Diseases of the Respiratory Tract Flashcards
Streptococcus pyogenes
[Bacterial disease of the upper respiratory system]
Group A strep
Gram positive cocci, chains, beta-hemolytic, ~80 serovars/strains based on differing M PROTEINS
Virulence factors: M proteins degrade C3b (bacteria cannot be opsonized), hyaluronic acid capsule (similar to human hyaluronic acid), protein G inhibits antibody functions, C5a peptidase
Different strains may or may not have differing exotoxins
Strep sore throat (pharyngitis)
Symptoms: local inflammation and fever, pharyngitis, tonsillitis, red spots with pus
Spread by respiratory droplets
Post-streoptococcal sequelae
Follows acute infections cause by Streptococcus pyogenes
Sequelae begins 1-3 weeks after acute illness due to the production of antibodies to the M proteins
Acute Rheumatic Fever- leading cause of heart disease in young in third world countries
Recurrent infections damage hear valves from cross reactive (molecular mimicry) and create antibodies to M proteins that will bind to our mitral valve proteins, but dependent on MHC identity/M protein
Antibodies binding to tissues- TYPE II hypersensitivity
Symptoms: fever, joint pain, rash, uncontrollable body movement, carditis
Acute Glomerulonephritis- due to small immune complexes developing to strep antigens after clearing infection
Antigen/antibody complexes form- Type III hypersensitivity
Signs and symptoms: fever, fluid retention, high BP, blood and protein in urine
Diphtheria
[Bacterial disease of the upper respiratory system]
Causative agent: Corynebacterium diphtheriae- gram-positive rod, aerobic, nonmotile
Spread by respiratory droplets
Infection isn’t the problem, it is the toxin the bacteria produces (toxemia)
Bacteria that have colonized respiratory tract produce highly virulent diphtheria toxin- A-B toxin is absorbed by the blood stream in inactive form. Toxin is only activated after being taken into cell. Bacteria transduce the gene for the toxin via lysogenic conversion (must have the gene to be pathogenic).
Signs and symptoms: sore throat, fever, and malaise. Toxin causes both local and systemic pathology.
Formation of pseudomembrane in back of throat in response to infection/toxin. Tough grayish membrane is composed of fibrin, dead tissue, and bacteria cells. –>
Toxin is absorbed and disseminated through body and targets susceptible tissues of the body (where the B portion binds. Stops protein synthesis. Degenerative changes in these tissues, which include heart, muscle, peripheral nerves, adrenals, kidneys, liver and spleen.
Antitoxin immunity is essential due to virulence of toxin. Antibiotics do not neutralize toxin.
A component of the TDaP/DTap vaccine
Diphtheria toxoid first successful use of modified toxin as vaccine. Induces blocking antibodies which prevents toxin binding to target tissues.
The common cold
[Viral infection of the upper respiratory system]
Predominately caused by rhinovirus (100+ strains) and coronaviruses
Both are RNA viruses that can mutate (antigenic drift)
Signs and symptoms: sneezing, watery eyes, increased nasal secretions/mucous, congestion, usually no fever
Incubation period: 1-2 days. ID50 of 1
Loss of cillary action and cells
No production of lasting immunity following infection because organism mutates. No antibiotics.
Adenoviral pharyngitis
[Viral infection of the upper respiratory system]
Caused by adenovirus (50 types), DNA virus
Signs and symptoms: fever, sore throat, swollen lymph nodes, pus on tonsils, sometimes conjunctivitis of pneumonia
Self limiting, symptoms may last as long as 3 weeks and can progress into pneumonia
Pneumococcal Pneumonia
[Bacterial infection of the lower respiratory system]
Streptococcus pneumonia- gram positive, diplococcus with capsule (5-25% of healthy persons are carriers and virulence is based on carrier resistance)
Over 90 strains based on antibodies to capsule. Capsule is virulence mechanism.
Is the cause of over 60-80% of bacterial pneumonia.
Impairment of cilia is major factor in getting pneumonia
Seeing increasing antibiotic resistance
Capsular and conjugated vaccine developed from the capsules of 23 of the most common strains
Klesbiella Pneumonia
[Bacterial infection of the lower respiratory system]
Causative agent: Klebsiella pneumonia- gram negative rod
Capsule and endotoxin are virulence factors
Respiratory spread, can be normal flora
Many strains are completely resistant to antibiotics (KPC- Klesbiella pneumoniae carbapenamase). The majority of resistance factors are spread via transposons.
Infection entering the blood stream release endotoxin. Causing endotoxic shock, tissue damage, and death
Mycoplasmal Pneumonia
[Bacterial infection of the lower respiratory system]
Mycoplasma pneumoniae: very small, no cell wall, no capsule
Long incubation period (2-3 weeks), very slow growing.
Most common in persons aged 5 to 35 years
Causes primary atypical pneumonia/walking pneumonia. Low-grade fever, cough and headache. Symptoms can last for 3 weeks or more.
