Mhr Exam 2

Front 1

Protozoa, single-celled or multicellular?

Back 1

Single-celled

Front 2

Metazoa, aka?

Back 2

Helminths

Front 3

Metazoa, single-celled or mulicellular?

Back 3

Multicellular

Front 4

Name the three types of helminths we discussed

Back 4

Cestodes, trematodes, and nematodes

Front 5

Cestodes, aka?

Back 5

Segmented worms

Front 6

Trematodes, aka?

Back 6

Flatworms

Front 7

Nematodes, aka?

Back 7

Roundworms

Front 8

Hexopoda, aka?

Back 8

Lice, 6 legs, eg. crabs

Front 9

Arachnida, aka?

Back 9

Mites, 8 legs, eg. scabies

Front 10

Most prevalent parasitic infection worldwide

Back 10

Toxoplasmosis

Front 11

What are the four species of Plasmodium causing malaria? (that we are concerned with)

Back 11

P. Falciparum, P. Vivax, P. Ovale, P. malariae

Front 12

Life-stage of Plasmodium injected into human by mosquito

Back 12

Sporozoites

Front 13

Plasmodia infecting liver cells is in this life-cycle

Back 13

Exoerythrocytic cycle (out of blood)

Front 14

Life-stage of plasmodia developing in hepatocytes

Back 14

Merozoites

Front 15

Life-stage of Plasmodia in blood cells

Back 15

Ring-form trophozoites

Front 16

Red cells infected with plasmodia that has undergone replication cycle(s)

Back 16

Schizont

Front 17

Life-stage of plasmodia taken up by uninfected mosquito that will allow for infection of new host

Back 17

*gametocyte

Front 18

Species of Plasmodium that typically causes more rapid disease onset

Back 18

P. falciparum

Front 19

RBCs that can be infected by P. falciparum

Back 19

All stages of RBC development

Front 20

Does P. falciparum persist in liver after main bout of infection?

Back 20

No

Front 21

Can many stages of life-cycle be seen in RBCs infected with P. Vivax?

Back 21

Yes

Front 22

Which species can be identified in a blood smear by visible schizonts? (P. falciparum or P. vivax)

Back 22

P. vivax

Front 23

Main problem with malaria

Back 23

anemia

Front 24

Which species of Plasmodium shows >3% infection of RBCs on a blood-smear

Back 24

P. falciparum

Front 25

Which species of Plasmodium shows >1 ring-form trophozoite in a given RBC

Back 25

P. falciparum

Front 26

Two nuclear "dots" in a ring-form trophozoite is characteristic of what Plasmodium species

Back 26

P. falciparum

Front 27

What are the life-stages of P. falciparum visible in the blood

Back 27

Ring-form trophozoite, and gametocyte

Front 28

Differentiate between P. falciparum and P. vivax gametocytes

Back 28

P. falciparum - small, banana shaped
P. vivax - large, diffuse

Front 29

An added danger from P. falciparum

Back 29

Microthrombi (brain especially)

Front 30

Which plasmodium is associated with drug resistance

Back 30

P. falciparum

Front 31

Is babesia endemic in the US?

Back 31

Yes

Front 32

Transmission of babesia is through?

Back 32

Ticks

Front 33

Person at increased risk of severe reaction to babesia infection might have

Back 33

Splenectomy, immunosuppression

Front 34

Leishmania is transmitted by

Back 34

Sand-flies

Front 35

Life-stage of leishmania causing initial infection

Back 35

Promastigote

Front 36

Three main species of Leishmania

Back 36

L. tropica, L. braziliensis, L. donovani

Front 37

What cell type is the main target of Leishmania

Back 37

Macrophages

Front 38

What life stage of Leishmania multiplies in macrophage

Back 38

Intracellular amastigotes

Front 39

Leishmania tropica is characterized by (externally apparent)

Back 39

Progressive lesion, non-responsive to standard antibiotics

Front 40

Leishmania is diagnosed by

Back 40

Biopsy of lesion edge, presence of macrophages with intracellular asmastigotes

Front 41

Leishmania amastigotes can be identified by

Back 41

presence of a "bar" (mitochondrion)

Front 42

What is a characteristic of L braziliensis that differs from other species?

Back 42

Can escape blood and infect mucosal tissues

Front 43

What is characteristic of L donovani that differs from other species?

Back 43

Causes a "higher level", disseminated infection - Kala-azar dermal reaction

Front 44

What part of the adaptive immunity is protective against Leishmania infections?

Back 44

Th1 cells, (Th2 for Kala-azar of donovani infection)

Front 45

How does Trypanosoma transfer from its insect vector into a person

Back 45

Trypomastigotes are present in kissing bug defecation and invade bite site or mucosa

Front 46

What life-stage is Trypanosoma in when it infects an individual?

Back 46

Trypomastigote

Front 47

What type of cells will T. cruzi infect?

Back 47

All nucleated cells

Front 48

What life-stage of T. cruzi generally resides in tissue?

Back 48

Amastigotes

Front 49

What life-stage of T. cruzi can be found in circulating blood?

Back 49

Trypomastigotes

Front 50

What are some of the pathologies associated with T cruzi infections

Back 50

Cardiomegaly, megacolon, megaesophagus (and chagoma (swollen face))

Front 51

What are some common symptoms of acute Chagas disease (T cruzi infection)

Back 51

Fever, malaise, anorexia, edema, myocarditis, meningoencephalitis

Front 52

What is the intracellular life-stage of T cruzi?

Back 52

Amastigote

Front 53

How can the intracellular amastigote of T cruzi be identified histologically?

Back 53

Presence of a large mitochodrion within amastigote cytoplasm

Front 54

Which aspect of the adaptive immunity helps give the most protection against T cruzi infections?

Back 54

?Th1 cells?

Front 55

How are Trypanosoma brucei gambiense and T.b. rhodesiense transmitted?

Back 55

Tsetse fly bites

Front 56

What life stage is T. brucei in when it infects an individual

Back 56

metacyclic trypanosome

Front 57

Where does the infection from T. brucei present

Back 57

Chancre forms in bite wound

Front 58

Are there any intracellular stages with the African trypanosoma (T. brucei)?

Back 58

No

Front 59

Encephalomyelitis caused by T brucei can result in

Back 59

Sleepiness (African Sleeping Sickness)

Front 60

What is winterbottom sign and what is it associated with?

Back 60

Enlarged cervical lymph node, caused by T brucei

Front 61

What is special about T brucei's relationship with immune responses?

Back 61

Surface antigen variation, causes recurrent "waves" of parasitemia

Front 62

How is Toxoplasma gondii transmitted?

Back 62

Animal feces, especially cats.

Front 63

What parasitemia is often associated with owning cats

Back 63

Toxoplama gondii

Front 64

What life-stage is T gondii transmitted to humans in

Back 64

Oocyst

Front 65

What life-stage of T gondii infects liver cells

Back 65

Tachyzoites

Front 66

What pathologies are associated with a Toxoplasma gondii infection

Back 66

Brain lesions, chorioretinitis, hepatitis, lymphadenitis

Front 67

What are the risks to a fetus with a mother newly infected with toxoplasma

Back 67

Congenital hydrocephalus, mental retardation

Front 68

How is Entamoeba histolytica transmitted?

Back 68

Fecal-oral transmission

Front 69

What life-stage is Entamoeba histolytica transmitted to a new individual in?

Back 69

Quadranucleate cysts

Front 70

What pathologies are associated with E hystolitica

Back 70

Liver abscess, brain abscess, flask-shaped ulcers in colon

Front 71

What life-stage of E histolytica invades colon tissue

Back 71

Trophozoites

Front 72

What are the histological indicators for E histolytica over other protozoa?

Back 72

Dark staining ring around nucleus, and phagocytosed RBCs

Front 73

How is Giardia lamblia transmitted?

Back 73

Fecal-oral pathway

Front 74

What life-stage is G lamblia in when transmitted to an individual

Back 74

Quadranucleate cyst

Front 75

What life-stage of G lamblia infects surface of intestinal villi?

Back 75

Trophozoite

Front 76

What histological changes does a G lamblia infection cause

Back 76

flattening of intestinal villi

Front 77

What symptoms are commonly associated with a G lamblia infection

Back 77

Explosive, watery diarrhea

Front 78

What part of the adaptive immunity is protective against a giardia infection

Back 78

Secretory IgA

Front 79

How is Cryptosporidium parvum transmitted

Back 79

Fecal-oral transmission

Front 80

What life-stage is Cryptosporidium parvum transmitted in

Back 80

Sporulated oocyst

Front 81

What life-stage of Cryptosporidium parvum begins the spreading of infection to intestinal epithelia

Back 81

Sporozoites

Front 82

On intestinal surface Cryptosporidium parvum does what

Back 82

Undergoes sexual cycle, making macrogamont which releases oocysts

Front 83

What does Cryptosporidium parvum cause

Back 83

Severe diarrhea

Front 84

What can Cryptosporidium parvum cause in immunosuppressed individuals

Back 84

Wasting syndrome

Front 85

What is the mode of transmission for Trichomonas vaginalis

Back 85

Sexual intercourse

Front 86

What life-stage is Trichomonas vaginalis usually transmitted in

Back 86

Trophozoite

Front 87

What type of pathogen is Trichomonas vaginalis

Back 87

Extracellular GU pathogen

Front 88

Which microorganism has either DNA or RNA (not both)

Back 88

Viruses

Front 89

Are the ribosomes in bacteria the same ours?

Back 89

No

Front 90

Are the ribosomes in fungi the same as ours?

Back 90

Yes

Front 91

Are the ribosomes in viruses the same as ours?

Back 91

Trick question, viruses don't have ribosomes

Front 92

Describe the outer surface of a bacteria

Back 92

rigid wall, coated in peptidoglycan

Front 93

Describe the outer surface of fungi

Back 93

chitinous, rigid wall

Front 94

Describe the outer surface of viruses

Back 94

protein capsid
lipoprotein envelope

Front 95

Describe the outer surface of protozoa/helminths

Back 95

flexible membrane

Front 96

What is the target of many antibiotics (ie penicillin)

Back 96

peptidoglycan layer of wall

Front 97

Do bacteria have a nucleus?

Back 97

No, they have a nucleoid

Front 98

Describe transcription/translation in bacteria and its significance

Back 98

Transcription and translation are coupled, can occur at same time in same place, yields fast production and rapid growth

Front 99

Describe transcription/translation in bacteria and its significance

Back 99

Transcription and translation are coupled, can occur at same time in same place, yields fast production and rapid growth

Front 100

How many chromosomes are in a typical bacteria?

Back 100

One

Front 101

Describe the membrane bound organelles in a typical bacteria

Back 101

There are none

Front 102

How many chromosomes are in a typical bacteria?

