BIOL 220 Airborne Diseases

What is a positive vs. negative pressure room?

Positive: push air out = very little pathogens to enter when door is open

Negative: suck air in = pathogens enter + do not exit in order to contain pathogens (contagious disease with low LD50)

How can Airborne Diseases spread

Indirect contact/Transmission: Transmission of a pathogen/disease through a contaminated non-living object (Fomite)

Contact transmission: Droplet transmission (airborne particles spread less than 1 meter in distance)

Vehicle Transmission: Airborne transmission (airborne particles greater than 1 meter in distance)

What are common predisposing factor for airborne infections?

Weakened immune system: HIV/AIDS, Cancer and chemotherapy, Autoimmune diseases

Age: Elderly (65+), infants and young children (not well-developed adaptive immunity)

Life style: Smoking/Vaping, Alcohol abuse

Environmental conditions: Crowded conditions, Urban areas with high Air pollution, multigenerational family housing - children

What is the major port of entry for airborne diseases?

Respiratory Tract - Involved in breathing & gas exchange

Upper respiratory tract: Filters air before it enters the lungs

• Nose

• Nasal cavity

• Sinus

• Pharynx (throat)

• Larynx (voice box)

Lower respiratory tract: Facilitates gas exchange between Oxygen intake and carbon dioxide release

• Trachea (windpipe)

• Bronchi

• Bronchioles

• Alveoli

What are the general S/Sx for airborne diseases

• Fever + Chills, Fatigue, Headache and body aches

• Coughs (wet/dry), sneezing, running or stuffy nose, sore throat

• Shortness of breath and difficulty breathing

What are the Host Defenses against Airborne Pathogens

• Normal microbiota (Biological barrier + 1st line defense): found in the upper respiratory tract → competitive

exclusion

• Mucus + Nasal hair : Traps dusts, microbes and other particles → prevents antigens from entering the respiratory tract; has IgA

• Lysozyme: Lytic enzymes secreted by epithelial cells in our airways to break down peptidoglycan

• Ciliary escalator: helps clear mucus, dust, pathogens and other particles up and out of the respiratory tract

• Coughing and Sneezing reflex: Helps expel irritants or pathogens from entering the respiratory tract

What is Streptococcus and its different types? How do we use differential media to differentiate the diffferent types?

Streptococcus (Gram-positive Cocci + arranged in chains)

• Streptococcus pneumoniae vs. Streptococcus pyogenes

Use differential media to help identify Streptococcus bacteria + implement the proper treatment

• RBC’s act as a nutrient source on the agar → Hemolysis occurs (RBCs lysed by hemolysins, type I exotoxin)

• Alpha Hemolysis: Partial lysis/destruction of RBC → Green Zone → S. pneumoniae

• Beta Hemolysis: Complete lysis/destruction of RBC → Clear zone/yellow color → S. pyogenes

Streptococcal Pharyngitis: Alternative Name/Type of Infection, S/Sx, and Causative Agent

Alternative Name: “Strep Throat”

• Upper Respiratory tract infection

S/Sx:

• Inflammation of the throat & tonsils

• Throat feels sore and “scratchy” + white patches or streaks of pus

• Red spots on the roof of the mouth

• Fever

Causative Agent: Streptococcus pyogenes:

• Gram-positive cocci arranged in chains; group A streptococci (GAS)

Streptococcal Pharyngitis: Virulence Factor and Diagnosis

Virulence Factor:

• Beta hemolysin: completely lyses RBC’s (clear zone, yellow color)

• Strepto-kinase: dissolves/prevents blood clot formation

• Hyaluronidase: dissolves substances holding connective tissue cells together

• Capsules + M proteins: allow for adherence and escape of phagocytosis

Diagnosis:

• Serological testing of blood or other body fluids (rapid antigen detection tests) → Beta Hemolysis on blood agar

Streptococcal Pharyngitis: Prevention and Treatment

Prevention:

• Practicing good respiratory hygiene (Ex: cover mouth + nose via masks)

• Avoid sharing cups & utensils

Treatment: with Antibiotics (Penicillin or amoxicillin)

Scarlet Fever: Alternative Name/Type of Infection, S/Sx, and Causative Agent

Alternative Name: Scarlatina

• Upper respiratory tract infection

S/Sx: due to toxemia

• Sore throat & high fever → Type I Exotoxin: SuperAntigen

• Pastia’s Lines: red/purple lines that appear in skin folds → caused by erythrogenic toxins

• Flat red/pink rash that is Sandpaper-like on the chest and throughout the body → caused by the erythrogenic toxin that damages the blood capillaries under the skin

