MCB Exam 4 – Flashcards

1. Sub-Microscopic

2. Obligate intracellular parasite

3. Host specificity

4. Needs host 4 energy n protein synthesis

1. Nucleic acid

2. Capsid

3. Envelope

4. Spikes

1. Protects DNA/RNA against damage

2. Involved in recognizing the host surface

3. Facilitates nucleic acid penetration

Nucleic acids

Capsids

1. Lytic = kills host

2. Persistant = small amounts of virus, host lives

3. Transforming = changes genetics, causes cancer

4. Latent = hides in host, no effect on host

1. Cell lysis

2. Cell transformation can lead to cancer

3. Produces toxic products

4. Alters host structure such as nuclear or cytoplasm

1. Directly by trauma or insect bite

2. Thru mucous membranes of the resp. tract or alimentary tract.

1. Fast action

2. Adapts to host biochemical conditions

3. Able to resist host defense mechanisms

1. Attachment

2. Penetration

3. Un coating

4. Provision of energy

5. synthesis of Low MW compounds

6. Nucleic acid and protein synthesis

7. Assembly

8. Release

1. Inhibits the MHC I restricted Ag Presentation so no CD8 response

2. Inhibits MHC II restricted Ag presentation so no Ab, or Ag memory

3. Downregulates CD4 (T-helper cells)

4. Inhibits NK cell lysis

5. Intereferes with apoptosis

6. Evasion of humoral immunity

7. Inhibits cytokine action

1. Permissive or productive infection

2. Abortive or non-productive

3. Persistent

4. latent

5. Cytopathic effects (CPE)

1. Plaque formation in phage

2. Nuclear/cytoplasm enlargement

3. Nucleus changes

4. Cell fusion, syncytia formation

5. Lysosomes leaking

6. Viral budding, fibroblast

7. Changes in membranes

1. Attach/adsorb to the cell

2. Penetration by fusion or endocytosis

3. Eclipse period

4. Rise = virus particles are detectable

It is the pathogenic manifestations of a viral infection.

1. Flu like and systemic symptoms

2. Infection of the eye, oral, resp. tract

3. Gastroenteritis

4. Hepatitis

5. STDs

6. Hemorrhagic fevers

Cytopathology = Branch of pathology that studies and diagnoses diseases on the cellular level.

Immunopathology = Branch of medication that deals with the immune response associated w/the disease.  It includes the study of  the pathology of an organism, organ system, or disease w/ respect to the immunity/response.

A = Infectious Hepatitis

B = Serum Hepatitis

C

D

E

1. Sexual

2. Parenteral injecting

3. Perinatal

1. Prevent perinatal HBV transmission

2. Routine vaccines for all infants

3. Vaccinate

Flaviviridae

+ss RNA

1. Blood transfusions

2. IV drug users

3. Sex

Percutaneous

1. Injecting drug use

2. Transfusion

3. Contaminated equipment

4. Needlestick

5. Clotting factors b4 viral inactivation

Permucosal

1. Perinatal

2. Sexually

1. Contaminated equipment

2. Unsfae injection practices such as multiple dose medication vials

Only when women HCV-RNA positive at delivery

(higher incidence in HIV women)

1. Avoid direct exposure to blood

2. Cover cuts and sores on skin

3. Do not share items that may have blood on them

4. Do not donate blood, body organs, etc

1. Use condoms

2. Limit # of partners

3. Get vaccinated against Hep. B

Hep. B

It has reverse transcriptase

Contaminated equip = Hemodialysis

Unsafe injection = plasmapheresis

1. Hihgly efficient amoung injection drug users

2. Rapidly acquired after initiation

3. 4x more common then HIV

5. Prevalence 60-90% after 5 years

1. Inhibits nucleoside biosynthesis

2. Inhibits capping of mRNA

3. Inhibits RNA Poly.

Sympt = B (70K-160K; vs 3K- 54K)

;

Liver = C (8K-10K vs 5K-6K)