Back 102

One

Front 103

List the components of a Gram-positive bacterial cell wall

Back 103

Protein, multiple layers of peptidoglycan, teichoic acid, lipoteichoic acid

Front 104

Describe the membrane bound organelles in a typical baceria

Back 104

There are none

Front 105

List the components of a Gram-positive bacterial cell wall

Back 105

Protein, multiple layers of peptidoglycan, teichoic acid, lipoteichoic acid

Front 106

List the components of a Gram-negative bacterial cell wall

Back 106

Lipopolysaccharide, outer membrane, wall peptidoglycan, cell membrane

Front 107

List the components of a Gram-negative bacterial cell wall

Back 107

Lipopolysaccharide, outer membrane, wall peptidoglycan, cell membrane

Front 108

Describe transcription/translation in bacteria and its significance

Back 108

Transcription and translation are coupled, can occur at same time in same place, yields fast production and rapid growth

Front 109

Describe transcription/translation in bacteria and its significance

Back 109

Transcription and translation are coupled, can occur at same time in same place, yields fast production and rapid growth

Front 110

How many chromosomes are in a typical bacteria?

Back 110

One

Front 111

How many chromosomes are in a typical bacteria?

Back 111

One

Front 112

Describe the membrane bound organelles in a typical baceria

Back 112

There are none

Front 113

Describe the membrane bound organelles in a typical bacteria

Back 113

There are none

Front 114

List the components of a Gram-positive bacterial cell wall

Back 114

Protein, multiple layers of peptidoglycan, teichoic acid, lipoteichoic acid

Front 115

List the components of a Gram-negative bacterial cell wall

Back 115

Lipopolysaccharide, outer membrane, wall peptidoglycan, cell membrane

Front 116

List the components of a Gram-positive bacterial cell wall

Back 116

Protein, multiple layers of peptidoglycan, teichoic acid, lipoteichoic acid

Front 117

List the components of a Gram-negative bacterial cell wall

Back 117

Lipopolysaccharide, outer membrane, wall peptidoglycan, cell membrane

Front 118

What color do Gram-positive bacteria stain?

Back 118

Purple

Front 119

What color do Gram-negative bacteria stain?

Back 119

Pink/red

Front 120

Which type of bacteria have porins? (Gram-positive/negative)

Back 120

Gram-negative

Front 121

What main molecular subunits make up the peptidoglycan glycan chains?

Back 121

N-acetylglucosamine (NAG), and N-acetylmuramic acid (NAM)

Front 122

How do antibiotics like penicillin function?

Back 122

By blocking the peptido-glycan cross-linking

Front 123

What is the toxic component of LPS?

Back 123

Lipid A

Front 124

What are the main components of the LPS molecule on a bacterial cell wall?

Back 124

Lipid A, Core polysaccharide, O-specific chain polysaccharide

Front 125

Which type of bacteria will have LPS in their cell wall

Back 125

Gram-negative

Front 126

Are their introns in bacterial DNA?

Back 126

No

Front 127

Are there exons in bacterial DNA?

Back 127

Yes

Front 128

What are bacterial capsules made of?

Back 128

Polysaccharides

Front 129

Name a bacteria that does not have a capsule

Back 129

Anthrax (?actual name? anthracine?)

Front 130

Pneumococcal and meningiococcal vaccines target what bacterial structure

Back 130

Polysaccharide of capsule

Front 131

Gram-positive cocci include

Back 131

Streptococcus and staphylococcus

Front 132

Gram-positive, spore-forming rod, that is aerobic

Back 132

Bacillus (anthrax)

Front 133

Gram-positive, spore-forming rod, anaerobic

Back 133

Clostridium

Front 134

Gram-positive, non-spore-forming rod, nonfilamentous

Back 134

Cornybacterium, Listeria

Front 135

Gram-positive, non-spore-forming rod, filamentous

Back 135

Nocardia

Front 136

Gram-negative cocci

Back 136

Neisseria

Front 137

Gram-negative rod, facultative, straight, respiratory

Back 137

Haemophilus, bordetella, legionella

Front 138

Gram-negative rod, facultative, straight, zoonotic

Back 138

Brucella, Francisella, Pasturella, Yersinia

Front 139

Gram-negative rod, facultative, straight, enteric

Back 139

E.coli, Enterobacter, Serratia, Klebsiella, Salmonella, Shigella, Proteus

Front 140

Gram-negative rod, facultative, curved

Back 140

Campylobacter, heliobacter, Vibrio,

Front 141

Gram-negative rod, aerobic

Back 141

Pseudomonas

Front 142

Gram-negative rod, anaerobic

Back 142

Bacteroides

Front 143

Extracellular, acid fast

Back 143

Mycobacteria

Front 144

Obligate intracellular

Back 144

Rickettsia, Chlamydia

Front 145

Flexible, thin-walled bacteria ?spirochetes?

Back 145

Treponema, Borrelia

Front 146

Wall-less cells

Back 146

Mycoplasma

Front 147

Describe basic composition of normal flora

Back 147

mostly bacteria, some fungi

Front 148

Normal flora of skin

Back 148

Staphylococcus epidermidis

Front 149

Normal flora of nose

Back 149

Staphylococcus aureus

Front 150

Normal flora of mouth

Back 150

Viridans streptococci

Front 151

Normal flora of dental plaque

Back 151

Streptococcus mutans

Front 152

Normal flora of gingival crevices

Back 152

various anaerobes; Bacteroides, fusobacterium, streptococci, actinomyces

Front 153

Normal flora of throat

Back 153

Viridans streptococci

Front 154

Normal flora of colon

Back 154

Bacteroides fragilis, Eschericha coli

Front 155

Normal flora of vagina

Back 155

Lactobacillus, E.coli, group B strep

Front 156

EXAM QUESTION
What part of the adaptive immune system mainly handles pyogenic infections

Back 156

Humoral

Front 157

Granulomatous infections are normally handled by what part of the adaptive immunity?

Back 157

Cell-mediated

Front 158

Define virulence

Back 158

quantitative measure of pathogenicity (number required to cause infection), infectious dose

Front 159

Define reservoir

Back 159

normal habitat of organism

Front 160

Define fomites

Back 160

inannimate objects that can be a source of transmission

Front 161

List the stages of bacterial pathogenesis

Back 161

Transmission, Evasion, Adhesion, Colonization & Spread, Damage, Response, Progression or Resolution of disease

Front 162

Do certain Gram-positive or -negative bacteria produce exotoxin

Back 162

Either can

Front 163

Do gram-positive or -negative bacteria produce endotoxin

Back 163

Most Gram-negative (LPS)

Front 164

Is exotoxin secreted from the cell

Back 164

Yes

Front 165

Is endotoxin secreted from the cell

Back 165

No (LPS released during breakdown of bacterial cell wall)

Front 166

What type of molecule is exotoxin

Back 166

Polypeptide

Front 167

What type of molecule is endotoxin

Back 167

Lipopolysaccharide

Front 168

Where are the genes located for exotoxin

Back 168

Plasmid or bacteriophage

Front 169

Where are the genes located for endotoxin

Back 169

On the bacterial chromosome

Front 170

Which is relatively more toxic exotoxin or endotoxin?

Back 170

Exotoxin

Front 171

Clinical effects of endotoxin

Back 171

Fever, shock

Front 172

Mode of action of endotoxin

Back 172

Includes TNF and IL-1

Front 173

Antigenicity of exotoxin

Back 173

Induces high-titer Abs called antitoxins

Front 174

Antigenicity of endotoxin

Back 174

Poorly antigenic

Front 175

What is more heat-stable, endotoxin or exotoxin

Back 175

endotoxin

Front 176

List Koch's postulates

Back 176

1) Must always be found in similarly diseased animals, not in healthy ones. 2) Must be isolated from diseased animal and grown in pure culture. 3) Isolate must cause original disease in inoculated susceptible animal. 4) Must be reisolated from experimentally infected animal

Front 177

Name a bacteria that is considered to be uniformally penicillin resistant worldwide

Back 177

Neisseri gonorrhoeae

Front 178

Is antibiotic resistance an acquired trait?

Back 178

Y-E-S!

Front 179

What drug can be combined with certain antibiotics to increase their efficacy?

Back 179

Augmentin

Front 180

What can chloramphenicol cause?

Back 180

Aplastic anemia

Front 181

What is synergism?

Back 181

Combined antibiotic therapy

Front 182

List four reasons why bacteria may be drug resistant

Back 182

They acquire genes that encode resistance, Develop resistance on their own by mutation, Natural resistance, Pharmacokinetic factors

Front 183

What are plasmids?

Back 183

Small circular pieces of episomal (outside of chromosome) DNA

Front 184

Would it be appropriate to call the structure of plasmids "modular"

Back 184

Why of course

Front 185

What is the only important part of a plasmid in order for it to exist

Back 185

The site controlling replication, copy number, and incompatibility

Front 186

What are the four main module types that are found on a plasmid

Back 186

Replication, Conjugation, Mobilization, Passenger Genes

Front 187

What is conjugation as it relates to bacteria?

Back 187

Bacterial sex

Front 188

Is conjugation species specific?

Back 188

No, not really

Front 189

How do genes end up on plasmids?

Back 189

Transposons, jumping genes

Front 190

What are transposons?

Back 190

Short segments of DNA that have the ability to move from one length of DNA to another

Front 191

What are the essential parts of a transposon?

Back 191

Enzyme (transposase), specific labelling terminus (inverted repeats)

Front 192

Can antibiotic resistance genes become associated with transposons?

Back 192

Yes, we believe that this is part of how these genes can be transferred

Front 193

What is a potential mode of long-distance transmission of genes in bacteria

Back 193

Phage transmission

Front 194

What is a phage

Back 194

A bacterial virus

Front 195

If a patient has a susceptible strain to an antibiotic and adheres to the prescribed treatment are they likely to develop resistance? Why?

Back 195

No, acquisition is a rare event

Front 196

Will prophylactic administration of antibiotics promote the occurrence of resistance?

Back 196

Data suggests no

Front 197

If a patient initially responds to antibiotics and then becomes more ill, what most likely happened

Back 197

Infection from a second type of microbe ( as in nosocomial infection)

Front 198

What is the number one predictor of having a drug resistant ear infection

Back 198

The patient has used that antibiotic previously

Front 199

Main weapons against antibiotic resistance?

Back 199

Decreased use and appropriate use (removal of selective pressure)

Front 200

What is the number one cultured bacteria in a microbiology laboratory?

Back 200

Staphylococcus

Front 201

What do staphylococci look like on a gram-stained slide?

Back 201

Gram-positive (purple), cocci (rounded), in clusters. Look like bunches of grapes

Front 202

Gram-stain of staphylococci

Back 202

Gram-positive

Front 203

If you have gram-positive cocci that are catalase positive, what might you have

Back 203

Staphylococcus (?or micrococcus?)

Front 204

If you have gram-positive cocci that are catalse negative, what might you have?

