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484 Cards in this Set

  • Front
  • Back
Herpesviridae
Structure
dsDNA
Enveloped
Linear
Herpes Infection patterns
Lytic

Persistent

Latent or Transforming
Herpes Theraputic Agent
Thymidine Kinase
HSV attachement Site
Heparan Sulfate
glycoprotein found on many cells
Stages for HSV infection
Immediate: control gene transcription
Early: Polymerase and other enzymes
Late: protein synthesis
Epidemiology of HSV
Found in Secretions

Vaginal
Saliva
Vesicle
Towels
Glasses
Clinical Features of HSV
Oral cold, sores, fever, blisters and genital vesicles
HSV Eruptions are caused by
fever
UV light
menstruation
local irriation
Cowdry Type A acidophilic intranuclear inclusion bodies
HSV 1 and 2
Disease caused by HSV
Herpes pharyngitis
ocular keratitis
Herpetic whitlow
encephalitis (HSV 2)
Lab diagnosis for HSV
Tzank Smear

Virus isolation
Prevention of HSV
Avoid exposure
What is acyclovir
Its is used to mimic guanosine and prevent HSV
Thymidine Kinase
Receptor, therapeutic target
Binding site for EBV
CR2 of the B-cell
Outcomes after EBV binds to B-Cells
Permissive
Latent
Immortalization of B cells
EBV early Antigens
Early Antigen
Viral Capsid antigen
EBV Latent Antigens
Non permissive, EBNA and LMP
Kissing disease
EBV
Virus spreads for a lifetime
EBV
Children Asymptomatic
EBV
M.Tb
Infective Mononucleosis
EBV
Sore throat
Lymphadenopathy
Splenomegaly
Infective Mononucleosis
Burkitt's lymphoma
EBV
Nasopharyngeal Carcinoma
EBV
Lymphoproliferative Disease
EBV
Chromosome Effected with EBV
c-myc gene from chromosome 8/14 translocation
Downey Cells
Atyptical lymphocytes seen in EBV
Monospot Test
Heterophile Antibody for EBV
Antibodies tested for EBV
EA and EBNA
Which are the only organs that escape Tb infections
Tests and ovaries
Morphology of Neisseria meningitidis
Gram - Diplococci with a kidney bean shaped
Oxidase and catalase positive
N.Meningitidis
Oxidase test where dye changes color
N.Meningitidis
Polysaccharide capsule with 13 serologic groups A,B,C,Y and W135
N.Meningitidis
Normal flor of N.Meningitidis
Nose and throat
Move through sinuses and can even go to the brain
N.Meningitidis
Transmission of N.Meningitidis
Aerosols, college and school children
Effects children with later complement deficiency
N.Meningitidis
Contain antiphagocytic capusles and pilli
N.Meningitidis
H. Influenza
Purulent, headache, fever, stiffness
Meningitis which is caused by N.meningitidis and H.Influenza
Petechia, purpura, thrombosis of small blood vessels, septic shock
Meningococcemia which is caused by N.Meningitidis
Bilateral renal gland hemorrhagic necrosis
Waterhouse-Friderichsen syndrome which is caused by N.Meningitidis
Chocolate agar, Thayer-martin chocolate agar
N.Meningitidis
Vaccines of four polysaccharides A,C,Y and W135 MPSV4
N.Meningitidis
MCV4/MPSV4 vaccine
N.Meningitidis
3 main human pathogens of H. Haemophilus
H.influenza
H.ducreyi
H.aegyptius
Conjuctivitis (pink eye)
H.Aegyptius
Chancroid an STD
H.ducreyi
What do H.Haemophilus require for growth
Hemin the X factor
NAD
V factor
Structure of H.Influenza
Six capuslar antigenic types, Polyribitol ribose phosphate (PRP), Hib.
Non-typable strains that lack a capsule
H.influenza
Cause Otitis Media and Sinusitis
H.influenza
Epiglottitis
H.Influenza
Can cause obstruction
What is the basic characteristics of Mycobacteria
Aerobic, slow growing, non spore forming bacilli
Stain for Mycobacteria
Acid Fast
Main content of Mycobacteria
Mycolic acid, Lipid, making them very hydorphobic
Morphology of Mycobacteria Colonies
Yellow to orange, dry fraible colonies
What is the main mode of transmission of M.Tuberculosis, and how prevelent is it ?
Aerosol transmission and 1/3 of the world's population is infected
MOA of M.Tb
Blocks phagosome-lysosome fusion after being phagocytosed by the cell.
Severity of most M.Tb infections
Asymptomatic or latent
Cellular reactions of M.Tb
Epithelioid cells, macrophages containing bacteria for granulomas with necrotic centers that can be reactivated with stress
Main virulent factor of M.Tb
Cord Factor (a lipid) kills mice and induces granulomas
Symptoms of M.Tb in the lung
Cavitary lung disease (cough, bloody sputum, fever, chils, night sweats, weight loss)
Systemic Symptoms of Tb
Miliary (multiple foci) disseminated and extra pulmonary disease of many tissues
Drug resistant forms of Tb
MDR-TB (multi drug resistant) isoniazid/rifampin
XDR-TB (extreme drug resistant) quinolone and aminoglycoside
Diagnositic Tests for Tb
Tuberculin Skin Test (Mantoux)
Acid Fast Staining of SputumFluorescent Dyes
Culturing methods for Tb
Decontamination of sputum specimens with 2% sodium hydroxide
Egg based media
Lab Diagnosis test for Tb
IFN-gamma assays