1. Enveloped icosahedral capsid 100 nm

2. 9 Glycoproteins

3. 30 structural proteins, but codes for 120

4. Tegument is amorphous

5. No common family antigen

1. Alphaherpsesvirinae

2. Betaherpesvirinae

3. Gammaherpesvirinae

1. Genus Simplex virus = HSV1 and 2, B virus

2. Genus Varicella virus = varicella-zoster virus (chicken pox)

Genus Cytomegalovirus

Genus Roseolovirus

Double stranded linear

infectious

Neuro

Salivary gland

Lympho

1. Attachment - glycoproteins on viral envelope fuses with cell P.M.

2. Penetration - direct or endocytosis

3. Envelopes are acquired at inner nuclear membrane

4. Virions are released by reverse phagocytosis

5. Cell is not killed, but the functions are taken over by the virus

1. Fever blisters

2. Occurs early in life

3. Primary infection is 8-10 days

4. Latent infection is asymptomatic

;

In the nerves of the lower back

(sacral plexus)

1. Encephalitis

2. Keatoconjunctivitis

3. Pharyngitis

4. Esophaitis

5. Gladiatorum

6. Oral

7. Genital

8. Whitlow

1. Meningitis

2. Oral

3. Pharyngitis

4. Genital

5. Perianal

6. Whitlow

Encephalitis

Meningitis

1. Spread by resp. tract

2. Chicken pox = seasonal epidemics

3. Vesicular rash w/systemic infection

4. 2-2 1/2 wks long infection cycle

5. More severe in adults

6. Recurrent infection occurs

Shingles

Specific nerve

1. Infects and causes no obvious disease

2. Prego can abort fetus

3. Transmitted by saliva

4. Virus secreted in milk, saliva and semen

5. Major problem in immunosuppressed peeps

Mononucleosis

95%

HHV-8 is associated with Kaposi's sarcoma in AIDS patients

EBV is associated with Burkitt's lymphoma in AIDS patients and related w/ nasopharngeal carinoma in Africa

1. Alphavirus

2. Rubivirus = causes Measles

3. Arteriviruses

Respiratory illness

Aerosols

1. Cataracts

2. Mental retardation

3. Deafness

1. Encased by a fragile lipid envelope

2. Nonsegmented (-) sensed ssRNA w/ 6-10 genes separated by noncoding termination, polyadenylation and initiation signals.

3. Replication occurs in the cytoplasm

;

1. H, HN or G = glycoproteins mediate cell attachment

2. F(fusion) protein;= has 3 functions

H = Hemagglutinin

HN = Neuraminidase

1. Enables virus; to fuse to cell to form syncytia

2. Enable viral penetration by fusion of viral envelope w/ P.M.

3. Allows direct intercellular spread by cell to cell fusion (can now evade the bodys circulating Ab's, and allow transfer of infectious nucleocapsids to nearby cells)

1. Natural immunity against reinfection is effective

2. Passive immunization for the unimmunized (administer IgG)

3. Live vaccine

1. Subacute Sclerosing Panencephalitis

2. Subacute Measles Encephalitis

3. Acute Postinfectious Measles Encephalitis

1. Distorted face

2. Edematous enlargement of the salivary glands

3. Infants often asymptomatic or as a resp. infection.

1. Non-segmented, (-) sensed ssRNA

2. Helical nucleocapsid

3. Virion associated RNA-dependent RNA Poly

4. Similar gene order

5. Single 3' promoter

Filoviridae = Ebola

Paramyxoviridae = Measles, mumps

Rhabdoviridae = Rabies

1. Can infect all warm blooded animals

2. Causes acute, contagious infection of the CNS

3. 100% fatal once symptoms show

4. Occurs worldwide except Hawaii, Japan, Great Britian and smaller islands

1. Bite/scratch of an infected animal (99% of cases worldwide)

2. Aerosol transmission from a bat

3. Tissue transplants from infected human (eyes)

1. Enters vody and travels w/in neurons to the CNS

2. Causes encephalitis in the brain

3. Virus travels down the nerves and multiplies in many diff. organs

1. Early = nonspecific includes fever, headache, tiredness, etc

2. Progesses = Insomnia, anxiety, confusion, paralysis, hallucinations, hypersalivation, hydrophobia, hard to swallow

3. Late = Delirium, coma, Death

1. Preexposure Prophylaxis

2. Postexposure Prophylaxis

5 doses

Admin Rabies Immune Globulin

1. Wheel shaped, 70 nm

2. 2 concentric icosahedral capsids surrounding an inner core

3. dsRNA, 11 segments each coding for a viral protein

4. Non-eveloped

It has 6 serogroups (A-F)

Group A is the most common in humans

1. Infects intestinal cells and kills them

2. Initial infection most severe

3. Absorptive surface of intestine is reduced

4. Fluid accumulation in lumen = diarrhea

5. Disease is self limiting

6. Dehydration problems

Secretory IgA

Neutralizing IgG

Fecal-oral

(highly contagious)

;

Can survive for hrs on hands and days on surfaces!

