Upper Respiratory Tract Infection Flashcards
What is rhinitis (common cold)? What is the pathology?
Most common infections of the nasopharynx are viral
> Many types - rhinoviruses and coronaviruses >50 %
- Viral surface molecules bind to host cells, cilia or microvilli and resist removal by mucus flow
- Spread locally on mucosal surface
- Symptoms due to damage to epithelial surface and release of inflammatory molecules
- Transmission by sneezing (aerosols) and contaminated hands
Pathology: infection, viruses adsorbed, virus replicates, virus shedding occurs, host defences are activated (phagocytes), low grade overgrowth of bacterial commensals –> fluid becomes purulent, recovery (antibody production)
Name the viruses and bacteria that can cause acute pharyngitis and tonsilitis - sore throat
Most sore throats are caused by viruses
- Epstein-Barr viruses = occurs in 70-90 % of glandular fever patients
Bacteria
- Streptoccocus pyogenes = causes 10-20 % of acute pharyngitis; sudden onset; mostly in 5-10 year old children
- Diphtheria = Pharyngitis often mid, but toxic illness can be severe
- Influenzae = Epiglottis
What is the epstein-barr virus (EBV)? Describe its infection and clinical features, regional epidemioloigical disease variation; infection mononucleosis(glandular fever)
> Glandular fever/mono/kissing disease
EBV is spread by saliva
EBV is widespread – one of the most common viruses – infects nearly everyone •
- Causes different diseases in different populations
- Due to genetic predisposition or environmental co-factors In some populations it is oncogenic •
- Equatorial Africa: EBV causes Burkitt’s Lymphoma due to a genetic rearrangement in B cells, rare elsewhere in the world
- South China, Alaska, Tunisia and East Africa –> EBV causes nasopharyngeal cancer
- Elsewhere – Infectious mononucleosis (glandular fever) Also associated with neurological and hematological diseases
- Most EBV infections are asymptomatic
> EBV is a well adapted parasite
>Some develop glandular fever after 1-2 months
- Symptoms: fatigue, headcache, fever, swelling of lmyph nodes, sore throat
- Sometimes assoicated with chronic fatigue like syndrome
What is streptococcus pyogenes? Discuss its structural and virulent features, clincial features and characteristic haemolysis (destruction of blood cells)
- Gram-positive cocci
- Most common bacterial cause of sore throat (step throat)
- Bacteria attach to muscosal epithelium and cause damage by toxin production and local invasion
- Can be readily treated with penicillin but can occasionally have significant complications
- Complications
>Scarlet fever - some strains produce a toxin that spreads in the body producing a characteristic rash on the tongue and skin –> could indicate septicaemia
>Rheumatic fever- due to cross reactivity between antibodies against bacteria with self antigens (can lead to heart damage)
- 3 types of heamolysis determined on blood agar plates:
> Alpha haemolysis: incomplete destruction of RBC, greenish halo around bacterial growth
> Beta haemolysis: complete destruction of RBC, clear area around bacterial growth –> characteristic features of S.pyogene (group a)
> Gamma haemolysis: no destruction of RBC around baterial growth
What is diphtheria? Discuss its clinical features, properties of C.diphtheriae, pathogenesis and toxin mechanism
Causative organism –> Corynebacteria diphtheriae (not all strains can cause disease, only toxin producing stains) –> appear as gray colonies on blood agar
Clinical features
- Exotoxin causes damage to mucus membranes of respiratory tract
- Pharyngeal diphtheria causes acute respiratory obstruction
Epidemiology
- Very uncommon due to vaccination
Treatments and vaccines
- Treated with antitoxin and antibotics
- Toxoid accine –> combined with tetanus and pertusiss
Diphteria Pathogenesis: Toxin gene transfer
- The diphtheria toxin is carried by a bacteriophage
- Only strains of C. diphtheriae infected by a bacteriophage carrying the toxin producing gene can cause disease
- This is an example of specialised transduction
- Lysogenic conversion of C. diphtheriae following bacteriophage infection results in formation of a prophage including the toxin gene
Diphtheria Toxin Mechanism:
Diphttheria toxin inhbits protein sysnthesis resulting in cell death
- Consists of two sub-units A and B
- Subunit B binds to receptors on host cell surface
- Subunit A is the toxic segment and inhibits protein synthesis by inactivating a key protein involved in protein synthesis by the ribosome –> does this by covalently adding an ADP-ribose molecule to the EF2 protein –> common mechanism used by many bacterial exotoxins to inactivate proteins
- A single subunit A molecule is lethal to a cell within hours
Diphtheria clinical features
- Toxin acts on mucous membranes of the respiratory tract (destroys epithelium –> triggering an inflammtory response )
- Inflammtory exudate forms a greyish/green membrane in upper respiratory tract called a pseudomembrane –> causes acute severe respiratory obstruction
- Physical removal of the pseudomembrane results in damage to the underlying tissue
- Swollen neck due to enlarged lymph nodes and edema (bulll neck)
What is cytomegalovirus? Discuss its infection and clincial features
CMV called Human Herpes Virus 5
- Virus structure: dsDNA , isocahedral, enveloped
- Transmitted in bodily fluids, saliva, blood, urine,breast milk
- Multi-nucleated cells
Tissue tropism:
- Epithelial mucosa cells
- Monocytes: can remain latent for many years
- Common infection
Cytomegalovirus: Clinical findings
- Infection is asymptomatic in children and mild in adults
- Can cause a Glandular fever-like syndrome in some cases
- CMV becomes latent after primary infection – rarely reactivates in healthy individuals – only immunosuppressed
Congenital CMV –> vertical transmission: in utero, birthing, nursing with breast milk
>May not appear for 2 years e.g. hearing loss
CMV and AIDS (can cause serious disease in the immunosuppressed)
What is mumps? Describe pathogenesis, clincial features and complications
caused by Mumps rubulavirus
Family- Paramyxoviridae
ssRNA, enveloped
Pathogenesis
- Replication in nasopharynx and regional lymp nodes
- Viruses in blood 12-5 days after exposure with spread to tissues
- Mulltiple tissues infected during viraemia (viruses in blood)
- Mumps can be prevented by vaccination –> measles, mumps, rubella vaccine (MMR)
Clincal features
- Mumps incubation period is 14-18 days
- Early symptoms: pain in muscle group, malaise, headache, low-grade fever
- Classical symptoms of parotid gland swelling in 60-70%
- Up to 20% of infections asymptomatic
Complications
- Meningitis occurs in approximately 10% of cases
- Permanent neurologic sequelae are rare
- Mumps encephalitis (1–2 per 10 000 cases) –> Mortality around 1.0%.
- Permanent deafness about 1/20 000 infections
- Orchitis (testicular inflammation) 15-30% of clinical mumps cases in post-pubertal males, rarely causes infertility
What is H. influenzae? Describe its microbe features and pathogenesis
Gram-negative coccobacillus –> normal URT flora
- Capsular (typeable) and non-capsular strains (non-typeable)
- Six encapsulated serotypes based on distinct capsular polysaccharides (a-f)
- H. influenzae type b (Hib) is by far the most common serious disease causing strain
- Other strains can cause opportunisitc infections especially in the respiratory tract
Pathogenesis
- Type B polysaccharide capsule is the major virulence factor
>Encapsulated organisms can penetrate the epithelium of the nasopharynx and invade the blood
>Capsule gives resistance to phagocytosis and complement-mediated lys
- Hib does not produce texotoxins
- Hib can cause local respiratory infections and also systemic disease
- Meningitis is most common Hib disease – see later lecture
- Epiglotittis - inflammation of the windpipe – obstructive
- Life threatening condition