Assay for the production of IFNg by the patients blood cells is evidence of lymphocyte reaction with antigens
Main features of Mycobacterium Avium
Shares same microbiology as M.Tb
Effects those with pulmonary conditions, Immunodeficient, smokers.
MAC pathogensis
Patchy lung infiltrates
Which are the slow growing mycobacteria
M. Kansasii
M. Bovis
Which are the cutaneous pathogens
M. Ulcerans: tropical, skin grafts.
M. Marinum in swimming pools.
Microbiology of Mycobacterium Leprae and other names for it
Cannot be grown in culture

Leprosy or Hansen's disease
Transmission of M.Leprae
Contact, Aerosols, skin abrasion
Pathogenesis of M. Leprae
heavy tissue burden of bacteria.

tuberculoid has fewer bacteria in tissue
Rusty Sputum
Strep.Pneumo
Which immunosuppression is common among drug users
HIV
Prevention Immunization of H.Influenzae
Conjugate type b vaccine
The virulence factor of Listeria Monocytogens
Listeriolysin O
Gram positive, short motile bacilli with tumbling motion
Listeria Monocytogenes
Found in soil, Vegetations, and the feces of animals
Listeria Monocytogenes
Populations at risk of Listeria Monocytogens
High adult population like pregnant, risk of infants from non immune infected mothers.
Cells enter and enter enterocytes and attach to M cells
Listeria Monocytogenes
Action of Listeriolysin O in L.Monocytogens
Phagolysosome release
Actin based intracellular motility, moving cells to systemic sites
Listeria Monocytogenes
Stages of L.Monocytogens clinical infections
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.
CAMP test
Listeria Monocytogenes
Weak Beta hemolysis and cold enrichment
Listeria monocytogenes
Morphology of Rabies Virus
bullet shaped rhabdovirus, enveloped,helical,
negative sense ssRNA.
RNAdep-RNApoly
Rabies Virus
Rabies Epidemiology
Zoonotic from dogs, cats, mad dog disease.DOMESTIC ANIMALS
Virus binds acetylcholine receptors, moves up neural system to brain, then outward to cornea, hair roots and salivary glands.
Rabies Virus
Hydrophobia and paralysis
Rabies Virus
Negri bodies
Intracytoplasmic are viral aggregates in neural tissues seen in animal or post mortem human. In Rabies.
Fluorescent antibody test of animal tissue for virus presence
Rabies Virus
RT-PCR on saliva
Rabies Virus
Wound cleansing and Injection of HRIG as well as active immunization
Human rabies immune globulin is for prevention of Rabies.
small RNA viruses
Picornviridae
Virology of Poliomyelitis
Enterovirus, acid stable, 37 C growth, and its tissues target sepatartts it from other members.
Structure of Poliomyelitis
Positive ssRNA
Has four proteins that are rearranged after attachement and bind Ribosome.
Transmission of Poliomyelitis
Fecal-Oral
Contaminated Water
Pathogenesis of Poliomyelitis
- 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%
Lab test for Poliomyelitis
Throat swabs to cell culture early, from feces later, CSF variable recovery.
Prevention and Control of Poliomyeltis
- 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.
Poliomyelitis drug reactions
You would start with 2 Doses of the Salk vaccine and then administer
Structure of Arenaviruses
Enveloped, 2 ssRNA segments,
Replication of Arenaviruses
- 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.
Epidemiology of Arenavirus
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.
Types of Polyomavirus
JC and BK viruses
Epidemiology of JC and BK viruses
Water or Sewage, human exposure early in life, continual shedding through kidneys throughout life.
Pathogenesis of JC and BK Viruses
Polyomavirus as symptomatic except for cancer and suppressive therapy, causes progressive multifocal leukoncephalopathy, a demyelenating disease of what matter.
Lab test of JC and BK viruses
CSF, urine source, expansion by PCR.
Prevention control of JC and BK viruses
Avoid immunosuppressive therapy
Defective Measles Virus
Subacute Sclerosing Panencephalitis
Muscle Jerks or spasticity, blindness, personality and behavioral changes.
Subacute Sclerosing Panencephalitis
What kinds of viruses are arthropod born
RNA viruses, some are positive strand and some are negative strand.
Structure of Arbovirus
zoonotic RNA viruses
Main vectors for the Arbovirus
Mosquitoes
Family Togaviridae
Alpha Virus
EEE,WEE,VEE
Family Bunyaviridae
CA
LaCosse
Hanta
Types of Flaviviridea
Yellow Fever Virus
Dengue
West Nile
St. Louis Encephalitis Virus
Powassan Virus
Japanese B Encephalitis Virus
Hep. C Virus
Heptatitis G Virus
Pathogensis of Flavivirus
Mild systemic disease is usual, fever, chills, headache. Jap B may produce severe even fatal Encephalitis.
Structure of Togaviridae and Flaviviridea
Positive ssRNA enveloped viruses, cloak like cover that looks like a toga.
E1 and E2 peplomers are both found on the cover.
Flaviviruses that may produce servere hemorrhagic disease
Dengue and Yellow fever (liver disease)
Replication Process of Togaviridea
ssRNA positive-polyprotein synthesis and cleavage-negative strand RNA is made-progeny RNA
Epidemiology of EEE and WEE
Togaviruses
Birds Reservoir
Mosquitoes Vectors
Horses and Humans are dead end hosts
Sleeping sickness was seen in which diseases as well
Trypanosomas
African sleeping sickness
Pathogensis of EEE and WEE
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
Horse develops fatal sleeping sickness and mortality
EEE and WEE
Same course as EEE and WEE but is not as serious, very few cases in the USA
VEE
Chikungunya
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.
Epidemiology of West Nile Virus
Flavivirus that is worldwide.
Birds reservoir-Culex Mosquitoes vector
Pathogensis of West Nile Virus
90% assymptomatic
Fever, headache, chills, joint pain, flu like.
Encephalities Phase, near fatality.
How many antigenic types are there for dengue fever
Den 1 through Den 4
Lab Diagnosis for West Nile Virus
IgM
RT-PCR or Viral RNA recognition
Epidemiology of Saint Louis Encephalitis Virus
Flavivirus that is found in the Central and Eastern USA (missouri river).
Pathogenesis of SLEV
Asymptomatic and mild CNS.
Epidemiology of Powassan Virus
ssRNA, E1 and E2.
Ixodes ticks ar the reservoir and the vector.
North America and Canada
Pathogenesis of Powassan Virus
Flu like mild disease and encephalitis
Epidemiology of Japanese B
ssRNA,
Reservoirs are birds and pigs and the vector is a Culex (mosquito).
Japan and neighboring countries
Epidemeiology of Dengue fever
Tropical and subtropical areas where victors reside, Mosquitoes are the main vectors.
Human primates are reservoirs, sylvatic and urban cycles.
Pathogenesis of Japanese B
Mild flu like, and can be fatal more often than the above.
Pathogenesis of Dengue Fever
Break bone fever, headache, muscle and joint pain. Rash could be present but there is no encephalitis.
Major Risk from Dengue Fever
Dengue Hemorrhagic Fever (DHF)
Symptoms of Dengue Hemorrhagic Fever
Irritability, restless, heavy sweating with petechia, bleeding tendency.
Dengue Shock Syndrome (DSS)
Deteriorates with the accumulation of blood in the abdomen, abundant petechia, loss of blood pressure.

