Micro Uni 2

Front 1

Herpesviridae
Structure

Back 1

dsDNA
Enveloped
Linear

Front 2

Herpes Infection patterns

Back 2

Lytic

Persistent

Latent or Transforming

Front 3

Herpes Theraputic Agent

Back 3

Thymidine Kinase

Front 4

HSV attachement Site

Back 4

Heparan Sulfate
glycoprotein found on many cells

Front 5

Stages for HSV infection

Back 5

Immediate: control gene transcription
Early: Polymerase and other enzymes
Late: protein synthesis

Front 6

Epidemiology of HSV

Back 6

Found in Secretions

Vaginal
Saliva
Vesicle
Towels
Glasses

Front 7

Clinical Features of HSV

Back 7

Oral cold, sores, fever, blisters and genital vesicles

Front 8

HSV Eruptions are caused by

Back 8

fever
UV light
menstruation
local irriation

Front 9

Cowdry Type A acidophilic intranuclear inclusion bodies

Back 9

HSV 1 and 2

Front 10

Disease caused by HSV

Back 10

Herpes pharyngitis
ocular keratitis
Herpetic whitlow
encephalitis (HSV 2)

Front 11

Lab diagnosis for HSV

Back 11

Tzank Smear

Virus isolation

Front 12

Prevention of HSV

Back 12

Avoid exposure

Front 13

What is acyclovir

Back 13

Its is used to mimic guanosine and prevent HSV

Front 14

Thymidine Kinase

Back 14

Receptor, therapeutic target

Front 15

Binding site for EBV

Back 15

CR2 of the B-cell

Front 16

Outcomes after EBV binds to B-Cells

Back 16

Permissive
Latent
Immortalization of B cells

Front 17

EBV early Antigens

Back 17

Early Antigen
Viral Capsid antigen

Front 18

EBV Latent Antigens

Back 18

Non permissive, EBNA and LMP

Front 19

Kissing disease

Back 19

EBV

Front 20

Virus spreads for a lifetime

Back 20

EBV

Front 21

Children Asymptomatic

Back 21

EBV
M.Tb

Front 22

Infective Mononucleosis

Back 22

EBV

Front 23

Sore throat
Lymphadenopathy
Splenomegaly

Back 23

Infective Mononucleosis

Front 24

Burkitt's lymphoma

Back 24

EBV

Front 25

Nasopharyngeal Carcinoma

Back 25

EBV

Front 26

Lymphoproliferative Disease

Back 26

EBV

Front 27

Chromosome Effected with EBV

Back 27

c-myc gene from chromosome 8/14 translocation

Front 28

Downey Cells

Back 28

Atyptical lymphocytes seen in EBV

Front 29

Monospot Test

Back 29

Heterophile Antibody for EBV

Front 30

Antibodies tested for EBV

Back 30

EA and EBNA

Front 31

Which are the only organs that escape Tb infections

Back 31

Tests and ovaries

Front 32

Morphology of Neisseria meningitidis

Back 32

Gram - Diplococci with a kidney bean shaped

Front 33

Oxidase and catalase positive

Back 33

N.Meningitidis

Front 34

Oxidase test where dye changes color

Back 34

N.Meningitidis

Front 35

Polysaccharide capsule with 13 serologic groups A,B,C,Y and W135

Back 35

N.Meningitidis

Front 36

Normal flor of N.Meningitidis

Back 36

Nose and throat

Front 37

Move through sinuses and can even go to the brain

Back 37

N.Meningitidis

Front 38

Transmission of N.Meningitidis

Back 38

Aerosols, college and school children

Front 39

Effects children with later complement deficiency

Back 39

N.Meningitidis

Front 40

Contain antiphagocytic capusles and pilli

Back 40

N.Meningitidis
H. Influenza

Front 41

Purulent, headache, fever, stiffness

Back 41

Meningitis which is caused by N.meningitidis and H.Influenza

Front 42

Petechia, purpura, thrombosis of small blood vessels, septic shock

Back 42

Meningococcemia which is caused by N.Meningitidis

Front 43

Bilateral renal gland hemorrhagic necrosis

Back 43

Waterhouse-Friderichsen syndrome which is caused by N.Meningitidis

Front 44

Chocolate agar, Thayer-martin chocolate agar

Back 44

N.Meningitidis

Front 45

Vaccines of four polysaccharides A,C,Y and W135 MPSV4

Back 45

N.Meningitidis

Front 46

MCV4/MPSV4 vaccine

Back 46

N.Meningitidis

Front 47

3 main human pathogens of H. Haemophilus

Back 47

H.influenza
H.ducreyi
H.aegyptius

Front 48

Conjuctivitis (pink eye)

Back 48

H.Aegyptius

Front 49

Chancroid an STD

Back 49

H.ducreyi

Front 50

What do H.Haemophilus require for growth

Back 50

Hemin the X factor
NAD
V factor

Front 51

Structure of H.Influenza

Back 51

Six capuslar antigenic types, Polyribitol ribose phosphate (PRP), Hib.

Front 52

Non-typable strains that lack a capsule

Back 52

H.influenza

Front 53

Cause Otitis Media and Sinusitis

Back 53

H.influenza

Front 54

Epiglottitis

Back 54

H.Influenza
Can cause obstruction

Front 55

What is the basic characteristics of Mycobacteria

Back 55

Aerobic, slow growing, non spore forming bacilli

Front 56

Stain for Mycobacteria

Back 56

Acid Fast

Front 57

Main content of Mycobacteria

Back 57

Mycolic acid, Lipid, making them very hydorphobic

Front 58

Morphology of Mycobacteria Colonies

Back 58

Yellow to orange, dry fraible colonies

Front 59

What is the main mode of transmission of M.Tuberculosis, and how prevelent is it ?

Back 59

Aerosol transmission and 1/3 of the world's population is infected

Front 60

MOA of M.Tb

Back 60

Blocks phagosome-lysosome fusion after being phagocytosed by the cell.

Front 61

Severity of most M.Tb infections

Back 61

Asymptomatic or latent

Front 62

Cellular reactions of M.Tb

Back 62

Epithelioid cells, macrophages containing bacteria for granulomas with necrotic centers that can be reactivated with stress

Front 63

Main virulent factor of M.Tb

Back 63

Cord Factor (a lipid) kills mice and induces granulomas

Front 64

Symptoms of M.Tb in the lung

Back 64

Cavitary lung disease (cough, bloody sputum, fever, chils, night sweats, weight loss)

Front 65

Systemic Symptoms of Tb

Back 65

Miliary (multiple foci) disseminated and extra pulmonary disease of many tissues

Front 66

Drug resistant forms of Tb

Back 66

MDR-TB (multi drug resistant) isoniazid/rifampin
XDR-TB (extreme drug resistant) quinolone and aminoglycoside

Front 67

Diagnositic Tests for Tb

Back 67

Tuberculin Skin Test (Mantoux)
Acid Fast Staining of SputumFluorescent Dyes

Front 68

Culturing methods for Tb

Back 68

Decontamination of sputum specimens with 2% sodium hydroxide
Egg based media

Front 69

Lab Diagnosis test for Tb

Back 69

IFN-gamma assays

Assay for the production of IFNg by the patients blood cells is evidence of lymphocyte reaction with antigens

Front 70

Main features of Mycobacterium Avium

Back 70

Shares same microbiology as M.Tb
Effects those with pulmonary conditions, Immunodeficient, smokers.

Front 71

MAC pathogensis

Back 71

Patchy lung infiltrates

Front 72

Which are the slow growing mycobacteria

Back 72

M. Kansasii
M. Bovis

Front 73

Which are the cutaneous pathogens

Back 73

M. Ulcerans: tropical, skin grafts.
M. Marinum in swimming pools.

Front 74

Microbiology of Mycobacterium Leprae and other names for it

Back 74

Cannot be grown in culture

Leprosy or Hansen's disease

Front 75

Transmission of M.Leprae

Back 75

Contact, Aerosols, skin abrasion

Front 76

Pathogenesis of M. Leprae

Back 76

heavy tissue burden of bacteria.

tuberculoid has fewer bacteria in tissue

Front 77

Rusty Sputum

Back 77

Strep.Pneumo

Front 78

Which immunosuppression is common among drug users

Back 78

HIV

Front 79

Prevention Immunization of H.Influenzae

Back 79

Conjugate type b vaccine

Front 80

The virulence factor of Listeria Monocytogens

Back 80

Listeriolysin O

Front 81

Gram positive, short motile bacilli with tumbling motion

Back 81

Listeria Monocytogenes

Front 82

Found in soil, Vegetations, and the feces of animals

Back 82

Listeria Monocytogenes

Front 83

Populations at risk of Listeria Monocytogens

Back 83

High adult population like pregnant, risk of infants from non immune infected mothers.

Front 84

Cells enter and enter enterocytes and attach to M cells

Back 84

Listeria Monocytogenes

Front 85

Action of Listeriolysin O in L.Monocytogens

Back 85

Phagolysosome release

Front 86

Actin based intracellular motility, moving cells to systemic sites

Back 86

Listeria Monocytogenes

Front 87

Stages of L.Monocytogens clinical infections

Back 87

Early onset in utero, birth defects due to transplacental infection.
Late onset: infant meningitis
Adult disease: as symptomatic in health, mild flu like symptoms in healthy adults.

Front 88

CAMP test

Back 88

Listeria Monocytogenes

Front 89

Weak Beta hemolysis and cold enrichment

Back 89

Listeria monocytogenes

Front 90

Morphology of Rabies Virus

Back 90

bullet shaped rhabdovirus, enveloped,helical,
negative sense ssRNA.

Front 91

RNAdep-RNApoly

Back 91

Rabies Virus

Front 92

Rabies Epidemiology

Back 92

Zoonotic from dogs, cats, mad dog disease.DOMESTIC ANIMALS

Front 93

Virus binds acetylcholine receptors, moves up neural system to brain, then outward to cornea, hair roots and salivary glands.

Back 93

Rabies Virus

Front 94

Hydrophobia and paralysis

Back 94

Rabies Virus

Front 95

Negri bodies

Back 95

Intracytoplasmic are viral aggregates in neural tissues seen in animal or post mortem human. In Rabies.

Front 96

Fluorescent antibody test of animal tissue for virus presence

Back 96

Rabies Virus

Front 97

RT-PCR on saliva

Back 97

Rabies Virus

Front 98

Wound cleansing and Injection of HRIG as well as active immunization

Back 98

Human rabies immune globulin is for prevention of Rabies.

Front 99

small RNA viruses

Back 99

Picornviridae

Front 100

Virology of Poliomyelitis

Back 100

Enterovirus, acid stable, 37 C growth, and its tissues target sepatartts it from other members.

Front 101

Structure of Poliomyelitis

Back 101

Positive ssRNA
Has four proteins that are rearranged after attachement and bind Ribosome.

Front 102

Transmission of Poliomyelitis

Back 102

Fecal-Oral
Contaminated Water

Front 103

Pathogenesis of Poliomyelitis

Back 103

- Asymptomatic (90%) with intestinal invasion. Abortive infection (5%).
- Paralytic Poliomyelitis-less than 2% of infection. Pentrates bowel to blood to anterior horn of spinal cord and motor complex.
- Bulbar polio 75% of the 2% fatal, respiratory Muscle paralysis.
-Post-polio syndrome 20-80%

Front 104

Lab test for Poliomyelitis

Back 104

Throat swabs to cell culture early, from feces later, CSF variable recovery.