1. 1-3 day incubation period

2. May be asymptomatic

3. Mild to severe

4. Death due to dehydration and electrolyte loss

5. Fever, vomitting, watery diarrhea

6. Lasts 3-9 days

Oral Rehydration - glucose, H2O, electrolytes

If severe, IV fluid replacement

1. Good hygiene

2. Chemical disinfections

3. Breast feed newborns

4. Vaccinations*

1. Uncomplicated Rhinotracheitis

2. Respirtatory viral infection followed by bacterial pneumonia

3. Viral pneumonia

1. Higher death in young and old (decline in cellular immunity)

2. Binds to clarithin coated pit--forms a coated vesicle

3. Needs a low pH to cause fusion to endosome and uncoat

4. RNA replication occurs in cytoplasm then to nucleus

1. Ion channel blockers that inhibit the replication of influenza virus by targeting M2 protein

2. Block acidifications of endosomes which inhibits the fusion

3. Since no fusion, release of viral RNA is prevented 

1. Small ~ 30nm

2. Naked icosahedral = Infectious

3. ssRNA

4. (+) sensed

5. Replication occurs in cytoplasm

6. Can go directly into cell and be translated

1. Stable at pH 3 so can survive passage thru stomach

2. Spreads by fecal oral route

3. Multiplies in cytoplasm

4. Produces a large precursor protein that can undergo post tranlational cleavage

5. Cause variety of diseases

Primary = initial spread of virus in the blood from the the first site of infection

Secondary = Primary viremia that now affects  organs such as the skin, brain, muscle, liver, & meninges

1. Adsorption to specific receptors

2. Internalization in vesicles

3. Lowering of the pH in the vesicles

4. Exposure of Hydrophobic grps on the virus

1. Alimentary phase

2. Lymphatic phase

3. Viremic phase

4. Neurological phase

Meningitis (stiffness of neck or back)

Can lead to paralysis

Inactivated Polio Vaccine

Oral Polio Vaccine

Peeps who survived polio show muscular weakness and paralysis many yrs after infection and recovery.

Caused by death of individual nerve terminals in the motor units that remain after the initial polio attack. 

Maybe due to possible deterioration of nerves that are required to function for damanged nerves. (degeneration of motor neurons)

1. Measles

2. Mumps

3. Enterviruses (Polio, Cox B and Cox A7/9)

4. HSV

33 million had it

2 million died from it

Groups=

 M (Major)

 N (Non-O/ Non-M)

O (Outlier)

Clads = A, B, C, D, H, G, J, K

Subtypes = look at figure

1. Sex

2. Inoculation of infected blood/blood products

3. Mother to child

Yes

Transmission can occur before, during or after birth

Sex = 0.01-1.0%

Blood Transfusion = >90%

Mom = 12-50%

Sexual contact.

Likihood after 1st exposure = 0.1-1%, but globaly accounts for 65-80 (73%) % of all cases

1. Reverse transcritpase that converts ssRNA to dsDNA

2. Has integrase that allows it genome to get into host DNA

3. Viral envelope proteins

4. Has a viral core w/proteins (M protein, Capsid, Nucleoprotein)

5. Accessory proteins

Primary = Slight increase in the # of CD8+ T cells  in wk 6, but returns back down by wk 9.

CD4+ T cells decrease

Anti-gp120 dramatically increases from 0.

Clinical = CD8, CD4 and Anti-gp stay fairly the same, hence the latency. This occurs for ~ 6yrs

Symptomatic = Slight decrease in Anti-gp, Decrease in 1/2 # of CD8

Dramatic decline in CD4 in 2 yrs. By year 8 nearly 0 CD4 T cells. This is when AIDs will develop

After 8 yrs

CD4 T cells are nearly 0 at this time.