Spread may involve close contacts or closed populations in schools, the military, and families
Because mycoplasmas do not have a cell wall, they do not response to antibiotics that interfere with cell wall structure (Beta-lactam antibiotics)
No vaccine. Recurrent infections common.
Pertussis (Whooping cough)
[Bacterial infection of the lower respiratory system]
Bordetella pertussis- small gram negative aerobic rod
Virulence is due to capsula, fimbriae, and production of 2 toxins
Filamentous hemagglutinin- pilus that allows for attachment to cilia
Pertussis toxin also aids in bacterial binding to epithelial cells and causes mucous output, decrease ability of phagocytes, NK cells (binding by B subunit aids in colonization. A fragment is cleaved and enters the cell upon attachment)
Tracheal cytotoxin (breakdown component from Bordetella’s peptidoglycan) causes the death of the ciliated epithelial cells as well as the secretion of IL-1
Cattarhal Stage: colonization of the ciliated epithelium (the nasopharynx, trachea, bronchi, and bronchioles). disease with fever, malaise and coughing, which increases in intensity over 10 day period
Toxins cause death of ciliated epithelial cells, and build up of mucous
Bacteria can be cultured from injected tissues at this time and antibiotics can reduce severity of disease
Paroxysmal Stage: loss of ciliated epithelium cause mucous to accumulate and the infected person has prolonged and paroxysmal coughing that ends in a characteristic inspiratory gap (whoop)
Bacteria no longer present
Stage two may last as long as 6 weeks
Brain damage from severity of coughing that occurs in infants. Adults have milder form of disease resembling bronchitis
Component of the TDaP/DTaP vaccine. After childhood, need booster every 10 years. Increasing incidence of disease. Adult onset can appear to be chest cold/common cold.
Tuberculosis
[Bacterial infection of the lower respiratory system]
Mycobaterium tuberculosos- obligate aerobic bacilli, very slow generation time. unusual cell wall, waxy lipids, acid fast.
Is not an obligate intracellular bacterium, but it can reproduce and hide out in macrophages
Stage 1: Primary Infection
Breathe in organisms from respiratory droplet –> Bacteria are taken up and multiply in macrophages, chemotaxic response calls other phagocytes, forms tubercle/granuloma primarily in lung tissue, but also can spread to lymph nodes, other body tissues –> Caseous center is formed, may be calcified. Bacteria don’t grow, but may remain dormant/viable for years
In 9/10 individuals the immune system keeps infection controlled. Infection does not equal disease - LATENT TB INFECTION (Type IV hypersensitivity)
Stage 2: Active TB disease
Only 10% infected go on to this stage
Aging, stress, malnutrition, and HIV can be factors that allow disease to progress
Liquefaction occurs and caseous center enlarges and forms air-filled tubercle cavity, where bacteria can reproduce outside macrophages
Tubercle ruptures, releases bacilli into bronchiole/system
Cough results in aerosol of respiratory droplets containing organisms INFECTIOUS
Chronic infections often results in gradual spread of lesions in lungs
TB skin test- delayed type hypersensitivity, cell mediated response
Antibiotic therapy not always effective. Require at least 2 antibiotics due to slowness of reproduction allowing organism to become resistant. Therapy lasts months. DOTS therapy very effective. Antibiotic resistant TB developing.
Influenza
[Viral infections of the lower respiratory tract]
Influenza virus- segmented RNA virus, have hemagglutinin spikes (H)-binding, NEuraminidase spikes (N)- release on viral envelope
Spread by respiratory droplets
Drift- small change in hemagglutinin due to small mutation rate
Shift- abrupt major change in hemagglutinin from acquiring an RNA segment from another species of virus
Signs and Symptoms: headache, muscle aches, fever, reach peak in 6-12 hours, dry cough worsens over a few days, lingering hacking cough, fatigue, and generalized weakness for days or weeks
Infection kill ciliated epithelial cells
Avion/Bird flue- not spread person to person, much come into contact with infected birds
Treatment: IgA best prevention, try to induce a protective response prior to getting infection - creation of annual vaccine
Coccidioidomycosis (Valley Fever)
[Fungal infections of the respiratory tract]
Coccidioides immitis- dimorphic fungi, found primarily in desert of Western Hemisphere (mimcs TB)
Spread by arthroconidiaa which are inhaled: these develop into thick walled spherules containing fungal endospores, when they rupture, they spread and cause new spherules, inflammatory response to fungal infection
Fever, cough, chest pain
Histoplasmosis
[Fungal infections of the respiratory tract]
Histoplasma capsulatum- dimorphic fungi
Found in Mississippi flyway
Spread by bird/bat feces
Symptoms are more mild than Coccidiodies
Predominantly a disease of immunocompromised and spelunkers
Inhale endospore, change into yeast form–> These multiply in macrophages and cause granulomas