Front 105

Prevention and Control of Poliomyeltis

Back 105

- Salk inactivated polio vaccine (IPV), prevents disease but not intestinal infection. Was found to cause infection in some people.
- SaBin vaccine: Bowel infections will be eliminated, increase intestinal immunity. Immunity is spread from primary person, from person to person.

Front 106

Poliomyelitis drug reactions

Back 106

You would start with 2 Doses of the Salk vaccine and then administer

Front 107

Structure of Arenaviruses

Back 107

Enveloped, 2 ssRNA segments,

Front 108

Replication of Arenaviruses

Back 108

- L strand is negative with RNAdep-RNApoly.
Ambiesense strand that can be read as RNA in 2 directions (one end is positive while other end is negative).
- Contains host ribosomes to give sandy appearance in EM.

Front 109

Epidemiology of Arenavirus

Back 109

Lymphocytic Chroiomeningitis (LCM).Transmission through aerosol transmission of the fecal substance of the mouse or hamsters.
- Africa: Lassa fever, pulmonary hemorrhagic diseases with high percentage of death.

Front 110

Types of Polyomavirus

Back 110

JC and BK viruses

Front 111

Epidemiology of JC and BK viruses

Back 111

Water or Sewage, human exposure early in life, continual shedding through kidneys throughout life.

Front 112

Pathogenesis of JC and BK Viruses

Back 112

Polyomavirus as symptomatic except for cancer and suppressive therapy, causes progressive multifocal leukoncephalopathy, a demyelenating disease of what matter.

Front 113

Lab test of JC and BK viruses

Back 113

CSF, urine source, expansion by PCR.

Front 114

Prevention control of JC and BK viruses

Back 114

Avoid immunosuppressive therapy

Front 115

Defective Measles Virus

Back 115

Subacute Sclerosing Panencephalitis

Front 116

Muscle Jerks or spasticity, blindness, personality and behavioral changes.

Back 116

Subacute Sclerosing Panencephalitis

Front 117

What kinds of viruses are arthropod born

Back 117

RNA viruses, some are positive strand and some are negative strand.

Front 118

Structure of Arbovirus

Back 118

zoonotic RNA viruses

Front 119

Main vectors for the Arbovirus

Back 119

Mosquitoes

Front 120

Family Togaviridae

Back 120

Alpha Virus
EEE,WEE,VEE

Front 121

Family Bunyaviridae

Back 121

CA
LaCosse
Hanta

Front 122

Types of Flaviviridea

Back 122

Yellow Fever Virus
Dengue
West Nile
St. Louis Encephalitis Virus
Powassan Virus
Japanese B Encephalitis Virus
Hep. C Virus
Heptatitis G Virus

Front 123

Pathogensis of Flavivirus

Back 123

Mild systemic disease is usual, fever, chills, headache. Jap B may produce severe even fatal Encephalitis.

Front 124

Structure of Togaviridae and Flaviviridea

Back 124

Positive ssRNA enveloped viruses, cloak like cover that looks like a toga.
E1 and E2 peplomers are both found on the cover.

Front 125

Flaviviruses that may produce servere hemorrhagic disease

Back 125

Dengue and Yellow fever (liver disease)

Front 126

Replication Process of Togaviridea

Back 126

ssRNA positive-polyprotein synthesis and cleavage-negative strand RNA is made-progeny RNA

Front 127

Epidemiology of EEE and WEE

Back 127

Togaviruses
Birds Reservoir
Mosquitoes Vectors
Horses and Humans are dead end hosts

Front 128

Sleeping sickness was seen in which diseases as well

Back 128

Trypanosomas
African sleeping sickness

Front 129

Pathogensis of EEE and WEE

Back 129

Togoviridae
Virus attaches to monocytes and endothelial cells.
Flu like, headache, fever, muscle pain, photophobia.
Entry into the brain through small vessel endothelia.
Aseptic encephalitic phase generally resolves withough sequelae.
EEE is more serious than WEE

Front 130

Horse develops fatal sleeping sickness and mortality

Back 130

EEE and WEE

Front 131

Same course as EEE and WEE but is not as serious, very few cases in the USA

Back 131

VEE

Front 132

Chikungunya

Back 132

Bending over. More series disease than EEE, WEE or VEE. Restricted to Africa. An acute febrile disease with arthralgia, muscle pain lasting month or years. Hemorrhagic.

Front 133

Epidemiology of West Nile Virus

Back 133

Flavivirus that is worldwide.
Birds reservoir-Culex Mosquitoes vector

Front 134

Pathogensis of West Nile Virus

Back 134

90% assymptomatic
Fever, headache, chills, joint pain, flu like.
Encephalities Phase, near fatality.

Front 135

How many antigenic types are there for dengue fever

Back 135

Den 1 through Den 4

Front 136

Lab Diagnosis for West Nile Virus

Back 136

IgM
RT-PCR or Viral RNA recognition

Front 137

Epidemiology of Saint Louis Encephalitis Virus

Back 137

Flavivirus that is found in the Central and Eastern USA (missouri river).

Front 138

Pathogenesis of SLEV

Back 138

Asymptomatic and mild CNS.

Front 139

Epidemiology of Powassan Virus

Back 139

ssRNA, E1 and E2.
Ixodes ticks ar the reservoir and the vector.
North America and Canada

Front 140

Pathogenesis of Powassan Virus

Back 140

Flu like mild disease and encephalitis

Front 141

Epidemiology of Japanese B

Back 141

ssRNA,
Reservoirs are birds and pigs and the vector is a Culex (mosquito).
Japan and neighboring countries

Front 142

Epidemeiology of Dengue fever

Back 142

Tropical and subtropical areas where victors reside, Mosquitoes are the main vectors.
Human primates are reservoirs, sylvatic and urban cycles.

Front 143

Pathogenesis of Japanese B

Back 143

Mild flu like, and can be fatal more often than the above.

Front 144

Pathogenesis of Dengue Fever

Back 144

Break bone fever, headache, muscle and joint pain. Rash could be present but there is no encephalitis.

Front 145

Major Risk from Dengue Fever

Back 145

Dengue Hemorrhagic Fever (DHF)

Front 146

Symptoms of Dengue Hemorrhagic Fever

Back 146

Irritability, restless, heavy sweating with petechia, bleeding tendency.

Front 147

Dengue Shock Syndrome (DSS)

Back 147

Deteriorates with the accumulation of blood in the abdomen, abundant petechia, loss of blood pressure.

Occurs after second infection to the disease.

Front 148

The flooding and removal of standing water to prevent moquito breeding

Back 148

Yellow Fever

Front 149

Human, primates, sylvatic and urban cycles, also found in Aedes mosquitoes

Back 149

Yellow Fever

Front 150

Stage of Yellow Fever Pathogenesis

Back 150

Early: fever, nausea and abdominal pain
Late: pain and jaundice
Hemorrhagic: black vomit

Front 151

Lab for Yellow fever

Back 151

RT-PCR
Patient serum for immune response

Front 152

Bunyaviridea Structure

Back 152

Enveloped, negative, ssRNA, 3 segmented virus. RNApoly-RNAdep.

Front 153

Epidemiology of Bunyavirus

Back 153

Rodents urine and feces and spread by infected ticks

Front 154

California and La Crosse Viruses

Back 154

Type of Bunyavirus, as symptomatic. Nausea, vomiting, headache, seizure in true encephalitis.

Front 155

Feature of Hanatvirus

Back 155

Sin Nombre. Dust contaminated by urine and feces of white footed mice.

Front 156

Pathogensis of Hantavirus

Back 156

Pulmonary and Cardiac syndromes with a lot of loss of blood.

Front 157

Coltivirus-Colorado tick fever features

Back 157

dsRNA virus. They are plus strands in an mRNA, translation to RNAdep-RNApoly for genomic RNA forms

Front 158

Epi. of Colitivirus

Back 158

Mountain West, hard ticks.

Front 159

Pathogenesis of Coltivirus-Colorado tick fever

Back 159

Flu like symptoms to aseptic

Front 160

Scrapie and Mad cow disease, bovine spongiform encephalopathy (BSE)

Back 160

Prions proteins, that are a denatured proteins.

Front 161

Disease caused by prions in New Guniea

Back 161

Kuru, which is a transmissible neurologic disease that originated from cannabalism.

Front 162

Creutzfeldt-Jacob disease (CJD)

Back 162

dementia leading to death in the prion disease.

Front 163

Pathogenesis of prions

Back 163

Protease resistant proteins

Front 164

Name for prion proteins

Back 164

PrPc and PrPsc

Front 165

Prion type that binds to human cellular

Back 165

Scrapie type, and causes it to aggregate into amyloid fibers and/or vacuoles that accumulate in the brain.

Front 166

Symptoms of PrPsc

Back 166

Ataxia, dementia, behavioral changes, memory loss, development of spongiform lesion and amyloid deposit in the brain.

Front 167

Transmission by ingestion

Back 167

Prions

Front 168

Accumulation of PMN and other immune cells as well as debris

Back 168

Brain Abscess that is caused by post surgical procedure, or trauma. This later increase the cranial pressure.

Front 169

Organism pass through the nose from water. Into the nose and then to the brain where they can be fatal.

Back 169

Naegleria Fowleri

Front 170

Organism that is caused by those who wear contact lenses with no proper hygiene

Back 170

Acanthamoebae Castellani

Front 171

Pathogenesis of Taenia Solium

Back 171

Flatworm (cestode) which has a head (scolex) and proglottid segments

Front 172

Adult worm in swine intestine sheds eggs, hexacanth embryo (oncosphere) develops

Back 172

Taenia Solium parasitology

Front 173

Taenia Solium Lifecycle

Back 173

a. Eggs in water and soil ingested by swine
b. Oncosphere larvae penetrate gut, enter tissue
c. Swine develop tissue cysticerci (bladder worms)
d. If humans ingest hexacanth eggs, they hatch to
larval oncosphere that penetrates gut and
tissue cysticerci develop in lungs, brain, etc
e. If humans eat undercooked pork the typical cestode
develops in the gut from the cysticercus and sheds ova

Front 174

CNS effecting protozoa

Back 174

Trypanosomes Brucei, and Trypanosomes Brucei

Front 175

CNS Nematodes

Back 175

Toxocara Canis and T. Cati

Front 176

T.Canis and Cati Lifecycle

Back 176

a. Natural gut parasite of dogs and cats
b. Eggs ingested by humans and larvae develop but
wander in tissues and fail to complete life cycle

Front 177

Mycological CNS

Back 177

Cryptococcus Neoformans

Front 178

Spherical yeast with a capsule larger in diameter

Back 178

Cryptococcus Neoformans
H.Pylori

Front 179

Positive Urease Test

Back 179

Cryptococcus Neoformans

Front 180

Very slow growing yeasts that cause meningitis

Back 180

Cryptococcus Neoformans

Front 181

Neonate born in poor conditions with encephalitis

Back 181

HSV 2

Front 182

Cystic Fibrosis, with pneumonia, blue green sputum

Back 182

Pseudomona Aurigonsa

Front 183

Jelly sputum

Back 183

Klebsiella

Front 184

Lesions on face of cutanous touch and pain, Acid fast organism

Back 184

Leprae

Front 185

Sore throat, spleen and liver. Later LEADING TO SPLENIC RUPTURE

Back 185

EBV

Front 186

Triad of Meningitis

Back 186

Headache, Fever, Stiff Neck

Front 187

Drug of choice for Neisseria Meningitids

Back 187

Ceftriaxone

Front 188

Patient comes in with petechia and stiff neck

Back 188

N.Meningitidis

Front 189

Test for N. Meningitidis

Back 189

Blood, Urine, and Sputum

Front 190

Where do you never delay therapy in

Back 190

N.Meningitidis
Dont do CT or MRI

Front 191

Major concern for patient with Neissieria Meningitidis

Back 191

Intercranial Pressure

Front 192

Effects college, and people clustered in small places

Back 192

N.Meningitids

Front 193

Why do you use Chocolate agar plate for N.Meningitidis

Back 193

X and V heme

Front 194

Glucose and Maltose Positive

Back 194

N.Meningitidis

Front 195

Glucose and Maltose negative

Back 195

N.Gonorrheae

Front 196

What is the main drug for prophylaxis today

Back 196

Ceftriaxone and Refampin

Front 197

Main side effect of Rifampin

Back 197

Soft contact lenses causes a problem, Red coloration of the skin.