Occurs after second infection to the disease.
The flooding and removal of standing water to prevent moquito breeding
Yellow Fever
Human, primates, sylvatic and urban cycles, also found in Aedes mosquitoes
Yellow Fever
Stage of Yellow Fever Pathogenesis
Early: fever, nausea and abdominal pain
Late: pain and jaundice
Hemorrhagic: black vomit
Lab for Yellow fever
RT-PCR
Patient serum for immune response
Bunyaviridea Structure
Enveloped, negative, ssRNA, 3 segmented virus. RNApoly-RNAdep.
Epidemiology of Bunyavirus
Rodents urine and feces and spread by infected ticks
California and La Crosse Viruses
Type of Bunyavirus, as symptomatic. Nausea, vomiting, headache, seizure in true encephalitis.
Feature of Hanatvirus
Sin Nombre. Dust contaminated by urine and feces of white footed mice.
Pathogensis of Hantavirus
Pulmonary and Cardiac syndromes with a lot of loss of blood.
Coltivirus-Colorado tick fever features
dsRNA virus. They are plus strands in an mRNA, translation to RNAdep-RNApoly for genomic RNA forms
Epi. of Colitivirus
Mountain West, hard ticks.
Pathogenesis of Coltivirus-Colorado tick fever
Flu like symptoms to aseptic
Scrapie and Mad cow disease, bovine spongiform encephalopathy (BSE)
Prions proteins, that are a denatured proteins.
Disease caused by prions in New Guniea
Kuru, which is a transmissible neurologic disease that originated from cannabalism.
Creutzfeldt-Jacob disease (CJD)
dementia leading to death in the prion disease.
Pathogenesis of prions
Protease resistant proteins
Name for prion proteins
PrPc and PrPsc
Prion type that binds to human cellular
Scrapie type, and causes it to aggregate into amyloid fibers and/or vacuoles that accumulate in the brain.
Symptoms of PrPsc
Ataxia, dementia, behavioral changes, memory loss, development of spongiform lesion and amyloid deposit in the brain.
Transmission by ingestion
Prions
Accumulation of PMN and other immune cells as well as debris
Brain Abscess that is caused by post surgical procedure, or trauma. This later increase the cranial pressure.
Organism pass through the nose from water. Into the nose and then to the brain where they can be fatal.
Naegleria Fowleri
Organism that is caused by those who wear contact lenses with no proper hygiene
Acanthamoebae Castellani
Pathogenesis of Taenia Solium
Flatworm (cestode) which has a head (scolex) and proglottid segments
Adult worm in swine intestine sheds eggs, hexacanth embryo (oncosphere) develops
Taenia Solium parasitology
Taenia Solium Lifecycle
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
CNS effecting protozoa
Trypanosomes Brucei, and Trypanosomes Brucei
CNS Nematodes
Toxocara Canis and T. Cati
T.Canis and Cati Lifecycle
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
Mycological CNS
Cryptococcus Neoformans
Spherical yeast with a capsule larger in diameter
Cryptococcus Neoformans
Positive Urease Test
Cryptococcus Neoformans
Very slow growing yeasts that cause meningitis
Cryptococcus Neoformans
Neonate born in poor conditions with encephalitis
HSV 2
Cystic Fibrosis, with pneumonia, blue green sputum
Pseudomona Aurigonsa
Jelly sputum
Klebsiella
Lesions on face of cutanous touch and pain, Acid fast organism
Leprae
Sore throat, spleen and liver. Later LEADING TO SPLENIC RUPTURE
EBV
Triad of Meningitis
Headache, Fever, Stiff Neck
Drug of choice for Neisseria Meningitids
Ceftriaxone
Patient comes in with petechia and stiff neck
N.Meningitidis
Test for N. Meningitidis
Blood, Urine, and Sputum
Where do you never delay therapy in
N.Meningitidis
Dont do CT or MRI
Major concern for patient with Neissieria Meningitidis
Intercranial Pressure
Effects college, and people clustered in small places
