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DWT Exam 3 > Bacteriology > Flashcards

Bacteriology Flashcards

1
Q

Define antibiotic resistance

A

The ability of a microorganism to survive and multiply in the presence of an antimicrobial agent that would normally inhibit or kill that particular kind of organism

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2
Q

What are the 4 basic mechanisms of resistance?

A
  1. Prevent entry of drug
  2. Pump drug out of bacteria
  3. Inactivate drug
  4. Change target site for drug
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3
Q

What is intrinsic resistance?

A

Bacteria’s natural ability to resist effects
-all bacteria of a certain type posses this ability

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4
Q

What is acquired resistance?

A

The bacteria GAINS the ability to resist a drug, where is was previously susceptible
Tends to be found in some strains/subtypes
Mechanisms of acquired bacterial resistance -> mutation, acquisition of resistance genes

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5
Q

When are susceptibility tests indicated?

A
  1. young or critically ill patients
  2. infection is at a site that is normally sterile (difficult to treat, significant impact on health)
  3. When the bacterial pathogen present has unreliable predicted susceptibility, or if rapid development of resistance is suspected
  4. Failure of presumptive or confirmed bacterial infection to respond to previous treatment
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6
Q

When are susceptibility tests NOT indicated?

A
  1. When bacteria are predictably susceptible
  2. High level of efficiency of empiric therapy
  3. If multiple bacteria is isolated from abscesses or wounds
  4. Testing of non-pathogenic normal flora
  5. Testing the susceptibility of many strict anaerobes
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7
Q

What are the three most common susceptibility tests?

A
  1. Agar disk diffusion
  2. Broth dilution tests
  3. Gradient dilution tests
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8
Q

What is an antibiotic breakpoint?

A

A value that is established based on obtainable serum concentrations of the drug and based on PK/PD data
STANDARD, fixed dose regimens

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9
Q

What are the two factors in interpretations of breakpoints?

A

Second Part I: susceptible and resistant only directly refer to concentrations of antimicrobials used in vitro
Some microorganisms are responsive in vivo, but resistant in other tissue locations

Second Part II: Breakpoints don’t indicate the ability of the drug to penetrate to the site and act within the conditions found at the site
The predicted susceptibility in vitro may not correspond to clinical efficacy

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10
Q

What is the third factor in breakpoint interpretation?

A

In vitro susceptibility testing is generally only reliable when applied to common, rapidly growing microorganisms

Infections caused by slow growing bacteria are usually treated more reliably on the basis of published guidelines

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11
Q

What is the fourth factor in breakpoint interpretation?

A

Susceptibility test results are a prediction of the expected response, not a guarantee
Extraneous factors frequently influence the outcome of antimicrobial therapy

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12
Q

What are common features of the genus Mycoplasma?

A

They are the smallest bacteria with the smallest genome of any free-living organism
They have many nutritional deficiencies and need special growth conditions for diagnosis

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13
Q

What is different about the cell membrane of Mycoplasma?

A

There is no cell wall meaning that beta-lactam antibiotics have no effect
They stain poorly with gram stains -> hard to diagnose
Their cell membrane contains cholesterol, meaning serum is needed in media to culture

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14
Q

What cells do Mycoplasma prefer to invade?

A

They prefer to colonize mucosal surfaces or RBCs of the respiratory and urogenital tract

If attached to a RBC they become a hemotropic Mycoplasmas, and some may invade host cells

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15
Q

What two tropisms is the genus Mycoplasma split into?

A

Hemotropic Mycoplasmas

Non-hemotropic mycoplasmas

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16
Q

Can hemotropic mycoplasmas replicate on their own?

A

No, they require a host to replicate

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17
Q

List the source, transmission, target cell, pathogenesis, and clinical signs of hemotropic mycoplasmas

A

Source: Carrier animals
Transmission: Blood
Target cell: Erythrocytes
Pathogenesis: extravascular hemolysis
Clinical signs: hemolytic anemia, icterus

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18
Q

How is hemotropic mycoplasma typically diagnosed and treated?

A

Diagnosis: Blood smear, PCR, serology
Treatment: tetracyclines and supportive care

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19
Q

What disease is caused by mycoplasma haemofelis and how is it transmitted?

A

Disease: feline hemotrophic mycoplasmosis
Affects cats
Transmitted by blood, fleas, or through the placenta
Diagnosed through blood smears (bacteria, agglutination, ghost cells, spherocytes) and PCR

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20
Q

What is the source, transmission, target cell, and clinical signs of non-hemotropic mycoplasmas?

A

Source: Mucosal epithelia and carrier animals
Transmission: Direct contact, inhalation of aerosols, vertical transmission
Target cell: epithelium and mesothelium
Clinical signs: depend on target cell affected
conjunctivitis, sinusitis, pneumonia, polyserositis, polyarthritis, mastitis, urogenital disease

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21
Q

How is non-hemotropic mycoplasma typically diagnosed and how is it treated?