Front 198

Where do you have polymicrobial effects with N.Meningitidis

Back 198

Stronglyoides

Front 199

Patient with headache, fever and stiff neck, and HD (immunocompramised)

Back 199

Listeria Monocytogens

Front 200

How do you treat listeria ?

Back 200

B lactams. Ampicillins and Penicillins

Front 201

Patient has fever, lethargy and clears drain pipes and paralysis

Back 201

West Nile Virus

Front 202

Reduvid Bug, occurs when you scratch after the bug infestation

Back 202

Chagas disease, Typansomas Cruzei.

Front 203

Cycle of Tryp. Cruzei

Back 203

Dog-Reduvid-Human

Front 204

Which are the oldest Hepatitis Viruses

Back 204

Hepatitis A and B

Front 205

Structure of Hepatitis A Virus

Back 205

Naked, Postive ssRNA. HepaRNAvirus, hepatovirus from picoviridae family.

Front 206

Replication of Hep A

Back 206

It is NOT cytolytic

Front 207

Epidemiology of HAV

Back 207

Fecal-Oral tranmission, Survives in salt and fresh water. Oysters, clams, mussels are natural sources when eaten raw or poorly cooked. 50% of all acute hepatitis cases.

Front 208

Pathogenesis and Clinical of HAV

Back 208

Ingested virus moves to blood, liver hepatocytes and kupffer cells are infected, discharged in bile and stool, fecal oral spread of virus follows.
Incubation time 15-50 days.
No chronic infection or cancer association.

Front 209

Lab diagnosis of HAV

Back 209

Detection of HAV infection by anti-HAV IgM by ELISA. History of sea food consumption.

Front 210

Prevention of HAV

Back 210

Sanitation and cholorination of water. Avoid raw sea foods.
Inactive HAV vaccine for travelers.

Front 211

Structure of Hepatitis B Virus

Back 211

Enveloped, circular, partially dsDNA with reverse transcriptase and an RNA intermediate. HepaDNAviruses.

Front 212

Dane particle

Back 212

Found in HBV. A virion consisting of DNA and a capsid protein labeled as the hepatitis B virus core antigen (HBcAg)

Front 213

Australia Antigen

Back 213

HBV surface antigen HBsAg is an envelope antigen. There are 3 molecular forms S,M and L.

Front 214

Replication of HBV

Back 214

- HBsAg binds to unknown receptor
- The incomplete DNA strand is completed by a DNA polymerase present in the virion core.
- Viral genome moves to the host cell nucleus for transcription of mRNA.
- mRNA is a template for the RNAdep-DNApoly(reverse transcriptase or P protein) to make negative strand DNA from which the positive strand is made.
- Postive strand DNA made from the negative strand by a DNAdep-DNApoly is not completed due to premature packaging which results in incomplete DNA genomic Circles.
- Genome has been identified in hepatocellular carcinoma.

Front 215

Epidemiology of HBV

Back 215

Asymptomatic. Transmitted by blood, contaminated needles, tattoos, ear puncture, sex and childbirth. Called SERUM HEPATITIS.

Front 216

Pathogenesis and Clinical of HBV

Back 216

Incubation for 45 before symptoms and before progression to typical liver disease.
- Chronic Leads to cirrhosis, liver failure.
- Primary hepatocellular Carcinoma

Front 217

Lab diagnosis of HBV

Back 217

HBsAg and HBeAg are present in blood during the infection. HBeAg is a major indication of active infection. Anti HBsAg and anti HBeAg are present in late stage of the acute resolved disease.

Front 218

Prevention and Lab control of HBV

Back 218

Screeining of blood for HBsAg and HBeAg antigens.
Vaccination, early with dan particle harvested from blood of drug addicts, now with recombinant virus yeasts for med personal and high risk groups.
- Hepatitis immune globulin for acitive diasese.
-Lamivudine is used for chronic hep B, inhibits reverse transcriptase and interferon alpha.

Front 219

Structure of Hep. C virus

Back 219

Family Flaviviridae and the genus Hepacivirus. Enveloped, positive sense RNA.
-mRNA make polyprotein, cleavage enzyme.
-Beninds to receptor on hepatocytes and B cells and also coats itself with lipoproteins for attachment to lipoprotein receptors on hepatocytes.
-promotes its own survival by inhibiting interferon synthesis and apoptosis.

Front 220

Epidemiology of HCV and HGV

Back 220

Blood borne hepatitis, bu drug abuse, transfusion, skin puncture, tattoos.
High rate in aids patients

Front 221

Pathogenesis and Clinical Disease

Back 221

15% Asymptomatic
70% progress to HCC
15% progresses to Cirrohosis

Front 222

Lab diagonsis for HCV

Back 222

ELISA to detect anti-HCV globulin.
Western blot of virus protein from patient serum.

Front 223

Prevention of HCV

Back 223

INFa with ribavirin, 50% recovery. Mimics riboquanosine and inhibits nuceloside synthesis.

Front 224

Anolog Used for HCV vaccine

Back 224

Ribavirin is used as a Guanosine analog

Front 225

Structure of Hepatitis D virus

Back 225

-ssRNA, circular genome
-Genome is small and is surrounded by the delta antigen core protein which is then covered by HBsAb
- HDV attaches to host hepatocytes via its HBsAg coat, it replicates only in a person with an HBV infection.

Front 226

Which virus requires HBV to survive?

Back 226

Hepatitis D

Front 227

Spreads though blood, semen and secretions

Back 227

Hepatitis D and B

Front 228

Leads to fuliminant hepatitis

Back 228

Hepatitis D

Front 229

Co-infection

Back 229

Person having both HBV and HDV infections

Front 230

Superinfection

Back 230

HBV positive person with HDV who is also HBV positive, of course, may exacerbate hepatitis symptoms and lead to cirrhosis or chronic, persistent infections.

Front 231

Enteric Hepatitis

Back 231

HEV

Front 232

Fecal-Oral Transmission

Back 232

HAV and HEV

Front 233

Agents that cause Hepatitis

Back 233

Prominent:
Yellow fever
Leptospira interrogans
Other:
CMV
EBV
Adenovirus

Front 234

Microbiology of Rickettsia

Back 234

Gram Negative
Small Pleomorphic Cocci
Obligate intracellular
Peptidoglycan and weak Endotoxin

Front 235

Small rodents as reservoirs and arthropod vectors

Back 235

Rickettsia

Front 236

Frontal Headache, Fever and Rash

Back 236

Rickettsia

Front 237

Use phospholipase to escape phagolysosome and reproduce by binary fission

Back 237

Rickettsia

Front 238

Transmitted by Dermacentor Varibilis and Andersoni

Back 238

Dog Tick and wood tick that transmits Rickettsia

Front 239

Rash on the Extremities that spreads to the core

Back 239

Rocky Mountain Spotted fever that is caused by Rickettsia Rickettsii

Front 240

Found in cosmopolitan areas, and uses the house mouse and its mites as a reservoir

Back 240

Rickettsia akari

Front 241

Louse that uses the human body as a reservoir

Back 241

Tick (Pediculus humanus) that causes Rickettsia Prowazekii

Front 242

Reactivation of a Rickettsia Infection long after the primary infection

Back 242

Recurdescent (Brill Zinsser Disease)

Front 243

Rash starts out on the trunk and spreads outwards

Back 243

Rickettsia Typhi

Front 244

Test for Rickettsia

Back 244

Wei-Felix Test that test for Rickettsial Anti-bodies that cross react with proteus antigen and agglutinate.

Front 245

Prevention and control of Rickettsia

Back 245

Avoid Ticks

Front 246

The disease of the Orient (japan) that is found in the Rodents as the Reservoir and Chiggers and the vector

Back 246

Orientia Tsutsugamushi

Front 247

Genetically different, but the same as gram negative strains weakly morphology like Rickettsia

Back 247

Coxiella Burnetii and Q fever

Front 248

Small cell variant which is resistant to enviornment and large cell variant appears in the phagolysosome of monocytes, macrophages.

Back 248

Coxiella Burnetii and Q fever

Front 249

Pneumonia, Hepatitis, Subacute endocarditis

Back 249

Coxiella Burnetii and Q fever

Front 250

Obligate intracellular pathogens that survive in phagocytic vacuoles inside hematopoietic cell (RBC, granulocytes, monocytes and platelets

Back 250

Ehrlichia and Anaplasma

Front 251

Large reticulate body formed by assembly of elementary bodies, called morulae and then lytic release, lack petidoglycan and LPS

Back 251

Ehrlichia and Anaplasma

Front 252

Gram Negative Curved Rod/Spiral

Back 252

Helicobacter Pylori

Front 253

Breaks urea to CO2 and NH3, neutralizes gastric acid

Back 253

Urease, found in C.Neoformans and H.pylori

Front 254

Steps of H.Pylori Pathogenesis

Back 254

1. H. pylori penetrate the mucus layer of host stomach and adhere the surface of gastric mucosal epithelial cells.2. produce ammonia from urea by the urease, and the ammonia neutralize the gastric acid to escape from elimination.3. proliferate, migrate, and finally form the infectious focus.4. The gastric ulcer is developed by destruction of mucosa, inflammation and mucosal cell death.

Front 255

Clinical diseases of H.Pylori

Back 255

Chronic Gastritis that leads to:
1: PUD
2:Chronic superficial Gastritis
3: MALT B Cell lymphoma
4: Chronic atrophic Gastritis which later becomes gastric adenocarcinoma

Front 256

Upper abdominal pain, feeling of nausea of vomitting, and bleeding into GI tract

Back 256

H.Pylori

Front 257

Diagnosis of H.Pylori

Back 257

Urease Breath test, by ingestive radioactive urea and detecting the labelled CO2 in breath.