Back 204

Streptococcus or enterococcus

Front 205

How would you differentiate between Staph aureus and other Staph (eg S. epidermidis)

Back 205

Coagulase test. (+) = S. aureus, (-) Coagulase negative (eg. S. epidermidis)

Front 206

Is S. aureus hemolytic or non-hemolytic

Back 206

hemolytic

Front 207

Staphylococci are normal flora of what parts of the body

Back 207

Anterior nares, Mucous membranes, skin, GI tract, vagina

Front 208

List some of the virulence factors of S. aureus

Back 208

Protein A, Fibronectin-binding protein, Hemolysins, PV Leukocidin, Secreted enzymes (lipases, proteases, DNAses, Hyaluronidase, Catalase, Coagulase)

Front 209

What is Protein A of S aureus and what is its significance

Back 209

Major cell wall protein, binds Fc of IgG and prevents complement activation, reducing opsonization and phagocytosis

Front 210

What is the significance of fibronectin-binding protein in S aureus

Back 210

Assists as adhesion factor and helps colonize host

Front 211

If you have a patient with S aureus expressing PVL, where was it acquired

Back 211

Community acquired MRSA

Front 212

S aureus expressing PVL is associated with what diseases

Back 212

Skin infections, furunculosis, severe hemorrhagic pneumonia

Front 213

What does hyaluronidase do

Back 213

hydrolyzes matrix of connective tissue

Front 214

What does catalase do

Back 214

converts H2O2 to H2O, may counteract neutrophil attack

Front 215

What does coagulase do

Back 215

converts fibrinogen to fibrin (via prothrombin activation), May help prevent phagocytosis through poor WBC motility in fibrin clots

Front 216

What are the S aureus superantigen toxins

Back 216

Stephylococcal Scalded Skin Syndrome Toxin (SSSS), Toxic Shock Syndrom Toxin (TSST-1), Enterotoxins A-G

Front 217

What chemicals cause food poisoning from S aureus

Back 217

Enterotoxins A-G, heat stable

Front 218

What bacteria can cause impetigo

Back 218

S aureus or Group A Strep

Front 219

What is erysipelas

Back 219

Superficial cellulitis of skin with prominent lymphatic involvement

Front 220

With endocarditis caused by S aureus, what might one see on a patient

Back 220

Janeway spots, small embolic skin lesions

Front 221

What is SSSS caused by

Back 221

exfoliative toxins ETA and ETB (in infants)

Front 222

What are the symptoms of TSST-1

Back 222

High fever, rash resembling sunburn, desquamation, vomiting, diarrhea, hypotension, multi-organ involvement

Front 223

Short-onset food poisoning suggests

Back 223

S aureus

Front 224

Is S aureus susceptible to penicillin

Back 224

No, most strains are resistant

Front 225

What protein incurs penicillin resistance in S aureus

Back 225

beta-lactamase

Front 226

Can coagulase negative Staph (CONS) cause infection

Back 226

Yes, they are opportunistic

Front 227

Which coag. neg. Staph. is often associated with UTIs

Back 227

S saprophyticus

Front 228

Which coag. neg. Staph. is often associated with infections of implanted artificial devices? Why?

Back 228

S. epidermidis, produces "slime layer" which facilitates adherence and is a barrier to antibiotics

Front 229

Which Strep. are beta-hemolytic

Back 229

Group A strep, Group B strep

Front 230

Streptococci will have which result for a catalase test?

Back 230

Negative

Front 231

What does beta hemolysis mean?

Back 231

Complete hemolysis

Front 232

What determines a streptococcus "group"

Back 232

Carbohydrate antigens on cell surface

Front 233

What does alpha hemolysis mean

Back 233

Incomplete hemolysis, can see a "greening" on a blood-agar plate

Front 234

What is the "real" name for Group A Strep?

Back 234

S. pyogenes

Front 235

What is the "real" name for Group B Strep?

Back 235

S. agalactiae

Front 236

S. pyogenes is also known as

Back 236

Group A strep

Front 237

S agalactiae is also known as

Back 237

Group B strep

Front 238

What is the habitat for Group A strep

Back 238

Skin and mucous membranes

Front 239

What is the habitat for Group B strep

Back 239

GI tract, vagina, urethra

Front 240

What is the habitat for S. pneumoniae

Back 240

nasopharynx

Front 241

Enterococci and Group-D non-enterococci are found in

Back 241

GI tract

Front 242

Viridans strep are found in

Back 242

mouth, gums, teeth

Front 243

What is the appearance of streptococci on a gram-stained slide

Back 243

Gram positive (purple), cocci (rounded), in chains

Front 244

Which Strep is bacitracin susceptible

Back 244

Group A (S pyogenes)

Front 245

Describe some important S. pyogenes exotoxins

Back 245

Spe A & C (superantigens), Spe A,B,C cause scarlet fever

Front 246

Streptococcal pyrogenic exotoxins are involved in

Back 246

pathogenesis of strep. toxic shock syndrome, necrotizing fasciitis

Front 247

How does S pyogenes prevent attraction of phagocytic cells to infection site

Back 247

C5a peptidase

Front 248

What does streptokinase do

Back 248

Dissolves clots

Front 249

What virulence factor(s) do Strep and Staph have in common?

Back 249

Hyaluronidase

Front 250

Describe some ways that S pyogenes infectionscause damage

Back 250

Supprative - direct damage by organism and secreted enzymes, Post-infectious sequelae - from autoimmune response cause by strep Ags, Toxin-mediated - strep exotoxins secreted into bloodstream

Front 251

What is the number one cause of bacterial pharyngitis

Back 251

Group A strep (S pyogenes)

Front 252

What are the symptoms indicative of a Group A strep caused pharyngitis

Back 252

Red throat, petechiae on soft palate, grayish-whitish tonsillar exudates, enlarged and tender anterior cervical lymph nodes

Front 253

A patient presents complaining of a sore throat, you note a reddening of the pharynx, petechiae on soft palate, gray-white tonsillar exudate and enlarge lymph nodes... diagnosis?

Back 253

Bacterial pharyngitis caused by S pyogenes (Group A)

Front 254

S pyogenes is associated with what post infectious sequelae

Back 254

Acute rheumatic fever, and Acute glomerulonephritis

Front 255

What is a major reason to treat an S pyogenes infection in throat

Back 255

Prevention of acute rheumatic fever (NOT acute glomerulonephritis)

Front 256

What are some indicators of scarlet fever?

Back 256

Recent (?or current?) infection of S pyogenes followed by a "sandpaper-type" rash beginning on torso and spreading, white strawberry tongue proceeded by a red/pink strawberry tongue

Front 257

What are some diseases that Group B strep can cause and in whom

Back 257

Sepsis, meningitis, and pneumonia in newborns, elderly, and immunocompromised

Front 258

What function does the polysaccharide capsule of S agalactiae serve

Back 258

antiphagocytic

Front 259

Is S pneumoniae alpha, beta, or non-hemolytic

Back 259

Alpha

Front 260

Which Strep is optochin sensitive

Back 260

S pneumoniae

Front 261

How would S pneumoniae appear on a gram-stained slide

Back 261

Gram-positive (purple), diplococci (two rounded attached circle)

Front 262

On a culture of S pneumoniae with an antibiotic disc, what does the P stand for

Back 262

Pneumococcus (testing for optochin sensitivity)

Front 263

What bacteria is a common cause of otitis media

Back 263

S pneumoniae

Front 264

What is the most common cause of bacterial pneumonia

Back 264

S pneumoniae

Front 265

What is the number one virulence factor for S pneumoniae

Back 265

Its polysaccharide capsule

Front 266

What part of the adaptive immunity is protective against S pneumonia infection

Back 266

Humoral/Antibodies directed against the capsule

Front 267

Other than its capsule, what is a virulence factor for S pneumoniae

Back 267

Autolysins allowing release of pneumolysins that attack mammalian cell membranes

Front 268

You have a alpha-hemolytic strep. that is optochin resistant, what might this be

Back 268

Viridans streptococci

Front 269

What is the major risk of viridans (oral) strep.

Back 269

endocarditis

Front 270

How would enterococci appear on a gram-stained slide

Back 270

Gram-positive (purple), cocci (rounded) in pairs and short chains

Front 271

Which gram-positive cocci (that we have discussed) is bile salt tolerant

Back 271

Enterococci

Front 272

Enterococci are important causes to consider in which diseases?

Back 272

UTIs, endocarditis, intra-abdominal infections, bacteremia

Front 273

What are two species of enterococci that are commonly seen

Back 273

E. faecalis and E. faecium

Front 274

Are groups A,B,C, and G beta-hemolytic strep penicillin susceptible?

Back 274

Yes

Front 275

What common antibiotics might S pneumoniae be resistant to?

Back 275

Penicillin, erythromycin, clindamycin, trimetoprim/sulfamethoxazole

Front 276

Metazoa (Helminths) have what three main life-stages

Back 276

Eggs, larvae, adults

Front 277

What type of immunity is associated with controlling helminthic infections

Back 277

Type 2 immunity. Eosinophilia

Front 278

Describe the main characteristics of nematodes

Back 278

Nonsegmented roundworms, separate sexes, four larval molts

Front 279

What are the main infections caused by nematodes (generalized)

Back 279

Intestinal and tissue infections

Front 280

Ascaris lumbricoides in known commonly as

Back 280

giant roundworm

Front 281

How is Ascaris lumbricoides acquired in humans

Back 281

Eggs are ingested from soil or improperly prepared foods

Front 282

Where do the larvae of Ascaris lumbricoides hatch and where do they travel to (first)

Back 282

Small intestines, travel through blood to liver and then on

Front 283

Describe the path of migration of Ascaris lumbricoides after hatching

Back 283

Small intestines, liver, heart, lung capillaries, alveolar space, up trachea, reswallowed into small intestines

Front 284

How does an ascaris lumbricoides infection result in pneumonitis

Back 284

Th2 induced eosinohpilia in alveolar tissue caused by larval stage passing through can cause inflammation

Front 285

What is the major interleukin associated with the Th2 response to an helminthic infection

Back 285

?IL-5?

Front 286

How is a Trichuris trichiura infection acquired

Back 286

eggs are ingested from soil

Front 287

Where do the larvae of a Trichuris trichiura hatch

Back 287

Hatch in small intestine

Front 288

Does Trichuris trichiura invade body tissues?

Back 288

No

Front 289

Does Ascaris lumbricoides invade body tissues

Back 289

Yes (or at least they will puncture through tissues to get where they're going)

Front 290

Where do adult Trichuris trichiura mature

Back 290

Large intestine

Front 291

Where do Trichuris trichiura females "like" to lay their eggs? What does this cause

Back 291

Eggs lain around pararectal tissues, causes intense inflammation and can lead to a prolapsed rectum

Front 292

What is the common name for Trichuris trichiura?

Back 292

Whip worm

Front 293

What is the common name for Enterobius vermicularis?

Back 293

Pin worm

Front 294

How is an Enterobius vermicularis infection acquired?

Back 294

Eggs contaminate fingers or surfaces and are then ingested

Front 295

Where do Enterobius vermicularis larvae hatch

Back 295

Small intestine

Front 296

Where do adult Enterobius vermicularis mature?

Back 296

Large intestine

Front 297

Do Enterobius vermicularis invade body tissues?

Back 297

no

Front 298

What is the common name for Strongyloides stercoralis

Back 298

Threadworm

Front 299

How is a Strongyloides stercoralis infection acquired?

