Smallpox Pandemic ( orthopox virus)

1. The Rash

1.1. Virus localizes in small dermal blood vessels.

1.2. Epidermal cells are infected, producing skins lesions.

1.3. Dilation of capillaries in the dermis layer.

1.4. Inflammatory response develops in the dermis.

1.5. The cell swollens, cell membrane ruptures and vesicles are formed.

1.6. When the healing process starts, scabs are formed in the place of pustules.

1.7. During healing, dermis fills with granulation tissues that shrink.

1.8. Leaves localized facil pockmarks

1.9. The face has the largest amount of skin affections.

1.10. Can lead to extensive necrosis

2. Lesions of the Mucous Membranes

2.1. Pharynx, uvula, larynx, tongue and upper part of trachea and esophagus are the places where mucus membranes are affected with enanthem lesions.

2.2. There is a severe inflammation that may produce ulcers.

2.3. Extensive necrosis also appears.

3. Clinical Features

3.1. High fever

3.2. The rash

3.3. Skin lessions

3.4. Affections to mucus membranes

3.5. Weakness

3.6. Bleeding

3.7. Delirium

3.8. Delirium

3.9. Decay

3.10. Diarrhea

3.11. Fatigue

3.12. Widespred pain

4. Entry and Infection

4.1. Secretions from mouse and nose are the main source for human-to-human transmission

4.2. Patients are most infectious during the 1st week of rash.

4.3. Enters through respiratory track as the variola virus

4.4. Scabs form after rash dies and are made of cellular debris and interferon.

4.5. Transmission to others is through coughing out virions

5. How it attacks the body

5.1. Virus first expands locally trough the lymphatic system

5.2. Passes to blood vessels and locates in tiny capillaries of skin and mucuse of mouth and pharynx.

5.3. Then it expands to the skin without affecting vital organs.

5.4. Fever and lessions in the skin appear at the end of the incubation period.

5.5. The rush appears and blisters start to form

5.6. Blisters get full of pus forming pustules and expand joining with closer ones

5.7. Scabs form and under the scabs there are pustules that leave permanent scars on the skin.

6. Complications

6.1. Disseminated intravascular coagulation

6.2. Hypotension

6.3. Encephalitis

6.4. Cardiovascular collapse

6.5. Endothelial cells in the liver swollen and may lead to necrosis.

6.6. Liver becomes heavier

7. Immune Response

7.1. Macrophages and dendritic cells present antigens to t-cells

7.2. B-cells produce immunoglobulin with the aid of helper t-cells.

7.3. When the antibody fits the antigen, b-cell clonning starts.

7.4. B-cells specialize in antibody secreting plasma cells and long-living memory cells

7.5. T- cells develop antigen-specific receptors

7.6. T-cell responds with clonal expansion and also produce cytokines such as gammainterferon.

7.7. T-cells divide and specialize in helper t-cells, regulatory t-cells, cytotoxic,and memory t-cells.

7.8. Cytotoxic t cells that generate cytokine destroy viral proteins and attract other inflammatory cells to the infected area.

8. Bibliography:(Mayo Foundation for Medical Education and Research, 1998-2020) (National Academy of Sciences, 1999)