question 54

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

Answer 54

(Feline enteric coronavirus which is an alphacoronavirus 1)

Question 55

What cells does FIPV have a tropism for?

Answer 55

(Macrophages)

Question 56

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

Answer 56

(Cats less than 1 year of age)

Question 57

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

Answer 57

(Pyogranulomatous vasculitis)

Question 58

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

Answer 58

(Fibrinous pleuritis, peritonitis, and/or pericarditis)

Question 59

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

Answer 59

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

Question 60

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

Answer 60

(Intranuclear inclusion bodies)

Question 61

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

Answer 61

(Biosecurity)

Question 62

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

Answer 62

(Feline panleukopenia virus)

Question 63

Why does feline panleukopenia virus have a seasonal pattern?

Answer 63

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

Question 64

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

Answer 64

(Fetal death or cerebellar hypoplasia)

Question 65

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

Answer 65

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

Question 66

What are the two bovine viral diarrhea biotypes?

Answer 66

(Non-cytopathic and cytopathic)

Question 67

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

Answer 67

(Noncytopathic)

Question 68

Which biotype of BVD can result in persistently infected animals?

Answer 68

(Noncytopathic)

Question 69

BVD vaccines are made using which BVD biotype?

Answer 69

(Cytopathic)

Question 70

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

Answer 70

(Abortions and mummification)

Question 71

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

Answer 71

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

Question 72

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

Answer 72

(BVD mucosal disease)

Question 73

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

Answer 73

(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)

Question 74

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?

Answer 74

(Rinderpest)

Question 75

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

Answer 75

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

Question 76

What is the canine morbillivirus?

Answer 76

(Distemper)

Question 77

How is canine distemper virus spread?

Answer 77

(Aerosol droplets)

Question 78

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

Answer 78

(Recovery and lifelong immunity or neurologic disease and death)

Question 79

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

Answer 79

(More than 6 months)

Question 80

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

Answer 80

(Immune complex glomerulonephritis)