Back 299

Larvae penetrate unbroken skin, perhaps through hair follicle

Front 300

Describe the pathway that Strongyloides stercoralis larvae will travel before becoming an adult?

Back 300

Skin, Blood, Lungs, Up trachea, Small intestines

Front 301

What is a life-threatening complication of Strongyloides stercoralis in certain individuals

Back 301

In immunocompromised, eggs can hatch in intestines and invade large intestines leading to autoinfection and potentially hyperinfection and/or lead to bacterial sepsis

Front 302

What is the common name for Necator americanus

Back 302

Hookworm

Front 303

How does Necator americanus enter the body?

Back 303

Larva penetrates unbroken skin (like Strongyloides stercoralis)

Front 304

Describe the pathway that Necator americanus takes once it enters the body

Back 304

Skin, Bloodstream, Lungs Trachea, Small intestines

Front 305

Where do the adults of Necator americanus mature

Back 305

Small intestine

Front 306

What is a particular complication of Necator americanus infection

Back 306

Anemia due to metabolic demands put on body

Front 307

What is a difference that might be seen in a CBC between intestinal nematodes and tissue nematodes?

Back 307

Elevated peripheral eosinophils with tissue nematodes

Front 308

How does Trichinella spiralis enter the body

Back 308

Larvae are ingested in undercooked meat

Front 309

Describe the immediate events of Trichinella spirallis after entering the body

Back 309

Larvae released from nurse cells while in stomach, larvae enter small intestine and mature into adults

Front 310

How do female Trichinella spiralis "give birth" to progeny

Back 310

Newborn larvae are "shed" from female

Front 311

What happens to Trichinella spiralis larvae born in the small intestines

Back 311

Enter lymph, travel through bloodstream to various tissues

Front 312

What are some very serious pathologies associated with trichinella spiralis infection

Back 312

Heart failure and CNS damage ?due to severe inflammation?

Front 313

How does Dracunculus medinensis enter the body?

Back 313

Ingested as larvae inside copepods

Front 314

Once in the body, how does a Dracunulus medinensis infection proceed

Back 314

Larvae freed from copepods in small intestine penetrate intestinal wall then abdominal wall entering subcutaneous tissues and maturing to adults

Front 315

Where do adult Dracunulus medinensis reside and what happens to their progeny

Back 315

Adults mature in subcutaneous tissue and lymph nodes and larval progeny are released from blister

Front 316

What is the main clinical manifestation of a Dracunulus medinensis infection

Back 316

Lymphedema from blocked lymph nodes

Front 317

What Metazoan infection might someone with dogs or cats be at risk for

Back 317

Toxocara canis/cati

Front 318

How does Toxocara canis/cati spread to humans

Back 318

Eggs from dog/cat are ingested by human

Front 319

Where do Toxocara canis/cati larva hatch

Back 319

Small intestine

Front 320

What do Toxocara canis/cati larva do once hatched

Back 320

Penetrate intestinal wall and migrate via bloodstream. Disseminate similarly to Trichinella spiralis

Front 321

What are the complications associated with Toxocara canis/cati

Back 321

Intense inflammation in body tissues like the eye, CNS, and liver ~ 1 month after ingestion

Front 322

How does Wuchereria bancrofti enter the body

Back 322

Infected mosquito bites and deposits larvae on skin which enter through bite wound

Front 323

Once in the body, how does Wuchereria bancrofti spread

Back 323

from skin larvae enter lymphatics where adults mature, microfilariae then enter bloodstream at night

Front 324

What is one possible complication of Wuchereria bancrofti

Back 324

Sever lymphedema (elephantiasis)

Front 325

How does Onchocerca volvulus enter the human body

Back 325

infected blackfly deposits (vomits) larvae on skin which enter through bitewound

Front 326

Where do Onchocerca volvulus mature into adults

Back 326

within subcutaneous tissues and release microfilariae

Front 327

What is a potential complication of Onchocerca volvulus

Back 327

Blindness when larvae are deposited near eye causing intense Th2 response

Front 328

How does Loa loa enter the human body

Back 328

Infective fly deposits larva during meal onto skin and larvae enter through bite wound

Front 329

Where do adult Loa loa mature

Back 329

Subcutaneous tissues

Front 330

When do adult Loa loa release microfilariae into blood

Back 330

During the day (opposite of Wuchereria)

Front 331

What are the intermediate hosts for trematodes (in general)

Back 331

Snails and shellfish

Front 332

What are some general characteristics of trematodes

Back 332

Nonsegmented flatworms (flukes), adults have two suckers

Front 333

What is the infectious stage of trematodes for shelfish

Back 333

"Miracidia"

Front 334

What is the infectious stage of trematodes for mammals

Back 334

"Cercaria"

Front 335

What is the common name for Schistosoma mansoni/japonicum

Back 335

Blood/liver fluke

Front 336

What is the common name for Schistosoma haematobium

Back 336

Blood/bladder fluke

Front 337

What is the common name for Clonorchis sinensis

Back 337

Oriental liver fluke

Front 338

What is the common name for Paragonimus westermani

Back 338

Lung fluke

Front 339

How does Schistosoma mansoni enter the body

Back 339

Generally, from snail or shellfish, cercariae enter skin, such as through hair follicle

Front 340

Path of Schistosoma mansoni after entering body

Back 340

From skin, migrate to lungs the to liver

Front 341

Where do adult Schistosoma mansoni live

Back 341

Liver venules (in "constant copulation")

Front 342

How do Schistosoma mansoni eggs laid in liver venules escape body

Back 342

Proteases dissolve path either through biliary tree to intestine or directly to intestine, passed in feces

Front 343

What are some complications of Schistosoma mansoni infection

Back 343

Hepatitis leading to cirrhosis, portal hypertension

Front 344

What is an identifying feature of Schistosoma mansoni in a stool sample

Back 344

A lateral spine on the egg

Front 345

How does a Schistosoma japonicum infection differ from a Schistosoma mansoni infection?

Back 345

Larval forms may penetrate into other tissues causing problems other than hepatosplenomegally, CNS issues, cardiopulmonary issues, also possible for transverse myelitis. Otherwise the same

Front 346

How does a Schistosoma haematobium infection differ from a Schistosoma mansoni infection?

Back 346

Adults migrate to bladder and live in venous plexus releasing eggs into bladder/urine (different subsequent complications)

Front 347

What are some complications of S haematobium?

Back 347

Bladder inflammation/calcification and cancer

Front 348

If you think your patient has Schistosoma haematobium, what should you order to confirm this diagnosis

Back 348

Urine sample test

Front 349

How does Clonorchis sinensis enter the body

Back 349

Undercooked infected fish with metacercaria is ingested

Front 350

Describe the events after Clonorchis sinensis enters the body

Back 350

Larvae hatch in small intestine, larva enters bile ducts and adults mature there

Front 351

How does Clonorchis sinensis cause issues

Back 351

adults and their released eggs cause biliary obstructions

Front 352

How does Paragonimus westermani enter the body

Back 352

Consumption of raw or undercooked shellfish

Front 353

What are the events after Paragonimus westermani enters the body

Back 353

Worms hatch in small intestine, adults mature in lung, eggs released in lungs as cyst

Front 354

How do paragonimus westermani eggs escape the body

Back 354

Eggs dissolve path into alveoli and are coughed up

Front 355

What tests would you order for a patient you suspected of having Paragonimus westermani

Back 355

Sputum test

Front 356

What are some basic characteristics of Cestodes (tapeworms)

Back 356

They are segmented flatworms, have a scolex (head), and proglottids (body segment, infectious units)

Front 357

How is Taenia saginata contracted

Back 357

Cysticerci are ingested in undercooked beef

Front 358

Where do cysticerci escape and mature

Back 358

Escape in stomach, worms live and mature in small intestine

Front 359

How does Taenia saginata resist peristaltic contractions forcing it out of the body

Back 359

Scolex has four suckers which hold onto intestinal wall

Front 360

How does Taenia solium differ from Taenia saginatum

Back 360

T solium is from pigs and if you are infected with a gravid proglottid or eggs, onchospheres hatch in small intestine, penetrate tissues and form cysticercus in body tissues = inflammatory or scarring issues

Front 361

What is cysticercosis

Back 361

Infection from Taenia solium infecting various body tissues

Front 362

What is a possible CNS issues caused by cysticercosis

Back 362

Grand mal seizure

Front 363

How does Diphyllobothrium latum differ from Taenia saginata

Back 363

Contracted from fish

Front 364

How is Echinococcus granulosus contracted

Back 364

Eggs are ingested, passed from animal to human

Front 365

Describe the events immediately after Echinoccocus granulosus enters the body

Back 365

Oncospheres hatch in small intestine then enter bloodstream and penetrate tissues where cysts develop

Front 366

What is the most common cause of significant pneumonia in a newly diagnosed AIDS patient

Back 366

Pneumocystis

Front 367

What should you think about/consider when an immunocompromised (HIV/AIDS) patient presents with a GM seizure

Back 367

Toxoplasmosis

Front 368

What are the two main Neisseriae that we are concerned with?

Back 368

N. gonorrhoeae & N. meningitidis

Front 369

What is the appearance of Neisseria on a Gram-stained slide?

Back 369

Gram-negative (pink), diplococci (paired round), opposing ends flattened in kidney bean appearance

Front 370

What are some general features of Neisseria

Back 370

Gram-neg., diplococci, oxidase (+), strict aerobes, require added CO2 and enriched medium for growth

Front 371

Are Neiserria aerobes/anaerobes, oxidase (+)/(-), Gram (+)/(-)

Back 371

Strict aerobes, oxidase (+), Gram-neg.

Front 372

What is gene conversion, as it relates to bacteria (ie N gonorrheoeae)

Back 372

Recombination and shuffling of genes so that bacteria can express multiple pilins with different AA sequences

Front 373

What role to pili play in N gonorrhoeae

Back 373

Major virulence factor, enhance attachment of bacterium to host epithelial and mucosal cell surface, also inhibit phagocytosis

Front 374

What are the major virulence factors of N gonorroeae

Back 374

Pili, Outer membrane proteins (OMP I and OMP II, inhibit complemnet, promote invasion), IgA protease

Front 375

What is the primary manifestation of a non-disseminated N gonorrhoeae infection

Back 375

Pain and purulent discharge

Front 376

What are the possible results of an N gonorrhoeae infection in men? Women?

Back 376

Men-urethritis
Women-cervicitis, salpingitis, PID (could lead to ectopic pregnancy or sterility)

Front 377

What can be the manifestations of a disseminated N gonorrhoeae infection

Back 377

Fever, polyarthralgia, rash

Front 378

Other than reproductive organs, where might one observe an N gonorrhoeae infection

Back 378

Within the rectum or pharynx

Front 379

What is a risk to a baby being born to a mother with gonorrhea?

Back 379

Gonococcal ophthalmia neonatorum, prevent with eyedrops at birth

Front 380

What is presumptive evidence for a N gonorrhoeae infection in males?

Back 380

Gram stain of uretral exudates showing intracellular gram-negative diplococci (in females, neither sensitive nor specific)

Front 381

What is the gold standard for N gonorrhoeae diagnosis?