N.Meningitids
Why do you use Chocolate agar plate for N.Meningitidis
X and V heme
Glucose and Maltose Positive
N.Meningitidis
Glucose and Maltose negative
N.Gonorrheae
What is the main drug for prophylaxis today
Ceftriaxone and Refampin
Main side effect of Rifampin
Soft contact lenses causes a problem, Red coloration of the skin.
Where do you have polymicrobial effects with N.Meningitidis
Stronglyoides
Patient with headache, fever and stiff neck, and HD (immunocompramised)
Listeria Monocytogens
How do you treat listeria ?
B lactams. Ampicillins and Penicillins
Patient has fever, lethargy and clears drain pipes and paralysis
West Nile Virus
Reduvid Bug, occurs when you scratch after the bug infestation
Chagas disease, Typansomas Cruzei.
Cycle of Tryp. Cruzei
Dog-Reduvid-Human
Which are the oldest Hepatitis Viruses
Hepatitis A and B
Structure of Hepatitis A Virus
Naked, Postive ssRNA. HepaRNAvirus, hepatovirus from picoviridae family.
Replication of Hep A
It is NOT cytolytic
Epidemiology of HAV
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.
Pathogenesis and Clinical of HAV
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.
Lab diagnosis of HAV
Detection of HAV infection by anti-HAV IgM by ELISA. History of sea food consumption.
Prevention of HAV
Sanitation and cholorination of water. Avoid raw sea foods.
Inactive HAV vaccine for travelers.
Structure of Hepatitis B Virus
Enveloped, circular, partially dsDNA with reverse transcriptase and an RNA intermediate. HepaDNAviruses.
Dane particle
Found in HBV. A virion consisting of DNA and a capsid protein labeled as the hepatitis B virus core antigen (HBcAg)
Australia Antigen
HBV surface antigen HBsAg is an envelope antigen. There are 3 molecular forms S,M and L.
Replication of HBV
- 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.
Epidemiology of HBV
Asymptomatic. Transmitted by blood, contaminated needles, tattoos, ear puncture, sex and childbirth. Called SERUM HEPATITIS.
Pathogenesis and Clinical of HBV
Incubation for 45 before symptoms and before progression to typical liver disease.
- Chronic Leads to cirrhosis, liver failure.
- Primary hepatocellular Carcinoma
Lab diagnosis of HBV
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.
Prevention and Lab control of HBV
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.
Structure of Hep. C virus
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.
Epidemiology of HCV and HGV
Blood borne hepatitis, bu drug abuse, transfusion, skin puncture, tattoos.
High rate in aids patients
Pathogenesis and Clinical Disease
15% Asymptomatic
70% progress to HCC
15% progresses to Cirrohosis
Lab diagonsis for HCV
ELISA to detect anti-HCV globulin.
Western blot of virus protein from patient serum.
Prevention of HCV
INFa with ribavirin, 50% recovery. Mimics riboquanosine and inhibits nuceloside synthesis.
Anolog Used for HCV vaccine
Ribavirin is used as a Guanosine analog
Structure of Hepatitis D virus
-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.
Which virus requires HBV to survive?
Hepatitis D
Spreads though blood, semen and secretions
Hepatitis D and B
Leads to fuliminant hepatitis
Hepatitis D
Co-infection
Person having both HBV and HDV infections
Superinfection
HBV positive person with HDV who is also HBV positive, of course, may exacerbate hepatitis symptoms and lead to cirrhosis or chronic, persistent infections.
Enteric Hepatitis
HEV
Fecal-Oral Transmission
HAV and HEV
Agents that cause Hepatitis
Prominent:
Yellow fever
Leptospira interrogans
Other:
CMV
EBV
Adenovirus
Herpesviridae
Structure
dsDNA
Enveloped
Linear
Herpes Infection patterns
Lytic