• Strawberry tongue: Red & bumpy tongue covered with a white coating

Causative Agent: Streptococcus pyogenes

Scarlet Fever: Virulence Factor and Diagnosis

Virulence Factor:

• Beta hemolysin, Streptokinase, Hyaluronidase, Capsules + M proteins

• Erythrogenic toxin (also known as streptococcal pyrogenic exotoxins) made via lysogenic cycle: Toxin producing gene is on a bacteriophage → Viral infection of S. pyogenes leads to a prophage (hybrid genetic material) → S. pyogenes will now produce erythrogenic toxins

Diagnosis:

• Serological tests (Rapid antigen detection tests) + Beta hemolysis on blood agar

Scarlet Fever: Prevention and Treatment? What age group is this disease most common in?

Prevention: Practicing good respiratory hygiene

Treatment: Antibiotics (Penicillin & amoxicillin)

Most common in children (ages 5-15)

• Most common cause of death in children in the 1800

• Rare disease in today’s time

Rheumatic Fever: Alternative Name/Type of Infection and Causative Agent

Alternative Name/Type of Infection:

• Autoimmune Reaction Mechanism: S. pyogenes has M proteins and other antigens that mimic human tissues

in the heart, joints, and brain → immune system makes antibodies to fight the bacteria but the antibodies

mistakenly attack the body’s own tissues → inflammation

• Upper respiratory tract infection, on list of national notifiable diseases

Causative agent: Corynebacterium diphtheriae

• Gram Positive Bacilli

• Pleomorphic: Can exist in a variety of shapes like clubbed shaped

Rheumatic Fever: Virulence Factor and Treatment of Non-toxigenic strain

Non-toxigenic strain

• No exotoxin production

• Less severe S/Sx compared to toxigenic strain

• Mild sore throat, potential ear infection, and skin infections

• Chronic non-healing sores/ulcers on the skin

• Treatment with antibiotics + diphtheria antitoxin (DAT) is not helpful

Rheumatic Fever: Virulence Factor and Treatment of Toxigenic strain

Diphtheria strain: powerful exotoxin, lead to toxemia (produced via lysogeny by a bacteriophage)

• Causes heart and kidney damage → can lead to myocarditis and heart failure

• Nerve damage and partial paralysis

• Psuedomembrane: Thick & gray coating of dead tissue on pallet, nose and throat

• Difficulty breathing and swallowing

• Death (especially when untreated)

• Treatment with antibiotics & diphtheria antitoxin

Rheumatic Fever: Diagnosis and Prevention

Diagnosis:

• throat swab → culture swab

Prevention: Diphtheria vaccine (Based on age group)

1. DtaP (series of 5 shots for young children)

• Diphtheria, Tetanus, acellular Pertussis

2. TDaP (for pre-teens, 11-12 yrs)

• Tetanus, Diphtheria, acellular Pertussis

3. Td (for adults)

• Tetanus & Diphtheria toxoid (bacterial toxin that has been inactivated to trigger an immune response)

Pertussis: Alternative Name/Type of Infection, S/Sx, and Causative Agent

Alterative Name/Type of Infection

• Whooping Cough”

• Highly contagious bacterial infection + targets lower respiratory tract

Causative agent: Bordetella pertussis

• Gram-negative aerobic coccobacillus

S/Sx:

• 5–10 day incubation period; no symptoms

• Initially mild S/Sx: Cold like symptoms- Runny nose, mild cough, Fever, and sneezing = infectious without • showing severe coughing

• Progress to more severe S/Sx: Uncontrollable violet coughing; can last for weeks-months (also called

the 100-day cough)

Pertussis: Virulence Factor and Diagnosis

Virulence factors:

• Capsule production for the attachment to ciliated cells in the trachea

• Tracheal cytotoxin: damages ciliated cells and shuts down the ciliary escalator

Diagnosis: Culturing of throat mucus sample

Pertussis: Prevention and Treatment? How is it dangerous to babies?

Prevention: Pertussis Vaccine

1. DTaP (Diphtheria, Tetanus, acellular Pertussis)

2. TDaP (Tetanus, Diphtheria, acellular Pertussis)

Treatment: Antibiotics (Penicillin or Amoxicillin) + Supportive care (Rest + Fluids)

Dangerous in babies because of their tiny airways → respiratory complications, may get clogged by inflammation

Pneumonias: Alternative Name/Type of Infection and the two types of Pneumonias

Alternative Name/Type of Infection:

• Lower respiratory infection → inflammation + fluid build up in one or both lungs

2 Types of Pneumonias:

1. Typical: Caused by Bacteria (S. pneumoniae)

2. Atypical: Caused by other microorganisms that are Viral or Fungal

Typical Pneumonia: Alternative Name/Type of Infection, S/Sx, and Causative Agent

Alternative Name/Type of Infection:

• Pneumococcal Pneumonia

• Lower respiratory tract infection

Causative Agent: Streptococcus pneumoniae

• Gram-positive bacterium, Encapsulated diplococci + Very large capsules

• ~ 90 different serovars/strains

S/Sx:

• Acute

• Chest Pain, Fever, Chills, fatigue

• Fluid accumulation in the lungs (specifically at the alveoli level) → interfere with gas exchange

• RED FLAGS: Labored/rapid breathing + bluish lips, face or fingers + coughing up blood/mucus

Typical Pneumonia: Virulence Factor and Diagnosis

Virulence Factors:

• Production of Large capsules

• Alpha hemolysin – partially lyses Red Blood Cells (green zone)

Diagnosis:

• Blood tests, Alpha hemolysis on blood agar, presence of capsular antigen in patient’s urine

Typical Pneumonia: Prevention and Treatment

Prevention:

• pneumococcal conjugate vaccine PCV13/Prevnar 13

• Protects against 13 serovars/strains based on capsule structure

• Age is a predisposing factor

Treatment: Antibiotics (Penicillin/Amoxicillin)

Atypical Pneumonia: Causative Agents

Caused by non-bacterial Microbes/Biological Agents:

1. Influenza virus & Sar-CoV-2 → Viral Pneumonia

2. Pneumocystis jirovecii → Fungal Pneumonia (Typically seen in immunocompromised Hosts like HIV/AIDs patients)

Tuberculosis: Alternative Name/Type of Infection, S/Sx, and Causative Agent

Alternative Name/Type of Infection:

• Lower respiratory tract infection

• Leading cause of death from infectious diseases worldwide

• 1/3 of the world’s population has latent TB (Infected but inactive) = No symptoms, not contagious

Caused by Mycobacterium tuberculosis

• Acid-fast bacterium, bacilli, obligate aerobe

• High lipid content in cell walls; resists traditional staining methods

• Fungus-like growth

S/Sx/Chronic Symptoms from a ruptured tubercle:

• Persistent low grade fever, night sweats, weight loss, weakness

• Bloody cough – means alveolar damage

• In Miliary Tuberculosis: Bacterial spread from the primary infection site (alveolar of the lungs) to other areas of the lungs, liver, nervous system and even bone

• Tuberculosis encephalitis

• Tuberculous hepatitis

Tuberculosis: Virulence Factor and Diagnosis

Virulence Factor:

• Mycolic Acid (waxy lipid) in the cell wall

• Allows bacteria to escape phagocytosis and multiply in macrophages

• Resists lysosomal enzymes + drying out

Diagnosis:

(Step 1)

• Mantoux Test (Tuberculin skin tests)

• Subdermal injection of Tuberculin proteins → check for induration (raised bump or hardness) 48-72 hours later (Delayed immune reaction)

• T cells react to Tuberculin protein

• Positive reaction indicates current or previous infection

(Step 2)

• Patient X-ray/CT Scan → Look for calcified tubercule (white spots indicate tubercle formation)

• Positive chest x-ray means a current or previous infection

(Step 3)

• Acid fast Stain: Collect sputum (fluid at lung base) from the patient → Culture and isolate bacterial colonies → Run an acid-fast staining technique (Mycobacterium stains pink vs. Non-Mycobacterium stains blue)

Tuberculosis: Treatment

• Minimum of 6 months of multi drug therapy due to slow growth + dormancy

• Initial treatment: Multiple drug cocktail

• First-line drugs: most effective and least toxic treatments

• Second-line drugs: used when first line drug treatments are not effective

• Multi-drug-resistant (MDR) strains: resistant to first-line drugs

• Extensively drug-resistant (XDR) strains: resistant to second-line drugs

What is the Pathogenesis of Tuberculosis

1. Inhaled bacteria is phagocytized by alveolar macrophages → Mycolic Acid allows the bacteria to survive and multiply inside the macrophages = causes an inflammatory response

2. More macrophages are recruited → surround and isolate the bacterial infection inside a tubercle/granuloma (aggregation of activated macrophages trapping the bacteria inside)

2 possibilities after tubercle formation = Latent TB vs Miliary TB

Latent TB

• Bacteria stop growing in the tubercle lesion and the disease process stops for now → Causes the bacterial infection to remain dormant

• Tubercule heals and calcifies (Ranke complexes) → Can get reactivated if patient has a weakened immune system

Miliary TB

• Bacteria grow/multiply outside of macrophages

• Tubercle gets broken down → releasing the bacteria into the lungs and cardiovascular system → Leads to a systemic infection