Back 381

Nucleic acid amplification

Front 382

What are some things that help N meningitidis evade the immune system

Back 382

Pili and IgA proteases

Front 383

What type of immunity is protective against N meningitidis infection

Back 383

Antibody to capsule

Front 384

What is it about N meningitidis that can induce shock

Back 384

Lipooligosaccharide (LOS), triggers TNF and IL-1

Front 385

What does LOS on N meningitidis cause

Back 385

Can induce shock, also activates coagulation system causing disseminated intravascular coagulation

Front 386

What animal is the only natural host to N gonorrhoeae and N meningitidis

Back 386

Humans

Front 387

How is N menigitidis transferred from person-to-person

Back 387

via close respiratory droplets

Front 388

In whom do most cases of N meningitidis occur?

Back 388

Infants and young adults, 3-12 months most at risk

Front 389

What microbe is Waterhouse-Friderichsen syndrome associated with?

Back 389

N meningitidis, (endotoxic shock, DIC, bilateral hemorrhagic destruction of adrenal glands, circulatory collapse, death)

Front 390

Meningiococcemia

Back 390

Septicemia with petechial rash, associated with N meningitidis

Front 391

Among survivors of N meningitidis, what are the significant sequelae

Back 391

Neurological disabilities, amputation, hearing loss

Front 392

What is echymosis

Back 392

Coalesceing petechia

Front 393

How would a N meningitis infection be identified

Back 393

Gram stain of CSF, Culture of CSF and blood (on chocolate agar and increased CO2)

Front 394

Is it common for N meningitis to have penicillin resistance

Back 394

No

Front 395

What should be done for close contacts of a patient with N meningitis

Back 395

Prophylactic antibiotics

Front 396

What are the vaccine option for N meningitis

Back 396

Polysaccharide-diptheria toxoid conjugate vaccine - MCV4 (11-55yrs), Pollysaccharide vaccine (very young/old)

Front 397

What are the general characteristics of acinetobacter

Back 397

Gram-negative coccobacilli, oxidase neg., aerobic (SAME AS MORAXELLA)

Front 398

What does "exposure" to acinetobacter cause?

Back 398

Hospital acquired infections, particularly ventilator-associated pneumonia

Front 399

What are the general characteristics of Moraxella catarrhalis

Back 399

Gram-negative coccobacilli, oxidase positive, aerobic (SAME AS ACINETOBACTER)

Front 400

What can a Moraxella catarrhalis infection cause

Back 400

Otitis media, pneumoniae, conjunctivitis, and rarely CNS and joint infections

Front 401

Describe the general characteristics of Corynebacteria

Back 401

Small gram-positive, pleomorphic rods, tend to clump, non-motile, non-encapsulated, non-spore forming

Front 402

What is the normal habitat of Corynebacteria? exceptions?

Back 402

Normal flora of skin and respiratory tract, except for C. diptheriae

Front 403

In what populations does diphtheria occur?

Back 403

Non-immunized populations

Front 404

What does C diphtheriae cause and how is it spread?

Back 404

Causes local infection of throat or skin, spread as respiratory droplet

Front 405

How does C diphtheriae cause damage

Back 405

Local and systemic effects of diphtheria toxin which (ultimately) causes inhibition of preotein synthesis in the host

Front 406

What is the respiratory form of C diphteriae likely to present with

Back 406

A thick grayish exudate called a pseudomembrane on the tonsils, can obstruct airways

Front 407

If a patient presents with a swollen neck and a thick grayish, adherent exudate on their tonsils, what might a diagnosis be

Back 407

Respiratory form of C diphtheriae

Front 408

What are the generalized symptoms of a C diphtheriae infection caused by absorption of toxin

Back 408

Myocariditis (leads to congestive heart failure), Reversible paralysis of soft palate or eye muscles (or others), death from respiratory obstruction

Front 409

Describe how Cutaneous diptheria might appear

Back 409

Range from simple pustule to chronic non-healing ulcer, resolves with antitoxin Ab formaiton

Front 410

What other infection does cutaneous diphtheria look like

Back 410

Anthrax

Front 411

What is the diphtheria vaccine?

Back 411

DPT

Front 412

What is Corynebacterium jeikeium associated with? Why might it be difficult to treat?

Back 412

Wound infection, septicemia, endocarditis. Usually multi-resistant to antibiotics

Front 413

What is Corynebacterium urealyticum associate with?

Back 413

Chronic, recurrent UTIs

Front 414

Describe the general characteristics of Bacillus anthracis

Back 414

Gram-positive (purple), bacillus (elongated rod), "boxcar" or bamboo rod arrangement in chains, spore forming

Front 415

Describe the spores of Bacillus anthracis

Back 415

oval, central or terminal, do not take up stain

Front 416

Is Bacillus anthracis hemolytic or non-hemolytic

Back 416

Non-hemolytic

Front 417

What is the rod-form of Bacillus anthracis also known as?

Back 417

Vegetative form

Front 418

What is germination, as it relates to Bacillus anthracis

Back 418

Conversion of spores to vegetative (rod) bacilli

Front 419

What is the process of Bacillus anthracis converting from the vegetative (rod) form into the spore form

Back 419

Sporulation

Front 420

What are the three virulence factors of Bacillus anthracis

Back 420

poly-D-glutamic acid capsule, edema factor, lethal factor

Front 421

Describe the properties of the capsule surrounding Bacillus anthracis

Back 421

Composed of poly-D-glutamic acid, neg. charge inhibits phagocytosis by leukocytes

Front 422

What are the three proteins associated with exotoxins that Bacillus anthracis elaborates

Back 422

Protective antigen (PA), Edema factor (EF), Lethal factor (LF)

Front 423

What is the role of protective antigen elaborated by Bacillus anthracis

Back 423

Mediates internalization of edema factor and lethal factor into host cells

Front 424

Describe the effect of edema toxin (EF + PA) on cells from Bacillus anthracis

Back 424

Acts as calmodulin-dependent adenylate cyclase, increases cAMP, changes membrane permeability and EDEMA results

Front 425

If a patient has inhaled Bacillus anthracis, what might one expect to see as a result

Back 425

Widening of mediastinum with pleural effusions without infiltrates... (edema)

Front 426

Describes the effect of Lethal toxin (LF + PA) on cells from Bacillus anthracis

Back 426

Zinc dependent protease that interferes with signaling pathways of major phagocytic cells and can induce apoptosis and necrosis, hemorrhagic necrosis in tissues)

Front 427

What are the three clinically presenting forms of anthrax

Back 427

Cutaneous, Inhalational (Pulmonary), Gastrointestinal

Front 428

How might a person acquire gastrointestinal anthrax

Back 428

Consumption of contaminated materials such as with rotting meat

Front 429

What is the appearance of cutaneous anthrax

Back 429

Papule that develops into a painless black/red pustule - eschar

Front 430

What are the early symptoms of an inhalational Bacillus anthracis infection

Back 430

Malaise, fatigue, myalgia, mild fever, non-productive cough "FLU-LIKE"

Front 431

What are the intermediate symptoms of an inhalational Bacillus anthracis infection

Back 431

Positive blood cultures, mediastical lymphadenopathy, hemorrhagic pleural effusions (require drainage), severe dyspnea, hypoxemia, cyanosis, tachydcardia

Front 432

What are the late fulminant symptoms of an inhalational Bacillus anthracis infection

Back 432

Respiratory failure requiring intubation, meningitis, shock, high fatality rate

Front 433

How might you sample to diagnose a Bacillus anthracis infection in each of its three forms

Back 433

Cutaneous - swab of vesicle fluid, elcer/eschar
Inhalational - blood (CSF in meningeal)
Gastrointestinal - feces, vomitus, blood

Front 434

What cells does Listeria monocytogenes infect

Back 434

Monocytes, it's in the name

Front 435

Describe the characteristics of Listeria monocytogenes

Back 435

Gram-postive rod with "Chinese character clumping" pattern, may look like cocci in pairs, Catalase positive, tumbling motility at room temp

Front 436

What might Listeria monocytogenes on Gram-stain be confused with? How can you tell the difference

Back 436

Group B streptococcus. Listeria is catalase positive

Front 437

Is Group B strep catalase positive or negative

Back 437

Negative

Front 438

Is Listeria catalase positive or negative

Back 438

Positive

Front 439

What would be seen on a blood agar culture of Listeria monocytogenes

Back 439

Beta-hemolysis

Front 440

Does refrigeration suppress Listeria growth

Back 440

No

Front 441

What species of Listeria will infect humans

Back 441

Only L monocytogenes

Front 442

What is a risk of unpasteurized dairy products

Back 442

Listeria contamination causing food poisoning

Front 443

Which groups of people are at the highest risk for lysteriosis

Back 443

AIDS patients (300X), Pregnant women (20X, can be fatal to fetus), others normally at risk for infection

Front 444

Is listeria an intracellular or extracellular pathogen

Back 444

Intracellular

Front 445

What are the steps in pathogenesis of Listeria monocytogenes

Back 445

Phagocytosis; escape from phagolysosome by listeriolysin O (damages membranes); growth in cytosol and assemply of actin filament tail that form a pseudopod, spread to adjacent cells

Front 446

After initial infection with Listeria monocytogenes, is there an extracellular stage

Back 446

No, passes directly from one cell to the next

Front 447

What are the two most common clinical presentations of Listeria monocytogenes infections

Back 447

Septicemia and meningitis

Front 448

What are the risks of a pregnant mother contracting listeriosis (other than normal risks)

Back 448

Infection of child during birth, can also cause abortion or preterm delivery

Front 449

Does humoral immunity play a role in fighting a Listeria infection

Back 449

No

Front 450

How would Listeria monocytogenes infections be identified in a lab

Back 450

Culture of blood or CSF

Front 451

What are the general characteristics of Erysipelothrix rhusiopathiae

Back 451

Gram-positive filamentous rod, catalse negative

Front 452

If you have a patient who is a butcher, veterinarian. or fisherman with a skin infection, what might you consider as a cause

Back 452

Erysipelothrix rhusiopathiae

Front 453

What bacteria might we have if our patient presents with a gram-positive anaerobic rod

Back 453

Clostridium

Front 454

What bacteria might we have if a patient presents with a gram-negative anaerobic rod

Back 454

Bacteroides

Front 455

What enzymes that break down toxic oxygen intermediates are anaerobes missing

Back 455

Catalase, peroxidase, superoxide dismutase, etc.

Front 456

What might a clostridia species be confused with on a simple gram-stain slide

Back 456

A bacillus species, must take into account aerobic vs anaerobic

Front 457

What are the general characteristics of Clostridia

Back 457

Gram-positive anaerobic spore-forming rods, large & boxcar shaped, catalase negative

Front 458

What species of Clostridia (that we are concerned with) are found in soil

Back 458

C tetani, C botulinum

Front 459

Where is Clostridium perfringens normally found in humans

Back 459

Normal flora of vagina and GI tract

Front 460

What pathologies can Clostridium perfringens cause

Back 460

gas gangrene (myonecrosis), cellulitis, sepsis, food poisoning

Front 461

What is the most important exotoxin produced by C perfringens and what does it do?