A

Diagnosis: Presumptive, direct examination, serology, culture (low sensitivity), PCR

Treatment: tetracyclines, tylosin, aminoglycosides, macrolides, may need to cull

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22
Q

What species does Mycoplasma bovis affect and what are clinical signs associated with disease?

A

Cattle are affected

Clinical signs: mastitis, pneumonia, polyarthritis, otitis media in calves

Causes lots of economic loss and can persist in the environment for months

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23
Q

What are common characteristics of obligate intracellular bacteria?

A

They require host cells for replication
They have elaborate mechanisms for acquiring and invading host cells
They have multiple mechanisms for surviving within host cells
Dependence on host cells is usually nutritional

24
Q

What are different mechanisms of persistence and proliferation in the host cell?

A
  1. They multiply inside the vacuole (chlamydia, mycobacterium)
  2. They can survive the conditions in the phagolysosome (salmonella, yersinia, coxiella)
  3. They can escape the vacuole and proliferate in the cytoplasm (rickettsia)
25
Q

What disease is caused by coxiella burnetii and what are the transmission sources?

A

Disease: Q fever (reportable and ZOONOTIC)

Transmission sources: wildlife/tick cycle, sheep, goats, and cattle

26
Q

Briefly describe the replication of coxiella

A

Targets: monocytes, macrophages, and placental epithelial cells

Large cell variant: non-infectious, labile, metabolically active and replicating form -> INTRACELLULAR. replicate until they burst from the vacuole releasing the small cell variant

Small cell variant: infectious, highly resistant, inactive, non-replicating, extracellular form

27
Q

What are clinical signs of coxiella burnetii infection? (q fever)

A

Late term abortions and other reproductive signs

Animals may shed the bacteria even if they aren’t clinically affected

28
Q

What are common sources for infection with coxiella burnetii?

A

Secreted in milk, urine, feces, and repro secretions
Inhalation
Ingestion
Direct/venereal contact
Arthropods (ticks)
SCV resistant in environment

29
Q

How is coxiella burnetii diagnosed?

A

Presumptive -> necropsy and histopath
fetus and placenta

Direct detection -> cannot culture in lab, PCR!

Exposure to agent -> serology

30
Q

What does coxiella burnetii look like in humans?

A

Most will develop a flu-like illness with fever, fatigue, headache, muscle aches, weight loss, and cough

May progress to pneumonia and hepatitis and some may develop chronic q fever and endocarditis

31
Q

Briefly describe the reproductive cycle in the cell of chlamydia

A

Targets epithelial cells

Reticulate body is non infectious, labile, active, replicating form that has no cell wall. Multiplies through binary fission

Elementary body is the infectious, resistant, inactive form that does have a cell wall

Cell lyses and releases infectious elementary bodies

32
Q

List the target cell, source, transmission, and clinical signs of chlamydia infection

A

Target cell: epithelium
Source: diseased and carrier animals
Transmission: direct contact, inhalation, ingestion, sexual, and vertical
Clinical signs: conjunctivitis, sinusitis, polyarthritis, polyserositis, hepatitis, enteritis, encephalomyelitis, urogenital disease

33
Q

How is chlamydia typically diagnosed and treated?

A

Diagnosis is often presumptive, through serology, or PCR or cytology
Treatment is tetracyclines

Poses a public health risk as it is zoonotic

34
Q

What disease is caused by chlamydia psittaci and how is it transmitted?

A

Disease: Psittacosis, Chlamydiosis (zoonotic) affects primarily psittacine birds

Transmission: inhalation, ingestion, respiratory, feces, transmission to young thru feeding, viable in environment for 2 months

35
Q

What is the incubation period and clinical signs of chlamydia psittaci?

A

Incubation period: 3 days to weeks

Clinical signs: respiratory: nasal and ocular discharge, sneezing, conjunctivitis
GI: diarrhea
Liver: yellow droppings
Neurologic symptoms

Variable morbidity and mortality

36
Q

How is chlamydia psittaci typically diagnosed and treated?

A

Need a combination of tests
Cytology/Histopath -> choana, conjunctiva, liver
Serology -> antibody, antigen
PCR

Treatment: doxycycline or tetracycline, restrict Ca2+ access

Zoonotic -> flu-like symptoms in humans

37
Q

What do rickettsia, anaplasma, ehrlichia and neorickettsia have in common in regards to their pathogenesis

A

They are intracellular and use host cell resources

They are often transmitted through a biting insect

38
Q

List the disease caused by Rickettsia rickettsii and the host, resevoir, transmission, and target cell of the bacteria

A

Disease: Rocky Mountain Spotted Fever
Host: dogs, humans zoonotic, but not dog -> human
Reservoir: small wild animals and dogs
Transmission: vector, primarily dermacentor ticks
Target cell: endothelium

39
Q

Briefly describe the pathogenesis of Rickettsia rickettsii

A

The bacteria replicates in endothelial cells of small blood vessels, leading to an increase in permeability.