Persistent

Latent or Transforming
Herpes Theraputic Agent
Thymidine Kinase
HSV attachement Site
Heparan Sulfate
glycoprotein found on many cells
Stages for HSV infection
Immediate: control gene transcription
Early: Polymerase and other enzymes
Late: protein synthesis
Epidemiology of HSV
Found in Secretions

Vaginal
Saliva
Vesicle
Towels
Glasses
Clinical Features of HSV
Oral cold, sores, fever, blisters and genital vesicles
HSV Eruptions are caused by
fever
UV light
menstruation
local irriation
Cowdry Type A acidophilic intranuclear inclusion bodies
HSV 1 and 2
Disease caused by HSV
Herpes pharyngitis
ocular keratitis
Herpetic whitlow
encephalitis (HSV 2)
Lab diagnosis for HSV
Tzank Smear

Virus isolation
Prevention of HSV
Avoid exposure
What is acyclovir
Its is used to mimic guanosine and prevent HSV
Thymidine Kinase
Receptor, therapeutic target
Binding site for EBV
CR2 of the B-cell
Outcomes after EBV binds to B-Cells
Permissive
Latent
Immortalization of B cells
EBV early Antigens
Early Antigen
Viral Capsid antigen
EBV Latent Antigens
Non permissive, EBNA and LMP
Kissing disease
EBV
Virus spreads for a lifetime
EBV
Children Asymptomatic
EBV
M.Tb
Infective Mononucleosis
EBV
Sore throat
Lymphadenopathy
Splenomegaly
Infective Mononucleosis
Burkitt's lymphoma
EBV
Nasopharyngeal Carcinoma
EBV
Lymphoproliferative Disease
EBV
Chromosome Effected with EBV
c-myc gene from chromosome 8/14 translocation
Downey Cells
Atyptical lymphocytes seen in EBV
Monospot Test
Heterophile Antibody for EBV
Antibodies tested for EBV
EA and EBNA
Which are the only organs that escape Tb infections
Tests and ovaries
Morphology of Neisseria meningitidis
Gram - Diplococci with a kidney bean shaped
Oxidase and catalase positive
N.Meningitidis
Oxidase test where dye changes color
N.Meningitidis
Polysaccharide capsule with 13 serologic groups A,B,C,Y and W135
N.Meningitidis
Normal flor of N.Meningitidis
Nose and throat
Move through sinuses and can even go to the brain
N.Meningitidis
Transmission of N.Meningitidis
Aerosols, college and school children
Effects children with later complement deficiency
N.Meningitidis
Contain antiphagocytic capusles and pilli
N.Meningitidis
H. Influenza
Purulent, headache, fever, stiffness
Meningitis which is caused by N.meningitidis and H.Influenza
Petechia, purpura, thrombosis of small blood vessels, septic shock
Meningococcemia which is caused by N.Meningitidis
Bilateral renal gland hemorrhagic necrosis
Waterhouse-Friderichsen syndrome which is caused by N.Meningitidis
Chocolate agar, Thayer-martin chocolate agar
N.Meningitidis
Vaccines of four polysaccharides A,C,Y and W135 MPSV4
N.Meningitidis
MCV4/MPSV4 vaccine
N.Meningitidis
3 main human pathogens of H. Haemophilus
H.influenza
H.ducreyi
H.aegyptius
Conjuctivitis (pink eye)
H.Aegyptius
Chancroid an STD
H.ducreyi
What do H.Haemophilus require for growth
Hemin the X factor
NAD
V factor
Structure of H.Influenza
Six capuslar antigenic types, Polyribitol ribose phosphate (PRP), Hib.
Non-typable strains that lack a capsule
H.influenza
Cause Otitis Media and Sinusitis
H.influenza
Epiglottitis
H.Influenza
Can cause obstruction
What is the basic characteristics of Mycobacteria
Aerobic, slow growing, non spore forming bacilli
Stain for Mycobacteria
Acid Fast
Main content of Mycobacteria
Mycolic acid, Lipid, making them very hydorphobic
Morphology of Mycobacteria Colonies
Yellow to orange, dry fraible colonies
What is the main mode of transmission of M.Tuberculosis, and how prevelent is it ?
Aerosol transmission and 1/3 of the world's population is infected
MOA of M.Tb
Blocks phagosome-lysosome fusion after being phagocytosed by the cell.
Severity of most M.Tb infections
Asymptomatic or latent
Cellular reactions of M.Tb
Epithelioid cells, macrophages containing bacteria for granulomas with necrotic centers that can be reactivated with stress
Main virulent factor of M.Tb
Cord Factor (a lipid) kills mice and induces granulomas
Symptoms of M.Tb in the lung
Cavitary lung disease (cough, bloody sputum, fever, chils, night sweats, weight loss)
Systemic Symptoms of Tb
Miliary (multiple foci) disseminated and extra pulmonary disease of many tissues
Drug resistant forms of Tb
MDR-TB (multi drug resistant) isoniazid/rifampin
XDR-TB (extreme drug resistant) quinolone and aminoglycoside
Diagnositic Tests for Tb
Tuberculin Skin Test (Mantoux)
Acid Fast Staining of SputumFluorescent Dyes
Culturing methods for Tb
Decontamination of sputum specimens with 2% sodium hydroxide
Egg based media
Lab Diagnosis test for Tb
IFN-gamma assays

Assay for the production of IFNg by the patients blood cells is evidence of lymphocyte reaction with antigens
Main features of Mycobacterium Avium
Shares same microbiology as M.Tb
Effects those with pulmonary conditions, Immunodeficient, smokers.
MAC pathogensis
Patchy lung infiltrates
Which are the slow growing mycobacteria
M. Kansasii
M. Bovis
Which are the cutaneous pathogens
M. Ulcerans: tropical, skin grafts.
M. Marinum in swimming pools.
Microbiology of Mycobacterium Leprae and other names for it
Cannot be grown in culture

Leprosy or Hansen's disease
Transmission of M.Leprae
Contact, Aerosols, skin abrasion
Pathogenesis of M. Leprae
heavy tissue burden of bacteria.