Back 461

Alpha-toxin, phospholipase activity causing cell lysis,

Front 462

What is a result of the enterotoxin released by C perfringens

Back 462

Alters intestinal epithelial permeability, releasing fluid into the lumen

Front 463

What are some of the enzymes that promote gas gangrene caused by C perfringens

Back 463

Proteases, DNases, Hyaluronidase, Collagenases... liquefy tissues

Front 464

Other than Clostridium perfringens, what bacteria might cause gas gangrene (myonecrosis)

Back 464

Clostridium septicum

Front 465

What is gas gangrene usually due to?

Back 465

introduction of clostridium spores into tissues

Front 466

What are some risks from gas gangrene other than loss of tissue

Back 466

Toxins may be carried to other organs causing systemic effects such as shock, renal failure, or intravascular hemolysis... death

Front 467

What is an infection that has been associated with colon cancer

Back 467

Clostridium septicum

Front 468

A patient presents with nausea, abdominal cramps, and diarrhea between 8-18 hours after eating at a potluck party, you're thinking food-poisoning (it's not diabetes and not a broken arm). What organism might be responsible?

Back 468

Clostridium perfringens

Front 469

Enteritis necroticans (nectrotizing bowel disease) has a high mortality rate, what organism can be responsible for this

Back 469

Clostridium perfringens

Front 470

What disease is associated with abortions performed with inadequately sterilized instruments or "illegal abortions", what organism causes this

Back 470

Clostridial endometritis, caused by C perfringens

Front 471

What is a notable characteristic of C perfringens on a blood agar culture

Back 471

A double zone of hemolysis

Front 472

What is a common cause of botulism in the US

Back 472

Home canning of foods (improper)

Front 473

What is a cause of wound botulism

Back 473

Injection/use of black-tar heroin

Front 474

Botulism is caused by what organism

Back 474

Clostridium botulinum

Front 475

What does botulinum toxin do

Back 475

Blocks neurotransmitter release of Ach by blocking vesicles, muscle paralysis results

Front 476

Is the botulinum toxin release by Clostridium botulinum neutralized by stomach acid

Back 476

No

Front 477

What are the symptoms of food-borne/classic botulism

Back 477

double vision, blurred vision, symmetrical paralysis, difficulty swallowing, no fever or signs of sepsis

Front 478

What is a risk of feeding infants honey

Back 478

Infant botulism

Front 479

What are symptoms of infant botulism

Back 479

Constipation, feeding problems, lethargy, poor muscle tone, possible paralysis and respiratory arrest

Front 480

An infant presents with constipation, feeding problems, lethargy and poor muscle tone. He is wearing a Winnie the Pooh shirt with a sticky substance on it. What might your diagnosis be

Back 480

Infant botulism caused by Clostridium botulinum spores in honey

Front 481

What are the general characteristics of Clostridium tetani

Back 481

Anaerobic gram-positive, spore-forming, found in soil, animal feces

Front 482

What are most cases of Clostridium tetani infections caused by

Back 482

Puncture wounds

Front 483

What cells does tetanus toxin attack

Back 483

Peripheral neurons

Front 484

What does tetanus toxin do

Back 484

Blocks release of inhibitory neurotransmitter in peripheral neurons, causes unopposed contraction of muscles

Front 485

What is the vaccine against tetanus toxin

Back 485

DPT

Front 486

What does Clostridium difficile cause in humans

Back 486

antibiotic-associated diarrhea and pseudomembranous colitis

Front 487

What is the toxin produced by C difficile that is responsible for virulence

Back 487

Toxin B

Front 488

What is a risk for the patient after antibiotic treatment to cure a C difficile infection

Back 488

Relapse

Front 489

What is the number one nosocomial infection

Back 489

Clostridium difficile

Front 490

What is the predominant bacteria found in the human gut

Back 490

bacteroides

Front 491

What is an anaerobic gram-negative rod associated with head and neck infections pulmonary infections, brain abscesses, and genital tract infections

Back 491

Prevotella/Porphorymonas

Front 492

Fusobacteria are normal flora of what body parts

Back 492

Mouth, female genital tract, colon, can cause disease at any of these locations

Front 493

What anaerobic gram-positive rod should be of concern with implantable devices

Back 493

Propionibacterium acnes

Front 494

What conditions are associated with gram-negative enteric organisms

Back 494

Sepsis, Gastrointestinal infections, Urinary tract infections

Front 495

Almost all gram-negative enteric rods have their reservoirs where (either in humans or animals)

Back 495

GI tract

Front 496

What are the seven "F"s and what are they associated with

Back 496

Feces, finger, flies, food, fluids, fomites, fornication; associated with the fecal oral transmission of gram-negative enteric rods

Front 497

What is the pathogenesis of gram-negative enteric rods

Back 497

Toxin mediated or invasive (or both): fluid loss; inflammation/cell death; vascular effects

Front 498

Enterotoxins from gram-negative enteric rods typically effects what location and causes what

Back 498

Small intestine, causes watery diarrhea, nausea, vomiting

Front 499

Invasins released by gram-negative enteric bacteria are typically associated with what location and what can they cause

Back 499

Large intestines: bloody diarrhea, fever, cramps, leukocytes in stool, immune evasion

Front 500

What are the laboratory diagnostic tools used in evaluating gram-negative enteric rods

Back 500

Gram stain, lactose fermentation, H2S production, oxidase reaction, motility, presence of leukocytes in stool,

Front 501

How might a lactose test (organism grown on MacConkey agar) be helpful in identifying organisms in a stool sample

Back 501

Differentiating between lactose(+) organisms of normal flora (ie E coli) and lactose (-) organisms that are abnormal (ie Shigela)

Front 502

What genus might a gram negative anaerobic rod be

Back 502

Bacteroides, Fusobacterium or Prevotella

Front 503

What genus might a gram negative cocci be

Back 503

Neisseria, Moraxella, Acinetobacter

Front 504

What genus might a fastidious gram negative facultative/aerobic rod found intracellularly be from

Back 504

Legionella

Front 505

What genus might a fastidious gram negative facultative/aerobic rod found extracellularly be from

Back 505

Haemophilus, Bordetella, Campylobacter, Helicobacter

Front 506

What genus might a gram negative facultative/aerobic that is oxidase positive be from

Back 506

Pseudomonas, Vibrio, Campylobacter, Helicobacter

Front 507

What genus might a gram negative facultative/aerobic that is oxidase negative and lactose positive be from

Back 507

Klebsiella, Enterobacter, Serratia, Citrobacter (also E coli)

Front 508

What genus might a gram negative facultative/aerobic that is oxidase negative and lactose negative be

Back 508

Salmonella, Shigella, Proteus, Yersinia

Front 509

What species (and type) might a gram negative facultative/aerobic that is oxidase negative, lactose positive and sorbitol negative be

Back 509

E coli O157:H7

Front 510

What genus might a gram negative rod that is urease positive be from

Back 510

Proteus, Klebsiella, Helicobacter, Ureaplasma

Front 511

What are the Enterobacteriaceae?

Back 511

Facultative, oxidase neg, ferment glucose: E coli, Salmonella, Shigella, Proteus, Yersinia

Front 512

Describe the Vibrionaceae

Back 512

Facultative, curved rods, oxidase positive

Front 513

Describe the campylobacteriaceae

Back 513

Curved microaerophilic, oxidase positive

Front 514

Describe Helicobacter

Back 514

curved, microaerophilic, oxidase positive, urease positive

Front 515

Describe the Pseudomonadaceae

Back 515

aerobes, oxidase positive

Front 516

Which gram negative organisms tend to be less pathogenic Lactose positive or lactose negative

Back 516

Lactose positive

Front 517

What are the four types of E coli that can cause GI disorders

Back 517

Enterotoxigenic (ETEC)
Enteropathogenic (EPEC)
Enterohemorrhagic (EHEC)
Enteroinvasive (EIEC)

Front 518

What is the type of E coli that causes UTIs

Back 518

Uropathogenic E coli

Front 519

What is the type of E coli associated with sepsis and meningitis in neonates

Back 519

Encapsulated E coli

Front 520

What is the presentation of Enterotoxigenic E coli

Back 520

Traveller's diarrhea, watery for several days. Toxin mediated infection causes nausea, vomiting, NO blood or mucus in feces. Self limiting

Front 521

What type of immunity protects against Enterotoxigenic E coli

Back 521

IgA

Front 522

What is the pathogenesis of Enterotoxigenic E coli

Back 522

Eterotoxin release causes hypersecretion of chloride ions and water due to increases in cAMP and cGMP

Front 523

What are the virulence factors of Enterotoxigenic E coli

Back 523

Colonization factor antigens (CFA) on pili helping to bind to small intestine. Heat labile and heat stable enterotoxins

Front 524

An increase of intracellular cAMP in the small intestine epithelia caused by bacteria will cause what

Back 524

Increased leaking of Na and Cl into the intestinal lumen (water follows) causing watery diarrhea

Front 525

What is the reservoir of Enteropathogenic E coli

Back 525

The human colon (no animals)

Front 526

What is the presentation of Enteropathogenic E coli

Back 526

Watery diarrhea, mostly in infants and children in developing countries; fever and vomiting may occur; self-limiting

Front 527

What are the virulence factors of Enteropathogenic E coli

Back 527

Bundle-Forming Pili (BFP), can cause loss of microvili, No particular toxin

Front 528

What is the presentation of Enterohemorrhagic E coli (EHEC - O157:H7)

Back 528

Mild to copius Bloody diarrhea; severe abdominal pain/cramps; little or no fever

Front 529

If Enterohemorrhagic E coli (EHEC - O157:H7) progresses to hemorrhagic collitis, what can follow

Back 529

Hemolytic uremic syndrome leading to acute renal failure

Front 530

What is the pathogenesis of Enterohemorrhagic E coli (EHEC - O157:H7)

Back 530

Consumption of contaminated foods, less than 100 organisms is needed

Front 531

How does Enterohemorrhagic E coli (EHEC - O157:H7) cause its most severe damage

Back 531

Release of shiga-toxin that destroy LARGE intestine microvilli, toxin enters blood stream causing endothelial damage and platelet aggregation leads to kidney damage

Front 532

What is the presentation of Enteroinvasive E coli

Back 532

Fever and scant-bloody diarrhea with pus in young children in developing countries

Front 533

Where does Enteroinvasive E coli bind in the human body

Back 533

Large intestine (That's why we can see blood in patients' stool)

Front 534

Which two forms of E coli bind in the small intestine

Back 534

ETEC, EPEC

Front 535

In which form of E coli is fever common? Absent?