This leads to microvascular hemorrhage, vasculitis, thrombocytopenia, DIC, inc plasma loss, edema, shock, organ damage, oliguria/anuria, and hypotension

40
Q

How is rocky mountain spotted fever typically diagnosed and treated?

A

Clinical signs include: high fever and thrombocytopenia

Diagnosis: Lymph node FA, pCr, titers, and culture

Treatment: palliative, doxycycline

41
Q

List the disease caused by e. canis and e. ewingii, and list the host, vector, and target cell

A

Disease: canine ehrlichiosis -> affects dogs and cats
Host/Resevoir: other dogs
Vector: Rhipicephalus ticks
Target cell: WBCs, often see pancytopenia and decreased platelets

42
Q

How is ehrlichiosis diagnosed?

A

Serology -> snap 4dx test, serology titers
Cytology -> buffy coat, lymph node FNA
PCR -> synovial fluid examination
CBC -> thrombocytopenia

43
Q

What disease is caused by Ehrlichia Ruminatium? List the host, vector, and target cell

A

Disease: Heartwater disease (exotic and reportable)
Host/Resevoir: ruminants
Vector: amblyoma ticks
Target cells: endothelial cells and WBCs

44
Q

What are clinical signs associated with ehrlichia ruminatium?

A

Edema associated with endothelial damage often neurologic and respiratory

45
Q

How is ehrlichia ruminatium diagnosed and treated?

A

Diagnosis: blood smear, PCR, necropsy

Treatment: tetracyclines

46
Q

What disease is caused by Anaplasma Phagocytophilum? List the species affected, target cell, and clinical signs associated.

A

Disease: granulocytic anaplasmosis
Species affected: horses, dogs, humans
Target cells: neutrophils, endothelium
Clinical signs: leukopenia, arthritis, phelbitis, thrombocytopenia, limb edema, neuritis/ataxia

47
Q

How is anaplasma phagocytophilum diagnosed and treated?

A

Diagnosis: Buffy coat/ morulae -> inclusion body in neutrophil
PCR

Treatment: palliative, doxycycline, minocycline

48
Q

What disease is caused by anaplasma marginale? List the species affected and vector

A

Disease: bovine anaplasmosis
Species affected: cattle, other ruminants
Bos indicus is more resistant than Bos taurus
Young animals are more resistant than older animals
Endemic herds have little overt disease when compared to naive herds

Vector: dermacentor tick + 19 other kinds

49
Q

List the clinical signs, diagnosis, and treatment of anaplasma marginale

A

Clinical signs: fever, hemolytic anemia, abortion

Diagnosis: blood smear, PCR, necropsy

Treatment: tetracyclines

50
Q

What disease is caused by Neorickettsia helminthoeca? List the vector, definitive, and intermediate host

A

Disease: salmon poisoning disease
Vector: fluke infected with the bacteria
Definitive host: Canidae
Intermediate host: snail, salmonoids

51
Q

What is the target cell of Neorickettsia helminthoeca and what are the clinical signs associated?

A

Target cell: histocytes (tissue macrophages) of the intestines and mesenteric lymph nodes
Clinical signs: V/D, lymphadenopathy, inappetence, enteropathy due to chemokine release, edema, inflammation, hemorrhage

52
Q

How is neorickettsia helimthoeca diagnosed and treated?

A

Treatment: tetracycline for N. helminthoeca, praziquantel for the fluke

Diagnosis: fecal for fluke eggs, FNA of LN for N. helminthoeca, cytology or PCR

53
Q

What disease is caused by Neorickettsia risticii? List the terminal host, definitive host, fluke vectors, and intermediate hosts.

A

Disease: Potomac host fever
Terminal host: horse
Definitive host: bat
Fluke vector: acanthatrium spp, lecithodendrium spp
Intermediate host: snails, flies w/ water nymph stage

54
Q

What are the target cells and clinical signs associated with neorickettsia risticii?

A

Target cell: histiocytes (+/- enterocytes) likely chemokine induced enteropathy

Clinical signs: non-specific and colic, loose stool/D+, laminitis secondary to endotoxemia, abortion, 30% mortality rate

55
Q

How is Neorickettsia risticii diagnosed and treated?

A

Diagnosis: PCR on whole blood or feces

Treatment: oxytetracycline

Prevention: vax is available

DWT Exam 3 (6 decks)

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