Front 258

Treatment of H.Pylori

Back 258

Omeprzole, which is a proton pump inhibitor. Can also use a Macrolide, beta lactam, metronidazole.

Front 259

Main sign of an enteric infection

Back 259

Watery feces that occurs 3 or more in a 24 hour period.

Front 260

Characteristics of Staph Aureus

Back 260

Gram Positive
Cocci

Front 261

Catalase and Coagulase positive and grows in 7.5% NaCl

Back 261

Stap. Aureus

Front 262

Transmitted from food handlers and is usually found in salted ham, creamy dishes and custards, mayonnaise, salad dressings potato and egg salad.

Back 262

Stap. Aureus

Front 263

Found in food that is not kept refrigerated

Back 263

Stap. Aureus

Front 264

Heat stable at about 100C for 30 min, and can act as an emetic agent.

Back 264

Stap. Aureus

Front 265

Sudden onset (1 hr) of severe nausea and vomitting, headache, diarrhea. Usually self resolving in 24-48 hrs.

Back 265

Stap. Aureus

Front 266

Main prevention for staph. Aureus

Back 266

Education on food handling

Front 267

Gram positive spore forming rod that is aerobic

Back 267

Bacillus Cereus

Front 268

Contaminated food with soil, that is sometimes cooked and kept warm like rise, grains, root vegetables.

Back 268

Bacillus Cereus

Front 269

Occurs with ingested preformed heat stable toxin containing foods, usually associated with carbohydrate rich foods like boiled rice, paste and fried rice.

Back 269

Emetic Syndrome occurring during B.Cereus

Front 270

Entertoxin found in the emetic syndrome of Staph Aureus and B.Cereus

Back 270

Superantigen. Stimulates the vagus nerve leading to emetic response

Front 271

Onset of an emetic syndrome

Back 271

Rapid Onset 1-6 hours incubation period and symptoms last about 24 hours. Staph Aureus and B.Cereus

Front 272

Ingested of heat liable toxin that stimulate cAMP causing intestinal fluid secretion

Back 272

Diarrheal syndrome that occurs during B.Cereus infection

Front 273

Associated with protein rich foods, vegetables, pudding, vanilla and cause and milk

Back 273

Diarrheal syndrome that occurs during B.Cereus infection

Front 274

Onset of Diarrheal syndrome

Back 274

Slow onset at about 6-16 hrs with symptoms of watery diarrhea

Front 275

Gram positive spore forming rod that is anaerobe

Back 275

Clostridium botulinum and Clostridium Perfringens

Front 276

Ingestion of preformed toxin, trauma and wound infection, ingesting spore by infants

Back 276

Transmission of Clostridium botulinum

Front 277

Infants that are fed with honey

Back 277

clostridium botulinum

Front 278

Flaccid paralysis and bilateral descending

Back 278

clostridium botulinum

Front 279

Toxin associated with canned a variety of foods

Back 279

Toxin A and B found in Clostridium Botulinum

Front 280

Toxin grows in wounds, food, and is ingested

Back 280

clostridium botulinum

Front 281

Double and blurred vision, droopy eyelids, slurred speech, difficulty swallowing, dry mouth, and muscle weakness

Back 281

Symptoms of C.Botulinum

Front 282

Floppy Baby Syndrome

Back 282

Infant Botulism

Front 283

Prevention of Clostridium Botulism

Back 283

Heating of canned food before eating to inactivate toxin, do not feed honey to infants

Front 284

found in meat products, poultry and gravy

Back 284

Clostridium Perfringes

Front 285

Toxin from food poisoning that acts on the small intestine

Back 285

Clostridium Perfringes

Front 286

High effective Dose about about 10^8-9

Back 286

Clostridium Perfringes

Front 287

Incubation period for Clostridium Perfringes

Back 287

8-16 hours, duration could generally last 24 hours of less.

Front 288

Symptoms of Clostridium Perfringes

Back 288

Abdominal cramps, watery diarrhea, nausea-no fever or vomiting.

Front 289

What are the antigens found on Enterbacteriaceae

Back 289

O: Somatic antigen for ID
K for capsular or Vir for for virulence.
H for motile flagellarx

Front 290

Causes of non inflammatory diarrhea in travelers and infants in developing countries

Back 290

ETEC

Front 291

Non inflammatory diarrhea in the small intestine are caused by

Back 291

ETEC
EPEC
EAEC

Front 292

Inflammatory diarrhea of the small intestine

Back 292

EHEC
EIEC

Front 293

Virulence factors of E.Coli

Back 293

Exotoxins: Heat stable toxin, heat liable toxin, shiga like toxin.
Adhesion: Colonizing factor adhesion, bundle forming pili and aggregate adherence fimbriae

Front 294

Heat labile toxin actions of ETEC

Back 294

Similar to cholera toxin , A-B type.
Binds to GM1 ganglioside receptors on gut epithelial cells
The toxin has ADP- ribosyltransferase activity
Interacts with membrane protein (Gs) that regulates adenylate cyclase
Results in increase of cAMP which cause out flow of Cl ion from mucosal cells and inhibit Na ion absorption
Ion imbalance leads to water loss: diarrhea

Front 295

Heat stable toxin (ST) action ETEC

Back 295

binds to membrane guanylate cyclase receptor
Results in excess of cGMP (not cAMP) – blocks ion transport into cells; so water moves into the lumen

Front 296

Secondary Diarrhea of ETEC

Back 296

Watery diarrhea, abdominal cramps, nausea, low-grade fever IP: 1-3 days, Duration of illness 3 to >7 days Major cause of traveler’s diarrhea, and < 3 years old children in developing countries

Front 297

AAF

Back 297

Aggregates adherence fimbriae, bacterial clump into small aggregates, noninvasive, stacked bricks like baxter parallel rows via autoagglutination.

EAST1: some species produce ST like toxin (heat stable)

Shortening of microvilli, mononuclear infiltration, hemorrhage decreased fluid absorption.

Front 298

EAEC symptoms

Back 298

Persistent watery diarrhea
Infantile diarrhea in under developed countries
Can cause travelers diarrhea in HIV patient.

Front 299

Virulence factors of EPEC and EHEC

Back 299

Adhesion factors. Bundle forming pilli, patchy adherence followed by Tir insertion and intimin binding. Attaching effacing-wiping out of microvilli.

Front 300

Destruction of absorptive Microvilli

Back 300

EPEC

Front 301

Infantile diarrhea, cause of epidemics in newborn nurseries.

Back 301

EPEC

Front 302

EPEC symptoms

Back 302

Water diarrhea, fever, nausea, vomitting, non bloody stools

Front 303

Diagnosis of E.Coli

Back 303

Lactose fermenter. Using MacConkey and EMB.

Front 304

Morphology of Vibrio spp

Back 304

Comma shaped (curved) bacilli, Gram -, oxidase +. Motile with single polar flagella.

Front 305

Found in Contaminated water, and humans can be asymptomatic

Back 305

Vibrio Cholera

Front 306

Spread by Seafood

Back 306

HAV
V.Parahaemolyticus and V. vulnificus

Front 307

Rice Watery diarrhea

Back 307

Vibrio Cholera

Front 308

Virulence of V.Cholera and ETEC

Back 308

01 and 0139 strains. Cholera toxin binds to GM! ganglioside. Increase cAMP hyper secretion of electrolytes and water, chloride ion out, Na ion not absorbed.

Front 309

Thiosulfate Citrate Bile Salts Sucrose Agar

Back 309

Vibrio Cholera

Front 310

Test for V. Cholera

Back 310

Agglutination test using polyvalent sera anti-01 type and 0139.

Front 311

Loss of skin turgor

Back 311

Vibrio Cholera, due to dehydration

Front 312

Treatment of V.Cholrae

Back 312

IV infusion of sterile pyogen free solution containing NaCl, KCl, NaHCO3. Oral rehydration therapy. Tetracyline in sever cases.

Front 313

Cholrination of water supplies, sewage treatment

Back 313

V.Cholerae

Front 314

Primary Septicemia, Skin lesions and tissue necrosis, that follows the ingestion of contaminated seafood.

Back 314

V.Vulnificus

Front 315

Milder Diarrhea than V.Cholerae

Back 315

V.Vulnificus

Front 316

Morphology of Norovirus

Back 316

positive ssRNA, non-enveloped icosahedral, star of david like appearance.

Front 317

Found mainly in cruise ships and it causes 50% of food burned Gastroeneritis at about 23 million cases/year.

Back 317

Norovirues

Front 318

Sudden onset of diarrhea, nausea and vomiting, abdominal pain. Incubation for 1-2 days, duration of the disease is 2-3 days. Re-infection is possible for a person with weak immunity.

Back 318

Norovirues

Front 319

Has wheel like structure, and kills about 1/2 million children worldwide

Back 319

Reoviridae
Rotaviruses

Front 320

Rotavirus Morphology

Back 320

ds RNA (11 segments), non-enveloped, icosahedral nucleocaspid

Front 321

10-100 infection viral particle dose

Back 321

Rotavirus

Front 322

Kills children 6-24 months of age

Back 322

Rotavirus

Front 323

Triad of Rotavirus

Back 323

Fever, vomiting, Diarrhea

Front 324

Treatment of Rotavirus

Back 324

Rotavirus-specific immunoglobulin preparation, prevent by vaccine, RotaTeq, Rotarix-part of childhood vaccination.

Front 325

Strains of Adenovirus that are enteric

Back 325

Adenovirus 40/41

Front 326

Morphology of Adenovirus

Back 326

ds DNA, non enveloped, 12 protruding fibers (penton), several serotypes

Front 327

Fecal to oral transmission during the late fall and winter

Back 327

Adenovirus 40/41

Front 328

Second most common cause of viral infantlile diarrhea

Back 328

Astrovirus

Front 329

Morphology of Astrovirus

Back 329

postive ss RNA, non-enveloped , 8 serotypes, serotype 1 causes 65% of infections

Front 330

Herpesviridae
Structure

Back 330

dsDNA
Enveloped
Linear

Front 331

Herpes Infection patterns

Back 331

Lytic

Persistent

Latent or Transforming

Front 332

Herpes Theraputic Agent

Back 332

Thymidine Kinase

Front 333

HSV attachement Site

Back 333

Heparan Sulfate
glycoprotein found on many cells

Front 334

Stages for HSV infection

Back 334

Immediate: control gene transcription
Early: Polymerase and other enzymes
Late: protein synthesis

Front 335

Epidemiology of HSV

Back 335

Found in Secretions

Vaginal
Saliva
Vesicle
Towels
Glasses

Front 336

Clinical Features of HSV

Back 336

Oral cold, sores, fever, blisters and genital vesicles

Front 337

HSV Eruptions are caused by

Back 337

fever
UV light
menstruation
local irriation

Front 338

Cowdry Type A acidophilic intranuclear inclusion bodies

Back 338

HSV 1 and 2

Front 339

Disease caused by HSV

Back 339

Herpes pharyngitis
ocular keratitis
Herpetic whitlow
encephalitis (HSV 2)