Back 535

Common in EIEC, absent in ETEC

Front 536

What is the presentation of uropathogenic E coli

Back 536

UTI (more common in women); Cystitis (bladder infection with dysuria and frequent urination); Pyelonephritis (kidney infection with dysuria, fever, shaking chills, flank pain, nausea, vomiting)

Front 537

An eighteen year old, sexually active, patient complains of pain on frequent urination, flank pain, nausea, and fever. What is your diagnosis

Back 537

uropathogenic E coli

Front 538

Is uropathogenic E coli motile or non-motile

Back 538

Motile, helps in travelling up urinary tract

Front 539

What is the presentation of Extraintestinal (systemic) E coli

Back 539

Neonatal meningitis (can also be caused by Group B strep and Listeria), nosocomial (urinary catheter) infections in compromised

Front 540

What organisms can cause neonatal meningitis

Back 540

Extraintestinal E coli, Group B strep, Listeria

Front 541

What are some complications associated with Extraintestinal E coli infections

Back 541

Sepsis, endotoxic shock, pneumonia

Front 542

What organism causes a "true" dysentery type diarrhea? Describe this diarrhea

Back 542

Shigella; scant, bloody, mucus/pus, leukocyets in stool

Front 543

What is the presentation of Shigella

Back 543

Initial watery diarrhea, abdominal cramps, fever, dysentery diarrhea follows

Front 544

Where/what does Shigella bind and what happens to them, what are the immediate results

Back 544

Selectively binds M cells in LARGE intestine, taken in and escapes endosome to enter cytoplasm -> inflammation and cell death

Front 545

What can Shigella dysenteriae cause

Back 545

Hemolytic-uremic syndrome leading to renal failure similar to EHEC

Front 546

Does a shigella infection resolve itself?

Back 546

In most cases of healthy individuals, yes

Front 547

Both Shigella and Salmonella are lactose negative, how can they be told apart in the lab

Back 547

Shigella is H2S negative

Front 548

How often does Shigella enter the blood stream

Back 548

rarely

Front 549

What is the main reservoir of Shigella? Salmonella?

Back 549

Shigella-humans; Salmonella-animals

Front 550

Which requires more organisms to cause infection Shigella or Salmonella

Back 550

Salmonella

Front 551

Which can more easily invade the bloodstream, shigella or salmonella

Back 551

Salmonella

Front 552

Where does salmonella bind during initial infection

Back 552

BOTH small and large intestines

Front 553

In a patient you suspect of having Salmonella, what samples should you send to the lab

Back 553

BOTH stool and blood samples

Front 554

Is salmonella motile or non-motile

Back 554

Motile

Front 555

What is the reservoir of Salmonella typhi

Back 555

Chronic human carriers

Front 556

Why is Salmonella typhi so dangerous

Back 556

It can easily get into the bloodstream and can survive in macrophages

Front 557

"Rose spots" are associated with what microbe infection

Back 557

Salmonella typhi

Front 558

What species is most common bacterial cause of diarrheal disease

Back 558

Campylobacter jejuni

Front 559

Does campylobacter have a high or low infectious dose

Back 559

Low

Front 560

What is the presentation of campylobacter

Back 560

Watery to bloody diarrhea with fever and sever abdominal pain

Front 561

What tissues does campylobacter invade

Back 561

jejunum, ileum, and colon

Front 562

What autoimmune reaction is campylobacter jejuni associated with

Back 562

Guillain-Barre Syndrome

Front 563

Describe the labs for Campylobacter

Back 563

Fastidious, Gram(-) curved rod, oxidase (+)

Front 564

What is the presentation of Yersinia

Back 564

Bloody diarrhea, enterocolitis similar to salmonella and shigella after exposure to contaminated foods

Front 565

What is the source and what is the reservoir of Vibrio

Back 565

Animal source, human reservoir

Front 566

Is the infectious dose of vibrio high or low

Back 566

Very high

Front 567

What is the presentation of Vibrio

Back 567

"Rice Water" stools, watery and cloudy, copious amounts

Front 568

Where does Vibrio adhere

Back 568

Small intestines

Front 569

What toxin does Vibrio secrete

Back 569

Cholera toxin

Front 570

Other than Vibrio cholera, what are the other two Vibrio species to be aware of

Back 570

V parahemolyticus (dysenteric diarrhea), V vulnificus (septicemia risk)

Front 571

What are the lab diagnosis features of Vibrio

Back 571

Gram(-) curved rod, oxidase (+), very motile

Front 572

What organisms cause copious watery stool with no blood or pus, no tissue invasion, and is in the small intestine

Back 572

Vibrio cholerae, ETEC

Front 573

What organisms cause scant bloody stool with mucus and pus, has tissue invasion, and is in the large intestine

Back 573

Shigella, Entamoeba histolytica

Front 574

What organisms cause copious, thickened blood with no leukocytes, has tissue invasion and is in the large intestine

Back 574

EHEC

Front 575

What organisms cause copious liquid, bloody, or blood-tinged stool with pus, tissue invasion and is in the ileum and colon

Back 575

Salmonella, Campylobacter jejuni, Yersinia enterocolitica

Front 576

Food poisoning with an onset of 1-6 hours could be caused by

Back 576

Bacilus cereus, Staphylococcus aureus

Front 577

Food poisoning with an onset of 8-16 hours could be caused by

Back 577

Clostridium perfringens, Bacilus cereus

Front 578

Food poisoning with an onset of >16 hours could be caused by

Back 578

Campylobacter jejuni, Clostridium botulinum, E coli, Shigella

Front 579

What tissue does helicobacter colonize

Back 579

Stomach

Front 580

What enzymes does helicobacter release that help it to colonize the stomach

Back 580

Mucinase, ureases (releases ammonia)

Front 581

What are the laboratory diagnostic features of Helicobacter

Back 581

Gram(-) curved rod, oxidase(+), urease (+), motility(+), microaerophilic, urea breath test, endoscopy/biopsy culture

Front 582

What is the presentation of Klebsiella pneumoniae

Back 582

Bronchopneumonia, lung abscess, UTI, wound infections

Front 583

What is a notable virulence factor of Klebsiella pneumoniae

Back 583

Luxurious complex capsular polysaccharide

Front 584

A patient with respiratory Klebsiella pneumoniae infection will have sputum with what appearance

Back 584

Like currant jelly

Front 585

What are the laboratory diagnostic features of Klebsiella pneumoniae

Back 585

Short plump Gram(-) rod, lactose (+), Urease (+), non-motile

Front 586

What bacteria has a "swarming motility"

Back 586

Proteus

Front 587

What bacteria secrete urease

Back 587

Proteus, klebsiella, helicobacter

Front 588

What are some characteristics of Haemophilus influenzae

Back 588

Gram negative pleomorphic rods with fastidious growth requirements

Front 589

Are Haemophilus influenzae capsulated or unencapsulated

Back 589

Could be either depending on type

Front 590

Do Haemophilus influenzae require aerobic or anaerobic environments to grow

Back 590

Could be either (or both)

Front 591

What growth factors might Haemophilus influenzae require that are found in blood

Back 591

X factor - protoporphyrin IX, hemin precursor
V factor - NAD or NADP

Front 592

Which form of Haemophilus influenzae are normal flora of the upper respiratory tract

Back 592

Unencapsulated strains

Front 593

Haemophilus influenzae normally cause infections in what group of people

Back 593

Children

Front 594

Invasive diseases that can be caused by Haemophilus influenzae include what

Back 594

Meningitis, Epiglottitis, Cellulitis, Osteomyelitis, Sepsis, Pneumonia, Septic arthritis

Front 595

Noninvasive diseases that can be caused by Haemophilus influenzae include what

Back 595

Conjunctivitis, Sinusitis, Otitis media

Front 596

Why will Haemophilus influenzae not grow on normal blood agar, why does it require chocolate agar as growth media

Back 596

V-factor is inactivated in blood-agar and therefore is not available to H influenzae

Front 597

What is the major virulence factor of Haemophilus influenzae? What is protective against the bacteria?

Back 597

The capsule (PRP in type B), Ab against capsule in protective (must be specific to type of H influenzae

Front 598

What is an effect that the LOS on the outer membrane of Haemophilus influenzae has on respiratory epithelium

Back 598

Exerts a paralyzing effect

Front 599

List the major virulence factors of Haemophilus influenzae

Back 599

Capsule, LOS, IgA proteases

Front 600

Describe the pathogenesis of Haemophilus influenzae type b

Back 600

Infection by inhalation of infection droplets, invasion of blood stream (type b capsule is essential for invasion), replication in blood and seeding of various sites

Front 601

How might neurological sequelae occur in children who recover from Haemophilus influenzae type b

Back 601

Damage caused by organism itself as well by cytokine release in host response.

Front 602

Why might Haemophilus influenzae infection be rare during the first three months of life

Back 602

maternal antibody

Front 603

What organism is the cause of whooping cough in humans

Back 603

Bordetella pertussis

Front 604

What is whooping cough also known as

Back 604

pertussis

Front 605

What two organisms can produce pertussis-like symptoms in humans

Back 605

Bordetella pertussis and Bordetella parapertussis

Front 606

Describe the characteristics of Bordetella pertussis

Back 606

Gram negative rod, non-motile, only grows on special media containing starch or charcoal to remove fatty acids

Front 607

If you want laboratory confirmation that your patient has whooping cough, what must you indicate to the lab running samples

Back 607

That you are looking for Bordetella pertussis so that they can culture the sample on special media

Front 608

Is Bordetella pertussis invasive of body tissues

Back 608

No?

Front 609

What is the major virulence factor of Bordetella pertussis? Describe it

Back 609

Pertussis toxin, classic A-B toxin (A portion is toxic and enters cell, B is receptor)

Front 610

What does the Pertussis Toxin do upon entering the cell

Back 610

A toxin splits NAD into nicotinamide and ADP-ribose which inactivates G1 protein controlling adenylate cyclase activity leading to build up of cAMP causing the cell to secrete massive amounts of fluids and electrolytes

Front 611

What are the three stages of pertussis

Back 611

Catarrhal phase - Runny nose, malaise, fever
Paroxysmal phase - cough, vomiting, leukocytosis
Convalescence

Front 612

What stage of pertussis is the most contagious

Back 612

Catarrhal

Front 613

What are the diagnostic tools in identifying a patient with pertussis in the catarrhal (early) stage

Back 613

DFA (direct fluorescent antibody)
PCR
Serology (for IgG and IgA against B pertussis antigens)

Front 614

Describe the characteristics of Legionella

Back 614

Fastidious Gram-negative aerobic bacilli

Front 615

Most documented infections in the US by Legionella pneumophila have been

Back 615

serogroup 1 strains

Front 616

How is legionnaires disease (caused by legionella) acquired

Back 616

Inhalation of aerosolized water contaminated with Legionella pneumophila

Front 617

What organism is responsible for the short-onset disease known as Pontiac fever

Back 617

Legionella

Front 618

What people is Legionella most likely to infect

Back 618

The elderly and immunocompromised

Front 619

What are the expected symptoms of Legionnaires disease

Back 619

Varies from mild to severe pneumonia characterized by fever, cough and proressive respiratory distress

Front 620

An elderly patient presents with moderate pneumonia, fever, cough, and increasing respiratory distress. His wife reports that he had recently used their old jacuzzi. What might he have?