tuberculoid has fewer bacteria in tissue
Rusty Sputum
Strep.Pneumo
Which immunosuppression is common among drug users
HIV
Prevention Immunization of H.Influenzae
Conjugate type b vaccine
The virulence factor of Listeria Monocytogens
Listeriolysin O
Gram positive, short motile bacilli with tumbling motion
Listeria Monocytogenes
Found in soil, Vegetations, and the feces of animals
Listeria Monocytogenes
Populations at risk of Listeria Monocytogens
High adult population like pregnant, risk of infants from non immune infected mothers.
Cells enter and enter enterocytes and attach to M cells
Listeria Monocytogenes
Action of Listeriolysin O in L.Monocytogens
Phagolysosome release
Actin based intracellular motility, moving cells to systemic sites
Listeria Monocytogenes
Stages of L.Monocytogens clinical infections
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.
CAMP test
Listeria Monocytogenes
Weak Beta hemolysis and cold enrichment
Listeria monocytogenes
Morphology of Rabies Virus
bullet shaped rhabdovirus, enveloped,helical,
negative sense ssRNA.
RNAdep-RNApoly
Rabies Virus
Rabies Epidemiology
Zoonotic from dogs, cats, mad dog disease.DOMESTIC ANIMALS
Virus binds acetylcholine receptors, moves up neural system to brain, then outward to cornea, hair roots and salivary glands.
Rabies Virus
Hydrophobia and paralysis
Rabies Virus
Negri bodies
Intracytoplasmic are viral aggregates in neural tissues seen in animal or post mortem human. In Rabies.
Fluorescent antibody test of animal tissue for virus presence
Rabies Virus
RT-PCR on saliva
Rabies Virus
Wound cleansing and Injection of HRIG as well as active immunization
Human rabies immune globulin is for prevention of Rabies.
small RNA viruses
Picornviridae
Virology of Poliomyelitis
Enterovirus, acid stable, 37 C growth, and its tissues target sepatartts it from other members.
Structure of Poliomyelitis
Positive ssRNA
Has four proteins that are rearranged after attachement and bind Ribosome.
Transmission of Poliomyelitis
Fecal-Oral
Contaminated Water
Pathogenesis of Poliomyelitis
- 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%
Lab test for Poliomyelitis
Throat swabs to cell culture early, from feces later, CSF variable recovery.
Prevention and Control of Poliomyeltis
- 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.
Poliomyelitis drug reactions
You would start with 2 Doses of the Salk vaccine and then administer
Structure of Arenaviruses
Enveloped, 2 ssRNA segments,
Replication of Arenaviruses
- 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.
Epidemiology of Arenavirus
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.
Types of Polyomavirus
JC and BK viruses
Epidemiology of JC and BK viruses
Water or Sewage, human exposure early in life, continual shedding through kidneys throughout life.
Pathogenesis of JC and BK Viruses
Polyomavirus as symptomatic except for cancer and suppressive therapy, causes progressive multifocal leukoncephalopathy, a demyelenating disease of what matter.
Lab test of JC and BK viruses
CSF, urine source, expansion by PCR.
Prevention control of JC and BK viruses
Avoid immunosuppressive therapy
Defective Measles Virus
Subacute Sclerosing Panencephalitis
Muscle Jerks or spasticity, blindness, personality and behavioral changes.
Subacute Sclerosing Panencephalitis
What kinds of viruses are arthropod born
RNA viruses, some are positive strand and some are negative strand.
Structure of Arbovirus
zoonotic RNA viruses
Main vectors for the Arbovirus
Mosquitoes
Family Togaviridae
Alpha Virus
EEE,WEE,VEE
Family Bunyaviridae
CA
LaCosse
Hanta
Types of Flaviviridea
Yellow Fever Virus
Dengue
West Nile
St. Louis Encephalitis Virus
Powassan Virus
Japanese B Encephalitis Virus
Hep. C Virus
Heptatitis G Virus
Pathogensis of Flavivirus
Mild systemic disease is usual, fever, chills, headache. Jap B may produce severe even fatal Encephalitis.
Structure of Togaviridae and Flaviviridea
Positive ssRNA enveloped viruses, cloak like cover that looks like a toga.
E1 and E2 peplomers are both found on the cover.
Flaviviruses that may produce servere hemorrhagic disease
Dengue and Yellow fever (liver disease)
Replication Process of Togaviridea
ssRNA positive-polyprotein synthesis and cleavage-negative strand RNA is made-progeny RNA
Epidemiology of EEE and WEE
Togaviruses
Birds Reservoir
Mosquitoes Vectors
Horses and Humans are dead end hosts
Sleeping sickness was seen in which diseases as well
Trypanosomas
African sleeping sickness
Pathogensis of EEE and WEE
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
Horse develops fatal sleeping sickness and mortality
EEE and WEE
Same course as EEE and WEE but is not as serious, very few cases in the USA
VEE
Chikungunya
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.
Epidemiology of West Nile Virus
Flavivirus that is worldwide.
Birds reservoir-Culex Mosquitoes vector
Pathogensis of West Nile Virus
90% assymptomatic
Fever, headache, chills, joint pain, flu like.
Encephalities Phase, near fatality.
How many antigenic types are there for dengue fever
Den 1 through Den 4
Lab Diagnosis for West Nile Virus
IgM
RT-PCR or Viral RNA recognition
Epidemiology of Saint Louis Encephalitis Virus
Flavivirus that is found in the Central and Eastern USA (missouri river).
Pathogenesis of SLEV
Asymptomatic and mild CNS.
Epidemiology of Powassan Virus
ssRNA, E1 and E2.
Ixodes ticks ar the reservoir and the vector.
North America and Canada
Pathogenesis of Powassan Virus
Flu like mild disease and encephalitis
Epidemiology of Japanese B
ssRNA,
Reservoirs are birds and pigs and the vector is a Culex (mosquito).
Japan and neighboring countries
Epidemeiology of Dengue fever
Tropical and subtropical areas where victors reside, Mosquitoes are the main vectors.
Human primates are reservoirs, sylvatic and urban cycles.
Pathogenesis of Japanese B
Mild flu like, and can be fatal more often than the above.
Pathogenesis of Dengue Fever
Break bone fever, headache, muscle and joint pain. Rash could be present but there is no encephalitis.
Major Risk from Dengue Fever
Dengue Hemorrhagic Fever (DHF)
Symptoms of Dengue Hemorrhagic Fever
Irritability, restless, heavy sweating with petechia, bleeding tendency.
Dengue Shock Syndrome (DSS)
Deteriorates with the accumulation of blood in the abdomen, abundant petechia, loss of blood pressure.