Front 340

Lab diagnosis for HSV

Back 340

Tzank Smear

Virus isolation

Front 341

Prevention of HSV

Back 341

Avoid exposure

Front 342

What is acyclovir

Back 342

Its is used to mimic guanosine and prevent HSV

Front 343

Thymidine Kinase

Back 343

Receptor, therapeutic target

Front 344

Binding site for EBV

Back 344

CR2 of the B-cell

Front 345

Outcomes after EBV binds to B-Cells

Back 345

Permissive
Latent
Immortalization of B cells

Front 346

EBV early Antigens

Back 346

Early Antigen
Viral Capsid antigen

Front 347

EBV Latent Antigens

Back 347

Non permissive, EBNA and LMP

Front 348

Kissing disease

Back 348

EBV

Front 349

Virus spreads for a lifetime

Back 349

EBV

Front 350

Children Asymptomatic

Back 350

EBV
M.Tb

Front 351

Infective Mononucleosis

Back 351

EBV

Front 352

Sore throat
Lymphadenopathy
Splenomegaly

Back 352

Infective Mononucleosis

Front 353

Burkitt's lymphoma

Back 353

EBV

Front 354

Nasopharyngeal Carcinoma

Back 354

EBV

Front 355

Lymphoproliferative Disease

Back 355

EBV

Front 356

Chromosome Effected with EBV

Back 356

c-myc gene from chromosome 8/14 translocation

Front 357

Downey Cells

Back 357

Atyptical lymphocytes seen in EBV

Front 358

Monospot Test

Back 358

Heterophile Antibody for EBV

Front 359

Antibodies tested for EBV

Back 359

EA and EBNA

Front 360

Which are the only organs that escape Tb infections

Back 360

Tests and ovaries

Front 361

Morphology of Neisseria meningitidis

Back 361

Gram - Diplococci with a kidney bean shaped

Front 362

Oxidase and catalase positive

Back 362

N.Meningitidis

Front 363

Oxidase test where dye changes color

Back 363

N.Meningitidis

Front 364

Polysaccharide capsule with 13 serologic groups A,B,C,Y and W135

Back 364

N.Meningitidis

Front 365

Normal flor of N.Meningitidis

Back 365

Nose and throat

Front 366

Move through sinuses and can even go to the brain

Back 366

N.Meningitidis

Front 367

Transmission of N.Meningitidis

Back 367

Aerosols, college and school children

Front 368

Effects children with later complement deficiency

Back 368

N.Meningitidis

Front 369

Contain antiphagocytic capusles and pilli

Back 369

N.Meningitidis
H. Influenza

Front 370

Purulent, headache, fever, stiffness

Back 370

Meningitis which is caused by N.meningitidis and H.Influenza

Front 371

Petechia, purpura, thrombosis of small blood vessels, septic shock

Back 371

Meningococcemia which is caused by N.Meningitidis

Front 372

Bilateral renal gland hemorrhagic necrosis

Back 372

Waterhouse-Friderichsen syndrome which is caused by N.Meningitidis

Front 373

Chocolate agar, Thayer-martin chocolate agar

Back 373

N.Meningitidis

Front 374

Vaccines of four polysaccharides A,C,Y and W135 MPSV4

Back 374

N.Meningitidis

Front 375

MCV4/MPSV4 vaccine

Back 375

N.Meningitidis

Front 376

3 main human pathogens of H. Haemophilus

Back 376

H.influenza
H.ducreyi
H.aegyptius

Front 377

Conjuctivitis (pink eye)

Back 377

H.Aegyptius

Front 378

Chancroid an STD

Back 378

H.ducreyi

Front 379

What do H.Haemophilus require for growth

Back 379

Hemin the X factor
NAD
V factor

Front 380

Structure of H.Influenza

Back 380

Six capuslar antigenic types, Polyribitol ribose phosphate (PRP), Hib.

Front 381

Non-typable strains that lack a capsule

Back 381

H.influenza

Front 382

Cause Otitis Media and Sinusitis

Back 382

H.influenza

Front 383

Epiglottitis

Back 383

H.Influenza
Can cause obstruction

Front 384

What is the basic characteristics of Mycobacteria

Back 384

Aerobic, slow growing, non spore forming bacilli

Front 385

Stain for Mycobacteria

Back 385

Acid Fast

Front 386

Main content of Mycobacteria

Back 386

Mycolic acid, Lipid, making them very hydorphobic

Front 387

Morphology of Mycobacteria Colonies

Back 387

Yellow to orange, dry fraible colonies

Front 388

What is the main mode of transmission of M.Tuberculosis, and how prevelent is it ?

Back 388

Aerosol transmission and 1/3 of the world's population is infected

Front 389

MOA of M.Tb

Back 389

Blocks phagosome-lysosome fusion after being phagocytosed by the cell.

Front 390

Severity of most M.Tb infections

Back 390

Asymptomatic or latent

Front 391

Cellular reactions of M.Tb

Back 391

Epithelioid cells, macrophages containing bacteria for granulomas with necrotic centers that can be reactivated with stress

Front 392

Main virulent factor of M.Tb

Back 392

Cord Factor (a lipid) kills mice and induces granulomas

Front 393

Symptoms of M.Tb in the lung

Back 393

Cavitary lung disease (cough, bloody sputum, fever, chils, night sweats, weight loss)

Front 394

Systemic Symptoms of Tb

Back 394

Miliary (multiple foci) disseminated and extra pulmonary disease of many tissues

Front 395

Drug resistant forms of Tb

Back 395

MDR-TB (multi drug resistant) isoniazid/rifampin
XDR-TB (extreme drug resistant) quinolone and aminoglycoside

Front 396

Diagnositic Tests for Tb

Back 396

Tuberculin Skin Test (Mantoux)
Acid Fast Staining of SputumFluorescent Dyes

Front 397

Culturing methods for Tb

Back 397

Decontamination of sputum specimens with 2% sodium hydroxide
Egg based media

Front 398

Lab Diagnosis test for Tb

Back 398

IFN-gamma assays

Assay for the production of IFNg by the patients blood cells is evidence of lymphocyte reaction with antigens

Front 399

Main features of Mycobacterium Avium

Back 399

Shares same microbiology as M.Tb
Effects those with pulmonary conditions, Immunodeficient, smokers.

Front 400

MAC pathogensis

Back 400

Patchy lung infiltrates

Front 401

Which are the slow growing mycobacteria

Back 401

M. Kansasii
M. Bovis

Front 402

Which are the cutaneous pathogens

Back 402

M. Ulcerans: tropical, skin grafts.
M. Marinum in swimming pools.

Front 403

Microbiology of Mycobacterium Leprae and other names for it

Back 403

Cannot be grown in culture

Leprosy or Hansen's disease

Front 404

Transmission of M.Leprae

Back 404

Contact, Aerosols, skin abrasion

Front 405

Pathogenesis of M. Leprae

Back 405

heavy tissue burden of bacteria.

tuberculoid has fewer bacteria in tissue

Front 406

Rusty Sputum

Back 406

Strep.Pneumo

Front 407

Which immunosuppression is common among drug users

Back 407

HIV

Front 408

Prevention Immunization of H.Influenzae

Back 408

Conjugate type b vaccine

Front 409

The virulence factor of Listeria Monocytogens

Back 409

Listeriolysin O

Front 410

Gram positive, short motile bacilli with tumbling motion

Back 410

Listeria Monocytogenes

Front 411

Found in soil, Vegetations, and the feces of animals

Back 411

Listeria Monocytogenes

Front 412

Populations at risk of Listeria Monocytogens

Back 412

High adult population like pregnant, risk of infants from non immune infected mothers.

Front 413

Cells enter and enter enterocytes and attach to M cells

Back 413

Listeria Monocytogenes

Front 414

Action of Listeriolysin O in L.Monocytogens

Back 414

Phagolysosome release

Front 415

Actin based intracellular motility, moving cells to systemic sites

Back 415

Listeria Monocytogenes

Front 416

Stages of L.Monocytogens clinical infections

Back 416

Early onset in utero, birth defects due to transplacental infection.
Late onset: infant meningitis
Adult disease: as symptomatic in health, mild flu like symptoms in healthy adults.

Front 417

CAMP test

Back 417

Listeria Monocytogenes

Front 418

Weak Beta hemolysis and cold enrichment

Back 418

Listeria monocytogenes

Front 419

Morphology of Rabies Virus

Back 419

bullet shaped rhabdovirus, enveloped,helical,
negative sense ssRNA.

Front 420

RNAdep-RNApoly

Back 420

Rabies Virus

Front 421

Rabies Epidemiology

Back 421

Zoonotic from dogs, cats, mad dog disease.DOMESTIC ANIMALS

Front 422

Virus binds acetylcholine receptors, moves up neural system to brain, then outward to cornea, hair roots and salivary glands.

Back 422

Rabies Virus

Front 423

Hydrophobia and paralysis

Back 423

Rabies Virus

Front 424

Negri bodies

Back 424

Intracytoplasmic are viral aggregates in neural tissues seen in animal or post mortem human. In Rabies.

Front 425

Fluorescent antibody test of animal tissue for virus presence

Back 425

Rabies Virus

Front 426

RT-PCR on saliva

Back 426

Rabies Virus

Front 427

Wound cleansing and Injection of HRIG as well as active immunization

Back 427

Human rabies immune globulin is for prevention of Rabies.

Front 428

small RNA viruses

Back 428

Picornviridae

Front 429

Virology of Poliomyelitis

Back 429

Enterovirus, acid stable, 37 C growth, and its tissues target sepatartts it from other members.

Front 430

Structure of Poliomyelitis

Back 430

Positive ssRNA
Has four proteins that are rearranged after attachement and bind Ribosome.

Front 431

Transmission of Poliomyelitis

Back 431

Fecal-Oral
Contaminated Water

Front 432

Pathogenesis of Poliomyelitis

Back 432

- Asymptomatic (90%) with intestinal invasion. Abortive infection (5%).
- Paralytic Poliomyelitis-less than 2% of infection. Pentrates bowel to blood to anterior horn of spinal cord and motor complex.
- Bulbar polio 75% of the 2% fatal, respiratory Muscle paralysis.
-Post-polio syndrome 20-80%

Front 433

Lab test for Poliomyelitis

Back 433

Throat swabs to cell culture early, from feces later, CSF variable recovery.

Front 434

Prevention and Control of Poliomyeltis

Back 434

- Salk inactivated polio vaccine (IPV), prevents disease but not intestinal infection. Was found to cause infection in some people.
- SaBin vaccine: Bowel infections will be eliminated, increase intestinal immunity. Immunity is spread from primary person, from person to person.

Front 435

Poliomyelitis drug reactions

Back 435

You would start with 2 Doses of the Salk vaccine and then administer

Front 436

Structure of Arenaviruses

Back 436

Enveloped, 2 ssRNA segments,

Front 437

Replication of Arenaviruses

Back 437

- L strand is negative with RNAdep-RNApoly.
Ambiesense strand that can be read as RNA in 2 directions (one end is positive while other end is negative).
- Contains host ribosomes to give sandy appearance in EM.