1. High turnover of HIV and infected CD4 T cell loads

2. Persistant Immune activation

3. Destruction of host immune system

1. Fever

2. Lymphadenopathy (enlarged lympth nodes)

3. Pharyngitis

4. Rash

During the Acute infection

vRNA = 5 x 10^6

IP = 2,500

HIV-PBMC = >30,000

1. Adsorption to specific receptor

2. Penetration

3. Reverse transcriptase

4. vRNA transit

5. Integration into host DNA

6. Transcription

7. Transcript processsing

8. Translation/ Post translational processing

9. Capsid assembly/ budding

10. Capsid processing

1. Antibodies to prevent attachment

2. Fusion Protein inhibitor

3. RT Inhibitors, so cant make viral DNA

4. Integrase inhibitor so cant incorportate viral DNA into host DNA

5. Protease inhibitors so no posst translational processing

6. Zinc finger inhibitors to stop capsid assembly and processing

Highly Active Anti-Retroviral Therapy

Many anti-HIV drugs to treat HIV+ peeps.

Usually includes 1 NS Analog, 1 protease inhibitor and a non-nucleoside RT inhbitor or another NS analog

Gag-Pol precursor

Capsid

Matrix

Nucleoprotein

Protease

RT

Integrase

Env Precursor

Surface Env

Transmembrane

1. Complete history and physical

2. CBC and chemistry profile (include transaminases and lipid)

3. CD4+ T cell count

4. Plasma HIV RNA measurement

1. Maximal and durable suppression of virus load

2. Restoration or preservation of immunologic function

3. Improvement of quality of life

4. Reduction of HIV related morbidity and mortality

To decide whether or not treatment is needed.

If has a/symptomatic AIDs then treat.

 If Asymptomatic HIV then treatment should be offered (CD4 200-350).

If CD4 > 350 w/ RT-PCR > 55K then varies on treatment option. Now have >30% chance of getting AIDs.

If CD4 >350 but RT-PCR <55K then many would defer treatment. 

1. Resistance to drug = 70%

2. Low Drug [M+] at the viral replication site = 25%

3. Progressive decline of the immune system

1. Patient factors such as age, co morbidities, etc

2. No compliance, miss clinical appts

3. Drug side effects and toxicity

4. Pharmacokinetics factors such as metabolism is fast, food/fasting, drug-drug interactions, etc

5. Potency of antiretroviral regimen

NRTIs = 6-12 months

PIs = 2-3 months

NNRTIs = days-weeks

When 1 or more of the following occur:

1. Incomplete virologic response (failure to decrease HIV RNA)

2. Virologic rebound (Re-appearance of viremia after suppression. Shows resistance)

3. Immunologic failure (Persistant decline in CD4 T cell count)

4. Clinical failures (deterioration after 3 mo)

Highest cases were in Sub-Saharan Africa (Accounts for 70% of all cases and about 58% of all women in Africa have it), SE Asia and South America.

In 2003, the global total = 40 million have it and 3 million deaths from it and 5 million new infections.

RT is a high error prone enzyme that causes many mutations thus variations. 

The disease can spread by many different routes.

There are many different Clads and subtypes of HIV, hard to make 1 that fits all.  All have diff. properties/genes

Hep B.

(I'm not too sure, Hep A has 100 deaths a yr from this and Hep D has 35 deaths a yr. But Hep B is 150 deaths a year).

1. Fecal oral route (ingested)

2. Respiratory

(I'm like 90% positive about this)

Can go to the CNS and affect the brain.

Or can cause secondary viremia and affect other organs such as the skin, liver, muscle.

1. 25-50% of people

2. Symptoms occur 15-30 yrs after the original infection

1. Affected by Geography & environment ( with damp areas)

2. Associated w/ soil

3. Produce endospores for reproduction

4. Are usually inhaled

5. Recycle organics

6. Opportunistic

7. Major antibiotic producers

6.

Yeast

Mold

Round/oval

Budding

Ex: Candida

Hyphae

Branching

Longitudinal

1. Thrush

2. Yeast infection

3. Skin and Mucosal infections

Resides inside macrophages and neutrophils.