Occurs after second infection to the disease.
The flooding and removal of standing water to prevent moquito breeding
Yellow Fever
Human, primates, sylvatic and urban cycles, also found in Aedes mosquitoes
Yellow Fever
Stage of Yellow Fever Pathogenesis
Early: fever, nausea and abdominal pain
Late: pain and jaundice
Hemorrhagic: black vomit
Lab for Yellow fever
RT-PCR
Patient serum for immune response
Bunyaviridea Structure
Enveloped, negative, ssRNA, 3 segmented virus. RNApoly-RNAdep.
Epidemiology of Bunyavirus
Rodents urine and feces and spread by infected ticks
California and La Crosse Viruses
Type of Bunyavirus, as symptomatic. Nausea, vomiting, headache, seizure in true encephalitis.
Feature of Hanatvirus
Sin Nombre. Dust contaminated by urine and feces of white footed mice.
Pathogensis of Hantavirus
Pulmonary and Cardiac syndromes with a lot of loss of blood.
Coltivirus-Colorado tick fever features
dsRNA virus. They are plus strands in an mRNA, translation to RNAdep-RNApoly for genomic RNA forms
Epi. of Colitivirus
Mountain West, hard ticks.
Pathogenesis of Coltivirus-Colorado tick fever
Flu like symptoms to aseptic
Scrapie and Mad cow disease, bovine spongiform encephalopathy (BSE)
Prions proteins, that are a denatured proteins.
Disease caused by prions in New Guniea
Kuru, which is a transmissible neurologic disease that originated from cannabalism.
Creutzfeldt-Jacob disease (CJD)
dementia leading to death in the prion disease.
Pathogenesis of prions
Protease resistant proteins
Name for prion proteins
PrPc and PrPsc
Prion type that binds to human cellular
Scrapie type, and causes it to aggregate into amyloid fibers and/or vacuoles that accumulate in the brain.
Symptoms of PrPsc
Ataxia, dementia, behavioral changes, memory loss, development of spongiform lesion and amyloid deposit in the brain.
Transmission by ingestion
Prions
Accumulation of PMN and other immune cells as well as debris
Brain Abscess that is caused by post surgical procedure, or trauma. This later increase the cranial pressure.
Organism pass through the nose from water. Into the nose and then to the brain where they can be fatal.
Naegleria Fowleri
Organism that is caused by those who wear contact lenses with no proper hygiene
Acanthamoebae Castellani
Pathogenesis of Taenia Solium
Flatworm (cestode) which has a head (scolex) and proglottid segments
Adult worm in swine intestine sheds eggs, hexacanth embryo (oncosphere) develops
Taenia Solium parasitology
Taenia Solium Lifecycle
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
CNS effecting protozoa
Trypanosomes Brucei, and Trypanosomes Brucei
CNS Nematodes
Toxocara Canis and T. Cati
T.Canis and Cati Lifecycle
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
Mycological CNS
Cryptococcus Neoformans
Spherical yeast with a capsule larger in diameter
Cryptococcus Neoformans
Positive Urease Test
Cryptococcus Neoformans
Very slow growing yeasts that cause meningitis
Cryptococcus Neoformans
Neonate born in poor conditions with encephalitis
HSV 2
Cystic Fibrosis, with pneumonia, blue green sputum
Pseudomona Aurigonsa
Jelly sputum
Klebsiella
Lesions on face of cutanous touch and pain, Acid fast organism
Leprae
Sore throat, spleen and liver. Later LEADING TO SPLENIC RUPTURE
EBV
Triad of Meningitis
Headache, Fever, Stiff Neck
Drug of choice for Neisseria Meningitids
Ceftriaxone
Patient comes in with petechia and stiff neck
N.Meningitidis
Test for N. Meningitidis
Blood, Urine, and Sputum
Where do you never delay therapy in
N.Meningitidis
Dont do CT or MRI
Major concern for patient with Neissieria Meningitidis
Intercranial Pressure
Effects college, and people clustered in small places
N.Meningitids
Why do you use Chocolate agar plate for N.Meningitidis
X and V heme
Glucose and Maltose Positive
N.Meningitidis
Glucose and Maltose negative
N.Gonorrheae
What is the main drug for prophylaxis today
Ceftriaxone and Refampin
Main side effect of Rifampin
Soft contact lenses causes a problem, Red coloration of the skin.
Where do you have polymicrobial effects with N.Meningitidis
Stronglyoides
Patient with headache, fever and stiff neck, and HD (immunocompramised)
Listeria Monocytogens
How do you treat listeria ?
B lactams. Ampicillins and Penicillins
Patient has fever, lethargy and clears drain pipes and paralysis
West Nile Virus
Reduvid Bug, occurs when you scratch after the bug infestation
Chagas disease, Typansomas Cruzei.
Cycle of Tryp. Cruzei
Dog-Reduvid-Human
Which are the oldest Hepatitis Viruses
Hepatitis A and B
Structure of Hepatitis A Virus