Front 438

Epidemiology of Arenavirus

Back 438

Lymphocytic Chroiomeningitis (LCM).Transmission through aerosol transmission of the fecal substance of the mouse or hamsters.
- Africa: Lassa fever, pulmonary hemorrhagic diseases with high percentage of death.

Front 439

Types of Polyomavirus

Back 439

JC and BK viruses

Front 440

Epidemiology of JC and BK viruses

Back 440

Water or Sewage, human exposure early in life, continual shedding through kidneys throughout life.

Front 441

Pathogenesis of JC and BK Viruses

Back 441

Polyomavirus as symptomatic except for cancer and suppressive therapy, causes progressive multifocal leukoncephalopathy, a demyelenating disease of what matter.

Front 442

Lab test of JC and BK viruses

Back 442

CSF, urine source, expansion by PCR.

Front 443

Prevention control of JC and BK viruses

Back 443

Avoid immunosuppressive therapy

Front 444

Defective Measles Virus

Back 444

Subacute Sclerosing Panencephalitis

Front 445

Muscle Jerks or spasticity, blindness, personality and behavioral changes.

Back 445

Subacute Sclerosing Panencephalitis

Front 446

What kinds of viruses are arthropod born

Back 446

RNA viruses, some are positive strand and some are negative strand.

Front 447

Structure of Arbovirus

Back 447

zoonotic RNA viruses

Front 448

Main vectors for the Arbovirus

Back 448

Mosquitoes

Front 449

Family Togaviridae

Back 449

Alpha Virus
EEE,WEE,VEE

Front 450

Family Bunyaviridae

Back 450

CA
LaCosse
Hanta

Front 451

Types of Flaviviridea

Back 451

Yellow Fever Virus
Dengue
West Nile
St. Louis Encephalitis Virus
Powassan Virus
Japanese B Encephalitis Virus
Hep. C Virus
Heptatitis G Virus

Front 452

Pathogensis of Flavivirus

Back 452

Mild systemic disease is usual, fever, chills, headache. Jap B may produce severe even fatal Encephalitis.

Front 453

Structure of Togaviridae and Flaviviridea

Back 453

Positive ssRNA enveloped viruses, cloak like cover that looks like a toga.
E1 and E2 peplomers are both found on the cover.

Front 454

Flaviviruses that may produce servere hemorrhagic disease

Back 454

Dengue and Yellow fever (liver disease)

Front 455

Replication Process of Togaviridea

Back 455

ssRNA positive-polyprotein synthesis and cleavage-negative strand RNA is made-progeny RNA

Front 456

Epidemiology of EEE and WEE

Back 456

Togaviruses
Birds Reservoir
Mosquitoes Vectors
Horses and Humans are dead end hosts

Front 457

Sleeping sickness was seen in which diseases as well

Back 457

Trypanosomas
African sleeping sickness

Front 458

Pathogensis of EEE and WEE

Back 458

Togoviridae
Virus attaches to monocytes and endothelial cells.
Flu like, headache, fever, muscle pain, photophobia.
Entry into the brain through small vessel endothelia.
Aseptic encephalitic phase generally resolves withough sequelae.
EEE is more serious than WEE

Front 459

Horse develops fatal sleeping sickness and mortality

Back 459

EEE and WEE

Front 460

Same course as EEE and WEE but is not as serious, very few cases in the USA

Back 460

VEE

Front 461

Chikungunya

Back 461

Bending over. More series disease than EEE, WEE or VEE. Restricted to Africa. An acute febrile disease with arthralgia, muscle pain lasting month or years. Hemorrhagic.

Front 462

Epidemiology of West Nile Virus

Back 462

Flavivirus that is worldwide.
Birds reservoir-Culex Mosquitoes vector

Front 463

Pathogensis of West Nile Virus

Back 463

90% assymptomatic
Fever, headache, chills, joint pain, flu like.
Encephalities Phase, near fatality.

Front 464

How many antigenic types are there for dengue fever

Back 464

Den 1 through Den 4

Front 465

Lab Diagnosis for West Nile Virus

Back 465

IgM
RT-PCR or Viral RNA recognition

Front 466

Epidemiology of Saint Louis Encephalitis Virus

Back 466

Flavivirus that is found in the Central and Eastern USA (missouri river).

Front 467

Pathogenesis of SLEV

Back 467

Asymptomatic and mild CNS.

Front 468

Epidemiology of Powassan Virus

Back 468

ssRNA, E1 and E2.
Ixodes ticks ar the reservoir and the vector.
North America and Canada

Front 469

Pathogenesis of Powassan Virus

Back 469

Flu like mild disease and encephalitis

Front 470

Epidemiology of Japanese B

Back 470

ssRNA,
Reservoirs are birds and pigs and the vector is a Culex (mosquito).
Japan and neighboring countries

Front 471

Epidemeiology of Dengue fever

Back 471

Tropical and subtropical areas where victors reside, Mosquitoes are the main vectors.
Human primates are reservoirs, sylvatic and urban cycles.

Front 472

Pathogenesis of Japanese B

Back 472

Mild flu like, and can be fatal more often than the above.

Front 473

Pathogenesis of Dengue Fever

Back 473

Break bone fever, headache, muscle and joint pain. Rash could be present but there is no encephalitis.

Front 474

Major Risk from Dengue Fever

Back 474

Dengue Hemorrhagic Fever (DHF)

Front 475

Symptoms of Dengue Hemorrhagic Fever

Back 475

Irritability, restless, heavy sweating with petechia, bleeding tendency.

Front 476

Dengue Shock Syndrome (DSS)

Back 476

Deteriorates with the accumulation of blood in the abdomen, abundant petechia, loss of blood pressure.

Occurs after second infection to the disease.

Front 477

The flooding and removal of standing water to prevent moquito breeding

Back 477

Yellow Fever

Front 478

Human, primates, sylvatic and urban cycles, also found in Aedes mosquitoes

Back 478

Yellow Fever

Front 479

Stage of Yellow Fever Pathogenesis

Back 479

Early: fever, nausea and abdominal pain
Late: pain and jaundice
Hemorrhagic: black vomit

Front 480

Lab for Yellow fever

Back 480

RT-PCR
Patient serum for immune response

Front 481

Bunyaviridea Structure

Back 481

Enveloped, negative, ssRNA, 3 segmented virus. RNApoly-RNAdep.

Front 482

Epidemiology of Bunyavirus

Back 482

Rodents urine and feces and spread by infected ticks

Front 483

California and La Crosse Viruses

Back 483

Type of Bunyavirus, as symptomatic. Nausea, vomiting, headache, seizure in true encephalitis.

Front 484

Feature of Hanatvirus

Back 484

Sin Nombre. Dust contaminated by urine and feces of white footed mice.

Front 485

Pathogensis of Hantavirus

Back 485

Pulmonary and Cardiac syndromes with a lot of loss of blood.

Front 486

Coltivirus-Colorado tick fever features

Back 486

dsRNA virus. They are plus strands in an mRNA, translation to RNAdep-RNApoly for genomic RNA forms

Front 487

Epi. of Colitivirus

Back 487

Mountain West, hard ticks.

Front 488

Pathogenesis of Coltivirus-Colorado tick fever

Back 488

Flu like symptoms to aseptic

Front 489

Scrapie and Mad cow disease, bovine spongiform encephalopathy (BSE)

Back 489

Prions proteins, that are a denatured proteins.

Front 490

Disease caused by prions in New Guniea

Back 490

Kuru, which is a transmissible neurologic disease that originated from cannabalism.

Front 491

Creutzfeldt-Jacob disease (CJD)

Back 491

dementia leading to death in the prion disease.

Front 492

Pathogenesis of prions

Back 492

Protease resistant proteins

Front 493

Name for prion proteins

Back 493

PrPc and PrPsc

Front 494

Prion type that binds to human cellular

Back 494

Scrapie type, and causes it to aggregate into amyloid fibers and/or vacuoles that accumulate in the brain.

Front 495

Symptoms of PrPsc

Back 495

Ataxia, dementia, behavioral changes, memory loss, development of spongiform lesion and amyloid deposit in the brain.

Front 496

Transmission by ingestion

Back 496

Prions

Front 497

Accumulation of PMN and other immune cells as well as debris

Back 497

Brain Abscess that is caused by post surgical procedure, or trauma. This later increase the cranial pressure.

Front 498

Organism pass through the nose from water. Into the nose and then to the brain where they can be fatal.

Back 498

Naegleria Fowleri

Front 499

Organism that is caused by those who wear contact lenses with no proper hygiene

Back 499

Acanthamoebae Castellani

Front 500

Pathogenesis of Taenia Solium

Back 500

Flatworm (cestode) which has a head (scolex) and proglottid segments

Front 501

Adult worm in swine intestine sheds eggs, hexacanth embryo (oncosphere) develops

Back 501

Taenia Solium parasitology

Front 502

Taenia Solium Lifecycle

Back 502

a. Eggs in water and soil ingested by swine
b. Oncosphere larvae penetrate gut, enter tissue
c. Swine develop tissue cysticerci (bladder worms)
d. If humans ingest hexacanth eggs, they hatch to
larval oncosphere that penetrates gut and
tissue cysticerci develop in lungs, brain, etc
e. If humans eat undercooked pork the typical cestode
develops in the gut from the cysticercus and sheds ova

Front 503

CNS effecting protozoa

Back 503

Trypanosomes Brucei, and Trypanosomes Brucei

Front 504

CNS Nematodes

Back 504

Toxocara Canis and T. Cati

Front 505

T.Canis and Cati Lifecycle

Back 505

a. Natural gut parasite of dogs and cats
b. Eggs ingested by humans and larvae develop but
wander in tissues and fail to complete life cycle

Front 506

Mycological CNS

Back 506

Cryptococcus Neoformans

Front 507

Spherical yeast with a capsule larger in diameter

Back 507

Cryptococcus Neoformans
H.Pylori

Front 508

Positive Urease Test

Back 508

Cryptococcus Neoformans

Front 509

Very slow growing yeasts that cause meningitis

Back 509

Cryptococcus Neoformans

Front 510

Neonate born in poor conditions with encephalitis

Back 510

HSV 2

Front 511

Cystic Fibrosis, with pneumonia, blue green sputum

Back 511

Pseudomona Aurigonsa

Front 512

Jelly sputum

Back 512

Klebsiella

Front 513

Lesions on face of cutanous touch and pain, Acid fast organism

Back 513

Leprae

Front 514

Sore throat, spleen and liver. Later LEADING TO SPLENIC RUPTURE

Back 514

EBV

Front 515

Triad of Meningitis

Back 515

Headache, Fever, Stiff Neck

Front 516

Drug of choice for Neisseria Meningitids

Back 516

Ceftriaxone

Front 517

Patient comes in with petechia and stiff neck

Back 517

N.Meningitidis

Front 518

Test for N. Meningitidis

Back 518

Blood, Urine, and Sputum

Front 519

Where do you never delay therapy in

Back 519

N.Meningitidis
Dont do CT or MRI

Front 520

Major concern for patient with Neissieria Meningitidis

Back 520

Intercranial Pressure

Front 521

Effects college, and people clustered in small places

Back 521

N.Meningitids

Front 522

Why do you use Chocolate agar plate for N.Meningitidis

Back 522

X and V heme

Front 523

Glucose and Maltose Positive

Back 523

N.Meningitidis

Front 524

Glucose and Maltose negative

Back 524

N.Gonorrheae

Front 525

What is the main drug for prophylaxis today

Back 525

Ceftriaxone and Refampin

Front 526

Main side effect of Rifampin

Back 526

Soft contact lenses causes a problem, Red coloration of the skin.