Back 620

Legionnaires disease

Front 621

What are the expected symptoms of Pontiac fever

Back 621

No pneumonia, occurs in epidemic characterized by self-limited influenza-like manifestations

Front 622

What are some diagnostic tests for a patient infected with Legionella

Back 622

Sputum culture, DFA sputum stain, Urinary antigen, serum antibody

Front 623

What are the three main non-invasive gram-negative bacteria that Dr. S discussed

Back 623

Vibrio cholera, ETEC, EPEC

Front 624

Where is Pseudomonas aeruginosa found (in general)

Back 624

Everywhere, it is ubiquitous, "biofilm"

Front 625

What are the major characteristics of Pseudomonas aeruginosa

Back 625

Obligate aerobe, oxidase (+), motile, encapsulated by glycocalyx/slimelayer, minimal nutritional requirements, highly resistant to antibiotics, pigmented

Front 626

Suppose you found, in the lab, an obligate aerobe that is oxidase (+), motile, and forms slimy blue/green colonies, what might you have?

Back 626

Pseudomonas aeruginosa

Front 627

What is the only lactose negative organism that is oxidase positive?

Back 627

Pseudomonas aeruginosa

Front 628

What is a common mode of transmission of Pseudomonas in a hospital setting

Back 628

Respiratory therapy equipment

Front 629

How might Pseudomonas be transmitted

Back 629

On or in just about anything that is wet

Front 630

What are the virulence factors of Pseudomonas

Back 630

Pili & flagella for adherence/colonization
Glycocalyx
Proteolytic Enzymes
*Exotoxin A - like C diptheriae
Endotoxin-LPS

Front 631

CF patients are at increased risk for infection by what type of Gram negative bacteria?

Back 631

Pseudomonas aeruginosa

Front 632

What are likely sources or risk factors for development of a localized pseudomonas infection

Back 632

Wounds (esp burns)
Whirlpools & tubs

Front 633

What are the complications of a systemic Pseudomonas infection

Back 633

Just about everything you could imagine of systemic bacterial infections

Front 634

A patient presents with an infected burn wound coated in a white-ish green pus and smells of a fruity odor. What organism might be responsible for this infection

Back 634

Pseudomonas aeruginosa

Front 635

Is there a vaccine for Pseudomonas

Back 635

No

Front 636

What are the characteristics of Brucella

Back 636

Aerobic facultative intracellular parasite, small poorly staining, very hardy, prolonged incubation to culture

Front 637

What is the major virulence factor of Brucella

Back 637

LPS

Front 638

How is Brucella transmitted

Back 638

Contact with or consumption of infected fluids from animals (esp. cows)

Front 639

Does Brucella have a high or low infective dose

Back 639

Low

Front 640

What is it important to know about Brucella pathogenesis

Back 640

It can easily penetrate into the blood

Front 641

A dairy farm worker presents with chills, weight loss, depression, and pain in his joints. He also has a fever that rises during the day and decreases at night. What might he be infected with

Back 641

Brucella

Front 642

What organism causes tularemia (rabbit fever)

Back 642

Francisella tularensis

Front 643

Describe the characteristics of Francisella tularensis

Back 643

Gram-neg., small pleomorphic coccobacilli, lipid-rich capsule, strict aerobe, has endotoxin, no exotoxin, Facultative intracellular parasite)

Front 644

What is the mode of transmission for Francisella tularensis to humans

Back 644

Arthropod vectors (and deerfly) or animal contact/abrasions

Front 645

Is the infectious dose of Francisella tularensis high or low

Back 645

Very low

Front 646

What is the pathogenesis of Francisella tularensis

Back 646

Begins cutaneously as erythematous papule, ulcerates, persists, then organism spreads to RES system via lymph

Front 647

What are the symptoms of Tularemia

Back 647

Acute onset, flu-like chills, fever, headache, malaise, fatigue, anorexia and papules on skin as well as lymphadenopathy

Front 648

Is there a vaccine for tularemia

Back 648

Experimental live vaccine

Front 649

How is Tularemia diagnosed

Back 649

Clinical history (exposure), lab growth, Serodiagnosis is best (IgG titers)

Front 650

What organism causes "The Black Plague"

Back 650

Yersinia pestis

Front 651

What are the characteristics of Yersinia pestis

Back 651

Gram-neg. rod, bipolar staining, oxidase neg., LPS capsule, facultative intracellular

Front 652

What are the major virulence factors of Yersinia pestis

Back 652

LPS, capsule, many Yersinia Outer Proteins that inhibit effectiveness of immune response

Front 653

What is the infectious dose of Yersinia pestis

Back 653

Extremely low (1-10 orgs)

Front 654

If Yersinia pestsis loses its capsule, can it still cause disease?

Back 654

No

Front 655

What is the mode of transmission of Yersinia pestis

Back 655

Fleas transmitting bacteria from infected animals (squirrels and rats, etc)

Front 656

A patient presents with an enlarged lymph node, on physical exam you notice scratches on their hand. You ask if they have a cat, they say yes. What might the cause of the lymphadenopathy be

Back 656

Bartonella

Front 657

A patient presents with a wound from a dog bite that is developing cellulitis around it. Should you suture the wound? Why/Why not?

Back 657

No, Pasteurella grows better when wound is sutured

Front 658

What are the general characteristics of Spirochetes

Back 658

Long, slender, motile, flexible, gram(-) bacilli (corkskrew)

Front 659

What are the three spirochetes that we need to know

Back 659

T pallidum, Borrelia, Leptospira

Front 660

What organism causes syphilis

Back 660

T pallidum

Front 661

What organism causes lyme disease

Back 661

Borrelia

Front 662

How is T pallidum cultured in vitro

Back 662

It can't be, only grown in rabbit testes

Front 663

What is the pathogenesis of T. pallidum

Back 663

Transmission either sexual contact or transplacentally, enters via break in skin or penetration of mucous membranes, no exotoxin or endotoxin, **Injury may be due to prolonged DTH response**

Front 664

Primary syphilis presents with what approximately how long after innoculation

Back 664

3 weeks (at least), chancre on site of innoculation

Front 665

Secondary syphilis presents with what

Back 665

Rash that starts on plams and soles of feet, can also have systemic appearances (hepatitis, meningitis)

Front 666

Tertiary syphilis presents with what

Back 666

Gumma on skin (granulomatous lesion), degeneration of nervous system and cardiovascular problems

Front 667

What are some added risks of congenital syphilis

Back 667

Fetal death, spontaneous abortion, stillbirth

Front 668

How is the organism identified in a patient you suspect of having syphilis

Back 668

Can be visualized under darkfield microscopy from primary and secondary lesions (sometimes), Usually diagnosed by serological tests

Front 669

Which is larger T pallidum or Borrelia burgdorferi

Back 669

Borrelia burgdorferi

Front 670

What are some characteristics of Borrelia burgdorferi

Back 670

Large spirochete, flagellated, Do not make endo or exotoxins

Front 671

What is the most common vector-borne infection in the United States

Back 671

Lyme disease

Front 672

What is the pathogenesis of Borrelia burgdorferi (Lyme disease)

Back 672

Vector-born infection transmitted by deer/rodent tick

Front 673

What are some clinical findings associated with Borrelia burgdorferi

Back 673

Tick bite, Erythema migrans (potentially bulls-eye shaped rash) within 1-4 wks, joint pain and neruological complications (wks to mos), chronic arthritis and CNS disease (mos to yrs)

Front 674

What are the ways of identifying the organism in labs looking for Borrelia burgdorferi

Back 674

Can be cultured, but slow and difficult, serological tests, PCR

Front 675

What organisms that we have discussed present with relapsing fever

Back 675

Bartonella (~5 days), Borrelia recurrentis (~4-10 days)

Front 676

How is Leptospira interrogans contracted

Back 676

transmitted by food or water contaminated with animal urine or feces (swimming in contaminated water)

Front 677

How might one identify an atypical bacterial respiratory infection caused by mycoplasma or chlamydia instead of staph or strep

Back 677

Gradual onset of symptoms, non-productive and scant sputum, no bacteria on sputum smear, patchy pneumonia (not lobar)

Front 678

What bacteria have no cell wall

Back 678

Mycoplasma

Front 679

What are some characteristics of Mycoplasma

Back 679

No cell wall, lipid bilayer contains sterols, fastidious (require cholesterol) "fried egg" colony appearance

Front 680

Would penicillin be effective against Mycoplasma? Why?

Back 680

No, no cell wall for penicillin to act on

Front 681

What is the transmission of Mycoplasma pneumoniae

Back 681

Inhalation of infected respiratory droplets

Front 682

How does mycoplasma pneumoniae cause damage

Back 682

Binds and inhibits ciliary action so mucosa desquamates

Front 683

How is Mycoplasma pneumoniae identified in lab tests

Back 683

Seroligically (cultures too slow growing)

Front 684

What are two genital Mycoplasma

Back 684

Ureaplasma and M hominis

Front 685

What are the organisms that you would expect to produce Urease

Back 685

Helicobacter, Proteus, Klebsiella, Ureaplasma

Front 686

What organism is an obligate intracellular organism

Back 686

Chlamydiae

Front 687

What are the characteristics of Chlamydiae

Back 687

Obligate intracellular, dual-lipid bilayer, no peptidoglycan (still has LPS)

Front 688

What are the two forms that Chalmydiae are found in, in the body

Back 688

Reticulate body and elementary body (spore like)

Front 689

What organism is responsible for the most common STD

Back 689

Chalmydia trachomatis

Front 690

Is Chlamydia trachomatis invasive?

Back 690

Rarely

Front 691

What are some risks aside from those directly related to the infection of a Chlamydia trachomatis infection

Back 691

PID, sterility, atopic pregnancy

Front 692

How will Chlamydia trachomatis appear on a gram-stain

Back 692

it won't

Front 693

What does Chlamydophila pneumoniae cause

Back 693

Atypical pneumonia

Front 694

What does Chlamydophila psittaci cause and how is it transmitted

Back 694

Acquired from dried feces of parrot family birds, Atypical pneumonia

Front 695

Rickettsiae mainly cause problems where

Back 695

within the vasculature

Front 696

The rickettsiae are normally transmitted by what

Back 696

Arthropod vectors

Front 697

A patient presents with rash, fever, and headache, what should you be considering at this point?

Back 697

Rickettsia and other tick-borne infections

Front 698

What is a major virulence factor for Rickettsia

Back 698

Phospholipase A, causes damage and escape from phagolysosomes

Front 699

What organisms mobilize actin

Back 699

Listeria, Shigella, Rickettsia

Front 700

The vasculatory effects of Rickettsia will/may lead to what

Back 700

Rash, high fever, malaise, headache, vascular collapse (tissue anoxia, drop in BP, shock)

Front 701

Rocky Mountain Spotted Fever is caused by what organism

Back 701

Rickettsia rickettsii

Front 702

The rash associated with Rocky mountain Spotted Fever could be confused for what other disease

Back 702

Syphillis

Front 703

Coxiella burnetii (Q fever) is transmitted by what

Back 703

NOT by arthropods (exception among rickettsia) transmitted by inhalation or abrasion

Front 704

Coxiella burnetii causes what?

Back 704

Atypical pneumonia