Naked, Postive ssRNA. HepaRNAvirus, hepatovirus from picoviridae family.
Replication of Hep A
It is NOT cytolytic
Epidemiology of HAV
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.
Pathogenesis and Clinical of HAV
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.
Lab diagnosis of HAV
Detection of HAV infection by anti-HAV IgM by ELISA. History of sea food consumption.
Prevention of HAV
Sanitation and cholorination of water. Avoid raw sea foods.
Inactive HAV vaccine for travelers.
Structure of Hepatitis B Virus
Enveloped, circular, partially dsDNA with reverse transcriptase and an RNA intermediate. HepaDNAviruses.
Dane particle
Found in HBV. A virion consisting of DNA and a capsid protein labeled as the hepatitis B virus core antigen (HBcAg)
Australia Antigen
HBV surface antigen HBsAg is an envelope antigen. There are 3 molecular forms S,M and L.
Replication of HBV
- 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.
Epidemiology of HBV
Asymptomatic. Transmitted by blood, contaminated needles, tattoos, ear puncture, sex and childbirth. Called SERUM HEPATITIS.
Pathogenesis and Clinical of HBV
Incubation for 45 before symptoms and before progression to typical liver disease.
- Chronic Leads to cirrhosis, liver failure.
- Primary hepatocellular Carcinoma
Lab diagnosis of HBV
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.
Prevention and Lab control of HBV
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.
Structure of Hep. C virus
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.
Epidemiology of HCV and HGV
Blood borne hepatitis, bu drug abuse, transfusion, skin puncture, tattoos.
High rate in aids patients
Pathogenesis and Clinical Disease
15% Asymptomatic
70% progress to HCC
15% progresses to Cirrohosis
Lab diagonsis for HCV
ELISA to detect anti-HCV globulin.
Western blot of virus protein from patient serum.
Prevention of HCV
INFa with ribavirin, 50% recovery. Mimics riboquanosine and inhibits nuceloside synthesis.
Anolog Used for HCV vaccine
Ribavirin is used as a Guanosine analog
Structure of Hepatitis D virus
-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.
Which virus requires HBV to survive?
Hepatitis D
Spreads though blood, semen and secretions
Hepatitis D and B
Leads to fuliminant hepatitis
Hepatitis D
Co-infection
Person having both HBV and HDV infections
Superinfection
HBV positive person with HDV who is also HBV positive, of course, may exacerbate hepatitis symptoms and lead to cirrhosis or chronic, persistent infections.
Enteric Hepatitis
HEV
Fecal-Oral Transmission
HAV and HEV
Agents that cause Hepatitis
Prominent:
Yellow fever
Leptospira interrogans
Other:
CMV
EBV
Adenovirus
Microbiology of Rickettsia
Gram Negative
Small Pleomorphic Cocci
Obligate intracellular
Peptidoglycan and weak Endotoxin
Small rodents as reservoirs and arthropod vectors
Rickettsia
Frontal Headache, Fever and Rash
Rickettsia
Use phospholipase to escape phagolysosome and reproduce by binary fission
Rickettsia
Transmitted by Dermacentor Varibilis and Andersoni
Dog Tick and wood tick that transmits Rickettsia
Rash on the Extremities that spreads to the core
Rocky Mountain Spotted fever that is caused by Rickettsia Rickettsii
Found in cosmopolitan areas, and uses the house mouse and its mites as a reservoir
Rickettsia akari
Louse that uses the human body as a reservoir
Tick (Pediculus humanus) that causes Rickettsia Prowazekii
Reactivation of a Rickettsia Infection long after the primary infection
Recurdescent (Brill Zinsser Disease)
Rash starts out on the trunk and spreads outwards
Rickettsia Typhi
Test for Rickettsia
Wei-Felix Test that test for Rickettsial Anti-bodies that cross react with proteus antigen and agglutinate.
Prevention and control of Rickettsia
Avoid Ticks
The disease of the Orient (japan) that is found in the Rodents as the Reservoir and Chiggers and the vector
Orientia Tsutsugamushi
Genetically different, but the same as gram negative strains weakly morphology like Rickettsia
Coxiella Burnetii and Q fever
Small cell variant which is resistant to enviornment and large cell variant appears in the phagolysosome of monocytes, macrophages.
Coxiella Burnetii and Q fever
Pneumonia, Hepatitis, Subacute endocarditis
Coxiella Burnetii and Q fever
Obligate intracellular pathogens that survive in phagocytic vacuoles inside hematopoietic cell (RBC, granulocytes, monocytes and platelets
Ehrlichia and Anaplasma
Large reticulate body formed by assembly of elementary bodies, called morulae and then lytic release, lack petidoglycan and LPS
Ehrlichia and Anaplasma