Front 527

Where do you have polymicrobial effects with N.Meningitidis

Back 527

Stronglyoides

Front 528

Patient with headache, fever and stiff neck, and HD (immunocompramised)

Back 528

Listeria Monocytogens

Front 529

How do you treat listeria ?

Back 529

B lactams. Ampicillins and Penicillins

Front 530

Patient has fever, lethargy and clears drain pipes and paralysis

Back 530

West Nile Virus

Front 531

Reduvid Bug, occurs when you scratch after the bug infestation

Back 531

Chagas disease, Typansomas Cruzei.

Front 532

Cycle of Tryp. Cruzei

Back 532

Dog-Reduvid-Human

Front 533

Which are the oldest Hepatitis Viruses

Back 533

Hepatitis A and B

Front 534

Structure of Hepatitis A Virus

Back 534

Naked, Postive ssRNA. HepaRNAvirus, hepatovirus from picoviridae family.

Front 535

Replication of Hep A

Back 535

It is NOT cytolytic

Front 536

Epidemiology of HAV

Back 536

Fecal-Oral tranmission, Survives in salt and fresh water. Oysters, clams, mussels are natural sources when eaten raw or poorly cooked. 50% of all acute hepatitis cases.

Front 537

Pathogenesis and Clinical of HAV

Back 537

Ingested virus moves to blood, liver hepatocytes and kupffer cells are infected, discharged in bile and stool, fecal oral spread of virus follows.
Incubation time 15-50 days.
No chronic infection or cancer association.

Front 538

Lab diagnosis of HAV

Back 538

Detection of HAV infection by anti-HAV IgM by ELISA. History of sea food consumption.

Front 539

Prevention of HAV

Back 539

Sanitation and cholorination of water. Avoid raw sea foods.
Inactive HAV vaccine for travelers.

Front 540

Structure of Hepatitis B Virus

Back 540

Enveloped, circular, partially dsDNA with reverse transcriptase and an RNA intermediate. HepaDNAviruses.

Front 541

Dane particle

Back 541

Found in HBV. A virion consisting of DNA and a capsid protein labeled as the hepatitis B virus core antigen (HBcAg)

Front 542

Australia Antigen

Back 542

HBV surface antigen HBsAg is an envelope antigen. There are 3 molecular forms S,M and L.

Front 543

Replication of HBV

Back 543

- HBsAg binds to unknown receptor
- The incomplete DNA strand is completed by a DNA polymerase present in the virion core.
- Viral genome moves to the host cell nucleus for transcription of mRNA.
- mRNA is a template for the RNAdep-DNApoly(reverse transcriptase or P protein) to make negative strand DNA from which the positive strand is made.
- Postive strand DNA made from the negative strand by a DNAdep-DNApoly is not completed due to premature packaging which results in incomplete DNA genomic Circles.
- Genome has been identified in hepatocellular carcinoma.

Front 544

Epidemiology of HBV

Back 544

Asymptomatic. Transmitted by blood, contaminated needles, tattoos, ear puncture, sex and childbirth. Called SERUM HEPATITIS.

Front 545

Pathogenesis and Clinical of HBV

Back 545

Incubation for 45 before symptoms and before progression to typical liver disease.
- Chronic Leads to cirrhosis, liver failure.
- Primary hepatocellular Carcinoma

Front 546

Lab diagnosis of HBV

Back 546

HBsAg and HBeAg are present in blood during the infection. HBeAg is a major indication of active infection. Anti HBsAg and anti HBeAg are present in late stage of the acute resolved disease.

Front 547

Prevention and Lab control of HBV

Back 547

Screeining of blood for HBsAg and HBeAg antigens.
Vaccination, early with dan particle harvested from blood of drug addicts, now with recombinant virus yeasts for med personal and high risk groups.
- Hepatitis immune globulin for acitive diasese.
-Lamivudine is used for chronic hep B, inhibits reverse transcriptase and interferon alpha.

Front 548

Structure of Hep. C virus

Back 548

Family Flaviviridae and the genus Hepacivirus. Enveloped, positive sense RNA.
-mRNA make polyprotein, cleavage enzyme.
-Beninds to receptor on hepatocytes and B cells and also coats itself with lipoproteins for attachment to lipoprotein receptors on hepatocytes.
-promotes its own survival by inhibiting interferon synthesis and apoptosis.

Front 549

Epidemiology of HCV and HGV

Back 549

Blood borne hepatitis, bu drug abuse, transfusion, skin puncture, tattoos.
High rate in aids patients

Front 550

Pathogenesis and Clinical Disease

Back 550

15% Asymptomatic
70% progress to HCC
15% progresses to Cirrohosis

Front 551

Lab diagonsis for HCV

Back 551

ELISA to detect anti-HCV globulin.
Western blot of virus protein from patient serum.

Front 552

Prevention of HCV

Back 552

INFa with ribavirin, 50% recovery. Mimics riboquanosine and inhibits nuceloside synthesis.

Front 553

Anolog Used for HCV vaccine

Back 553

Ribavirin is used as a Guanosine analog

Front 554

Structure of Hepatitis D virus

Back 554

-ssRNA, circular genome
-Genome is small and is surrounded by the delta antigen core protein which is then covered by HBsAb
- HDV attaches to host hepatocytes via its HBsAg coat, it replicates only in a person with an HBV infection.

Front 555

Which virus requires HBV to survive?

Back 555

Hepatitis D

Front 556

Spreads though blood, semen and secretions

Back 556

Hepatitis D and B

Front 557

Leads to fuliminant hepatitis

Back 557

Hepatitis D

Front 558

Co-infection

Back 558

Person having both HBV and HDV infections

Front 559

Superinfection

Back 559

HBV positive person with HDV who is also HBV positive, of course, may exacerbate hepatitis symptoms and lead to cirrhosis or chronic, persistent infections.

Front 560

Enteric Hepatitis

Back 560

HEV

Front 561

Fecal-Oral Transmission

Back 561

HAV and HEV

Front 562

Agents that cause Hepatitis

Back 562

Prominent:
Yellow fever
Leptospira interrogans
Other:
CMV
EBV
Adenovirus

Front 563

Microbiology of Rickettsia

Back 563

Gram Negative
Small Pleomorphic Cocci
Obligate intracellular
Peptidoglycan and weak Endotoxin

Front 564

Small rodents as reservoirs and arthropod vectors

Back 564

Rickettsia

Front 565

Frontal Headache, Fever and Rash

Back 565

Rickettsia

Front 566

Use phospholipase to escape phagolysosome and reproduce by binary fission

Back 566

Rickettsia

Front 567

Transmitted by Dermacentor Varibilis and Andersoni

Back 567

Dog Tick and wood tick that transmits Rickettsia

Front 568

Rash on the Extremities that spreads to the core

Back 568

Rocky Mountain Spotted fever that is caused by Rickettsia Rickettsii

Front 569

Found in cosmopolitan areas, and uses the house mouse and its mites as a reservoir

Back 569

Rickettsia akari

Front 570

Louse that uses the human body as a reservoir

Back 570

Tick (Pediculus humanus) that causes Rickettsia Prowazekii

Front 571

Reactivation of a Rickettsia Infection long after the primary infection

Back 571

Recurdescent (Brill Zinsser Disease)

Front 572

Rash starts out on the trunk and spreads outwards

Back 572

Rickettsia Typhi

Front 573

Test for Rickettsia

Back 573

Wei-Felix Test that test for Rickettsial Anti-bodies that cross react with proteus antigen and agglutinate.

Front 574

Prevention and control of Rickettsia

Back 574

Avoid Ticks

Front 575

The disease of the Orient (japan) that is found in the Rodents as the Reservoir and Chiggers and the vector

Back 575

Orientia Tsutsugamushi

Front 576

Genetically different, but the same as gram negative strains weakly morphology like Rickettsia

Back 576

Coxiella Burnetii and Q fever

Front 577

Small cell variant which is resistant to enviornment and large cell variant appears in the phagolysosome of monocytes, macrophages.

Back 577

Coxiella Burnetii and Q fever

Front 578

Pneumonia, Hepatitis, Subacute endocarditis

Back 578

Coxiella Burnetii and Q fever

Front 579

Obligate intracellular pathogens that survive in phagocytic vacuoles inside hematopoietic cell (RBC, granulocytes, monocytes and platelets

Back 579

Ehrlichia and Anaplasma

Front 580

Large reticulate body formed by assembly of elementary bodies, called morulae and then lytic release, lack petidoglycan and LPS

Back 580

Ehrlichia and Anaplasma

Front 581

Gram Negative Curved Rod/Spiral

Back 581

Helicobacter Pylori

Front 582

Breaks urea to CO2 and NH3, neutralizes gastric acid

Back 582

Urease, found in C.Neoformans and H.pylori

Front 583

Steps of H.Pylori Pathogenesis

Back 583

1. H. pylori penetrate the mucus layer of host stomach and adhere the surface of gastric mucosal epithelial cells.2. produce ammonia from urea by the urease, and the ammonia neutralize the gastric acid to escape from elimination.3. proliferate, migrate, and finally form the infectious focus.4. The gastric ulcer is developed by destruction of mucosa, inflammation and mucosal cell death.

Front 584

Clinical diseases of H.Pylori

Back 584

Chronic Gastritis that leads to:
1: PUD
2:Chronic superficial Gastritis
3: MALT B Cell lymphoma
4: Chronic atrophic Gastritis which later becomes gastric adenocarcinoma

Front 585

Upper abdominal pain, feeling of nausea of vomitting, and bleeding into GI tract

Back 585

H.Pylori

Front 586

Diagnosis of H.Pylori

Back 586

Urease Breath test, by ingestive radioactive urea and detecting the labelled CO2 in breath.

Front 587

Treatment of H.Pylori

Back 587

Omeprzole, which is a proton pump inhibitor. Can also use a Macrolide, beta lactam, metronidazole.

Front 588

Main sign of an enteric infection

Back 588

Watery feces that occurs 3 or more in a 24 hour period.

Front 589

Characteristics of Staph Aureus

Back 589

Gram Positive
Cocci

Front 590

Catalase and Coagulase positive and grows in 7.5% NaCl

Back 590

Stap. Aureus

Front 591

Transmitted from food handlers and is usually found in salted ham, creamy dishes and custards, mayonnaise, salad dressings potato and egg salad.

Back 591

Stap. Aureus

Front 592

Found in food that is not kept refrigerated

Back 592

Stap. Aureus

Front 593

Heat stable at about 100C for 30 min, and can act as an emetic agent.

Back 593

Stap. Aureus

Front 594

Sudden onset (1 hr) of severe nausea and vomitting, headache, diarrhea. Usually self resolving in 24-48 hrs.