Acquired by inhalation

Zoophilic

Antrhopophilic

Scalp

Feet

Skin

Groin

Toes

Itching

1. Eukaryotic, unicellular

2. In 2 forms: cysts or trophoziote

3. Classified based on there locomation

4. Fecal-oral route

5. H2O borne also

6. Anaerobic

Infectious = Cyst form

Growing = Trophozoite

1. Severe infections resemble ARDS

2. Causes large pulmonary lesions that become nodules = Histoplasmoma

3. Granuolmatosis and fibrosis that infects lymph nodes

4. If chronic have diseased upper lobes of lung

5. Progressive is usually fatal

6. Can infect choroid

7. African version selectively affects skin, soft tissues and bone not lungs.

Urine

Feces

Sweat

Tears

Breastmilk

Semen

Vaginal

Saliva

1. Wash bedding in very hot water (125 F)

2. Avoid sex w/ infected peeps

3. Dry clean clothing

4. Vacuum living room

5. Dont share clothes/towels/bedding

6. Notify school

Plasmodium

Female Anopheles Mosquitoes

Enters the Exo-Erythrocytic Cycle

It affects the liver

1. Recurrent high fever

2. Chills

3. Headache

4. Anemia

5. Splenomegaly

6. Weakness

Can cause Splenomegaly.

The Red pulp of the spleen is the cemetary for RBC.  The spleen enlarges because it has alot of dead RBCs.

600 million/yr

Use DDT

1. Leishmaniasis

2. Malaria

Fecal-ral

Sexual

1.  (4pairs of flagella) Flagellated protozoan parasite

2. 1 celled organism

3. Lack ER, Mito, GA and Lyso

4. Protective outer shell

5. Anaerobic

6. Aerotolerant

Fecal oral

Water/food borne

Intestinal

Pulmonary

tracheal

100%

25-75%

1. Persistent fevers, may cycle

2. Night sweats

3. Fatigue

4. Weakness

5. Appetite loss

6. Weight loss

1. Selective toxicity (kill organism not man)

2. Reach the site of infection at inhibitory [M+]

3. Penetrate and bind to target (avoid inactivation and extrusion)

1. Cell wall synthesis (we lack this)

2. Protein synthesis (ribosomes)

3. Nucleic acid synthesis

4. Cell membrane function

1. Clycoserine

2. Glycopeptides

3. Bacitracin

4. Beta lactams

1. Aminoglycosides

2. Tetracyclines

3. Chloramphenicol

1. Gentamicin

2. Streptomycin

3. Amikacin

4. Neomycin

Bacteriostatic

Bactericidal

1. Treatment for severe sepsis

2. Needs O2 for entry into cells

3. Fat insoluble = not absored orally

4. Toxic to kidney and inner ear

It has a nitrobenzene nucleus that blocks peptidyl transferase blocking the protein synthesis.

(Bacteriostatic)

1. Trimtethoprim

2. Sulfonamides

Quinolones

DNA gyrase

1. Azoles = no synthesis of ergosterol

2. Polyenes (Amp.B) = binds to sterols and causes leakage of components then causes cell death.

1. Chromosomally mediated resistance= mutant selection

2. Plasmid mediated resistance = spread of ressitance plasmid

3. Plamid mediated resistance on transposon = spread of resistance gene

They can physically and chemically remove the drug.

1. Alter target = lowers affinity for antibacterial

2. Alter the uptake = pump drug out of cell

3. Drug inactivation = enzyemes that kill the antibacterial agent

1. Dont dispense antibiotics w/out Rx

2. Control misuse of antibiotics

3. Antibiotic policies

4. Surveillance of use coupled w/ monitoring emerging patterns of resistance

5. Control use in industry

1. Flagella

2. Adhesins (attaches to stomach lining)

3. Urease enzyme (neutralizes acid so bacteria can grow)

Bacteria can turn sucrose into Glucan (polymer).

Glucan allows the formation of biofilm.

Biofilm covers bacteria and provides anaerobic growing conditions for bacteria.

Fermentation occurs w/ sucrose.

This decreases pH

Decreased ph softens enamel

1. Hep A and B

2. Influenza

3. Measles, Mumps, Rubella (MMR)

4. Polio

5. Rabies

6. Smallpox

7. Varicella-Zoster