Back 594

Stap. Aureus

Front 595

Main prevention for staph. Aureus

Back 595

Education on food handling

Front 596

Gram positive spore forming rod that is aerobic

Back 596

Bacillus Cereus

Front 597

Contaminated food with soil, that is sometimes cooked and kept warm like rise, grains, root vegetables.

Back 597

Bacillus Cereus

Front 598

Occurs with ingested preformed heat stable toxin containing foods, usually associated with carbohydrate rich foods like boiled rice, paste and fried rice.

Back 598

Emetic Syndrome occurring during B.Cereus

Front 599

Entertoxin found in the emetic syndrome of Staph Aureus and B.Cereus

Back 599

Superantigen. Stimulates the vagus nerve leading to emetic response

Front 600

Onset of an emetic syndrome

Back 600

Rapid Onset 1-6 hours incubation period and symptoms last about 24 hours. Staph Aureus and B.Cereus

Front 601

Ingested of heat liable toxin that stimulate cAMP causing intestinal fluid secretion

Back 601

Diarrheal syndrome that occurs during B.Cereus infection

Front 602

Associated with protein rich foods, vegetables, pudding, vanilla and cause and milk

Back 602

Diarrheal syndrome that occurs during B.Cereus infection

Front 603

Onset of Diarrheal syndrome

Back 603

Slow onset at about 6-16 hrs with symptoms of watery diarrhea

Front 604

Gram positive spore forming rod that is anaerobe

Back 604

Clostridium botulinum and Clostridium Perfringens

Front 605

Ingestion of preformed toxin, trauma and wound infection, ingesting spore by infants

Back 605

Transmission of Clostridium botulinum

Front 606

Infants that are fed with honey

Back 606

clostridium botulinum

Front 607

Flaccid paralysis and bilateral descending

Back 607

clostridium botulinum

Front 608

Toxin associated with canned a variety of foods

Back 608

Toxin A and B found in Clostridium Botulinum

Front 609

Toxin grows in wounds, food, and is ingested

Back 609

clostridium botulinum

Front 610

Double and blurred vision, droopy eyelids, slurred speech, difficulty swallowing, dry mouth, and muscle weakness

Back 610

Symptoms of C.Botulinum

Front 611

Floppy Baby Syndrome

Back 611

Infant Botulism

Front 612

Prevention of Clostridium Botulism

Back 612

Heating of canned food before eating to inactivate toxin, do not feed honey to infants

Front 613

found in meat products, poultry and gravy

Back 613

Clostridium Perfringes

Front 614

Toxin from food poisoning that acts on the small intestine

Back 614

Clostridium Perfringes

Front 615

High effective Dose about about 10^8-9

Back 615

Clostridium Perfringes

Front 616

Incubation period for Clostridium Perfringes

Back 616

8-16 hours, duration could generally last 24 hours of less.

Front 617

Symptoms of Clostridium Perfringes

Back 617

Abdominal cramps, watery diarrhea, nausea-no fever or vomiting.

Front 618

What are the antigens found on Enterbacteriaceae

Back 618

O: Somatic antigen for ID
K for capsular or Vir for for virulence.
H for motile flagellarx

Front 619

Causes of non inflammatory diarrhea in travelers and infants in developing countries

Back 619

ETEC

Front 620

Non inflammatory diarrhea in the small intestine are caused by

Back 620

ETEC
EPEC
EAEC

Front 621

Inflammatory diarrhea of the small intestine

Back 621

EHEC
EIEC

Front 622

Virulence factors of E.Coli

Back 622

Exotoxins: Heat stable toxin, heat liable toxin, shiga like toxin.
Adhesion: Colonizing factor adhesion, bundle forming pili and aggregate adherence fimbriae

Front 623

Heat labile toxin actions of ETEC

Back 623

Similar to cholera toxin , A-B type.
Binds to GM1 ganglioside receptors on gut epithelial cells
The toxin has ADP- ribosyltransferase activity
Interacts with membrane protein (Gs) that regulates adenylate cyclase
Results in increase of cAMP which cause out flow of Cl ion from mucosal cells and inhibit Na ion absorption
Ion imbalance leads to water loss: diarrhea

Front 624

Heat stable toxin (ST) action ETEC

Back 624

binds to membrane guanylate cyclase receptor
Results in excess of cGMP (not cAMP) – blocks ion transport into cells; so water moves into the lumen

Front 625

Secondary Diarrhea of ETEC

Back 625

Watery diarrhea, abdominal cramps, nausea, low-grade fever IP: 1-3 days, Duration of illness 3 to >7 days Major cause of traveler’s diarrhea, and < 3 years old children in developing countries

Front 626

AAF

Back 626

Aggregates adherence fimbriae, bacterial clump into small aggregates, noninvasive, stacked bricks like baxter parallel rows via autoagglutination.

EAST1: some species produce ST like toxin (heat stable)

Shortening of microvilli, mononuclear infiltration, hemorrhage decreased fluid absorption.

Front 627

EAEC symptoms

Back 627

Persistent watery diarrhea
Infantile diarrhea in under developed countries
Can cause travelers diarrhea in HIV patient.

Front 628

Virulence factors of EPEC and EHEC

Back 628

Adhesion factors. Bundle forming pilli, patchy adherence followed by Tir insertion and intimin binding. Attaching effacing-wiping out of microvilli.

Front 629

Destruction of absorptive Microvilli

Back 629

EPEC

Front 630

Infantile diarrhea, cause of epidemics in newborn nurseries.

Back 630

EPEC

Front 631

EPEC symptoms

Back 631

Water diarrhea, fever, nausea, vomitting, non bloody stools

Front 632

Diagnosis of E.Coli

Back 632

Lactose fermenter. Using MacConkey and EMB.

Front 633

Morphology of Vibrio spp

Back 633

Comma shaped (curved) bacilli, Gram -, oxidase +. Motile with single polar flagella.

Front 634

Found in Contaminated water, and humans can be asymptomatic

Back 634

Vibrio Cholera

Front 635

Spread by Seafood

Back 635

HAV
V.Parahaemolyticus and V. vulnificus

Front 636

Rice Watery diarrhea

Back 636

Vibrio Cholera

Front 637

Virulence of V.Cholera and ETEC

Back 637

01 and 0139 strains. Cholera toxin binds to GM! ganglioside. Increase cAMP hyper secretion of electrolytes and water, chloride ion out, Na ion not absorbed.

Front 638

Thiosulfate Citrate Bile Salts Sucrose Agar

Back 638

Vibrio Cholera

Front 639

Test for V. Cholera

Back 639

Agglutination test using polyvalent sera anti-01 type and 0139.

Front 640

Loss of skin turgor

Back 640

Vibrio Cholera, due to dehydration

Front 641

Treatment of V.Cholrae

Back 641

IV infusion of sterile pyogen free solution containing NaCl, KCl, NaHCO3. Oral rehydration therapy. Tetracyline in sever cases.

Front 642

Cholrination of water supplies, sewage treatment

Back 642

V.Cholerae

Front 643

Primary Septicemia, Skin lesions and tissue necrosis, that follows the ingestion of contaminated seafood.

Back 643

V.Vulnificus

Front 644

Milder Diarrhea than V.Cholerae

Back 644

V.Vulnificus

Front 645

Morphology of Norovirus

Back 645

positive ssRNA, non-enveloped icosahedral, star of david like appearance.

Front 646

Found mainly in cruise ships and it causes 50% of food burned Gastroeneritis at about 23 million cases/year.

Back 646

Norovirues

Front 647

Sudden onset of diarrhea, nausea and vomiting, abdominal pain. Incubation for 1-2 days, duration of the disease is 2-3 days. Re-infection is possible for a person with weak immunity.

Back 647

Norovirues

Front 648

Has wheel like structure, and kills about 1/2 million children worldwide

Back 648

Reoviridae
Rotaviruses

Front 649

Rotavirus Morphology

Back 649

ds RNA (11 segments), non-enveloped, icosahedral nucleocaspid

Front 650

10-100 infection viral particle dose

Back 650

Rotavirus

Front 651

Kills children 6-24 months of age

Back 651

Rotavirus

Front 652

Triad of Rotavirus

Back 652

Fever, vomiting, Diarrhea

Front 653

Treatment of Rotavirus

Back 653

Rotavirus-specific immunoglobulin preparation, prevent by vaccine, RotaTeq, Rotarix-part of childhood vaccination.

Front 654

Strains of Adenovirus that are enteric

Back 654

Adenovirus 40/41

Front 655

Morphology of Adenovirus

Back 655

ds DNA, non enveloped, 12 protruding fibers (penton), several serotypes

Front 656

Fecal to oral transmission during the late fall and winter

Back 656

Adenovirus 40/41

Front 657

Second most common cause of viral infantlile diarrhea

Back 657

Astrovirus

Front 658

Morphology of Astrovirus

Back 658

postive ss RNA, non-enveloped , 8 serotypes, serotype 1 causes 65% of infections

Front 659

Common Cause of Diarrhea in Day Care centers and mainly effects children <15 years.

Back 659

Shigella spp.

Front 660

Gram negative rods, non lactose frementers, H2S-, non motile

Back 660

Shigella spp.

Front 661

Only transmissible between humans with now animal reservoir

Back 661

Shigella spp.

Front 662

Flies, Feces, Food, Fingers with low infectious dose

Back 662

Shigella spp.

Front 663

Entertoxins of Shigella

Back 663

ShET1 and ShET2, which blocks the absorption of electrolytes, glucose, and amino acids from the intestinal lumen causing-watery diarrhea.

Front 664

Shiga toxins (AB)

Back 664

S.dysenteriae. Cytotoxin- Stx= shiga -(vero) toxins. Kills intestinal epitheilal and endothelial cells= blood diarrhea.

Front 665

Non symptoms, Watery flooded by dysentry bloody diarrhea

Back 665

Bacillary dysentry seen in shigellosis by Shigella toxin.

Front 666

HUS (Hemolytic Uremic Syndrome)

Back 666

S. Dysenteriae. Acute hemolysis and renal failure. Primary disease of infants and children (6 months to 4 years) ~ 15% mortality

Front 667

Reiter's Syndrome

Back 667

Autoimmune. S.flexneri. Triad of arthritis, urethritis, and conjuctivitis.

Front 668

Treatment for Shigella spp.

Back 668

Rehydration, anti biotics to protect contacts. DO NOT ADMINISTER ANTI DIARRHEAL COMPOUNDS WHICH INHIBIT PERISTALSIS. It is a reportable disease in the US.

Front 669

Hektoen Enteric Agar

Back 669

Shigella spp. for non lactose fermenters, faint green.

Front 670

G -, non lactose fermenter. produce H2S and MOTILE

Back 670

Salmonella spp.

Front 671

Found in poultry, eggs, dairy products, and lizards

Back 671

Salmonella spp.

Front 672

Hektoen Agar, H2S positive

Back 672

Salmonella spp.

Front 673

Grow inside the macrophage and resist killing by the phagosome

Back 673

Salmonella spp.

Front 674

Gastroenteritis and osteomyelitis

Back 674

Salmonella spp. effacing mainly sickle cell patients.

Front 675

Effects mainly older people, immunocompromised patients, sickle cell,prosthetic valve or vascular grafts.

Back 675

Salmonella spp.