B3 Flashcards
List the bacteria and viral agents causing tonsillitis, otitis & sinusitis
Tonsillitis & Pharyngitis : Influenza virus , Rhinovirus , Adenovirus , Streptococcus pyrogens (most common)
Otitis : Influenza virus , parainfluenza virus , Streptococcus pyogenes, mycoplasma pneumonia, Candida albicans
Sinusitis : Rhinovirus , influenza virus, streptococcus pneumoniae, haemophillus influenza
Describe the etio-pathogenesis with emphasis on the mechanism of action of the toxin of Corynebacterium diphtheriae
Diphtheria toxin- primary virulence factor , have 2 fragments - A(active) , B (binding)
B for binds to the host cell receptors and help in the entry of fragment A.
A - gets internalized into the cell
Mechanism of DT
Fragments A is the active fragment , which cause ADP ribosylation of elongation factor ( EF-2) then leads to inhibition of EF-2 then leads to inhibition of translation step of protein synthesis . Cell death
Pathogenesis
A) Bacilli is non-invasive , present & multiply only at local site (pharynx) and secrete the exotoxin which spread via bloodstream to various organs, leads to local(respiratory) and systemic (cutaneous) symptoms
B) Exotoxin causes necrosis of the epithelial cells & liberates serous & fibrinous materials which forms a greyish white pseudo-membrane.
C) The membrane bleeds on being dislodged. Surrounding tissue is inflamed & edematous.
Describe the clinical manifestations and complications of Diphtheria.
Clinical manifestations
A) Faucial diphtheria - DT leads to necrosis of the epithelium and exudate formation.
- leads to formation of mucosal ulcers, lined by a tough leathery greyish white pseudo membrane coat ( inner bank surround by RBC and bacteria)
B) Extension of psedomembrane - it may extend into larynx and bronchial airways, results in fatal airway obstruction leading to asphyxia.
C) Bull neck appearance - characterised by massive tonsillar swelling & neck edema.
Complications
A) Neurological manifestations ( presented with cranial nerve involvement ,peripheral neuropathy, ciliary paralysis)
B) Myocarditis (associated with arrhythmias and dilated cardiomyopathy
List the prophylactic measures for Diphtheria
Vaccination- induce the antitoxin production
Children - gives at 2,3,5 months while booster dose administered at 18 months ( DTaP-IPV-HiB-HepB) and seven years old.
Post exposure prophylaxis
Booster dose of diphtheria vaccine + penicillin G
6 in 1vaccine
Diphtheria , tetanus , pertussis , polio , and Hib
List the defence mechanism of respiratory tract
A)Secretory products - Secretory IgA & nonspecific antibacterial substances in respiratory secretions
B) Tracheobronchial tree - branching architecture traps particles on the airway lining.
C) Mucociliary clearance - cilia and mucous lining of the trachea help in clearing or killing the potential pathogens
D) Alveolar macrophages - ingest and subsequently destroy the pathogens of LRT which gain access into the lungs.
Describe the Pathogenesis of pneumonia caused by Streptococcus pneumoniae , Haemophillus influenza and Klebsiella pneumonia
S.pneumonia-inhalation of encapsulated pneumococci; colonisation of the alveoli triggers an inflammatory response; plasma, blood and inflammatory cells fill the alveoli; pain results from involvement of nerve endings
Klebsiella pneumoniae : Aspiration of colonised mucus droplets from the throat. Destruction of lung tissue and abscess formation common ; infection spreads via blood to others body tissue.
List the preventive strategies against bacterial pneumonia
S.pneumonia : Treatments : antibiotics .Prevention: Polysaccharide vaccine against 23 serotypes; conjugate vaccine against 13 serotypes
K.pneumonia: A combination of antibiotics
List the agents responsible for primary atypical pneumonia
Mycoplasma , Legionella , Chlamydophila
Describe the etiology, Pathogenesis , clinical features & prophylaxis for whooping cough.
Etiology: Gram negative coccobacillus , obligate aerobe , causes whooping cough , encapsulated , non fermenter
Pathogenesis :
1)Bordetella pertussis bacterium enters the airway via droplets
2) It binds to ciliates epithelial cells & multiplies, colonizing the nasopharyx.
3) It produces multiple toxins ( B- attach to cell surface ; A - enter the cells & activate regulation of cAMP then causing increased mucus formation & decrease phagocytic formation ) which damage mucosal cells.
4)PT produces cyclic AMP& disrupt normal intracellular, increases mucus secretion & impairing mucus secretion & impairing immune response initially.
5) Pertussis ( Whooping Cough) Respiratory syndrome consisting of severe fits of paroxysmal coughing & stridor
Clinical manifestations
-3stages
A) Catarrhal phase
- Lasts for 1-2 weeks
-Characterized by common cold like nonspecific symptoms
-Highly infectious stage
- In this stages , both smear and cultures are positive
Paroxysmal phase
- Last for 1-6 weeks
- Less infectious
- Smear and culture may become negative
- sounds like “whooping cough”
Convalescent phase
- Lasts for 1-3 months
- The frequency and severity of coughing gradually decrease
Prophylaxis - vaccine (Dtap -IPV- HiB- HepB vaccine) (6 in 1 vaccine)
At 2,3 ,5 months + booster at 18 months old
State Antigenic Structure of mycobacterium tuberculosis complex
Cell wall ( insoluble antigens) antigens - Lipoarabinomannan(LAM) : facilitates the survival of tubercle bacilli within the macrophages, also used as a target antigen for the TB diagnosis.
Cytoplasmic (soluble) antigens : use in serodiagnosis of TB
List the rapid grower of mycobacteria
M.fortuitum, M. Chelonae
Describe the transmission , Pathogenesis , clinical manifestation & complication of tuberculosis
Transmission : through airborne (transmission of aerosols) , at least 10^4 bacilli/mL in sputum is required for an effective transmission.
**Pathogenesis:
A) Droplet nuclei containing tubercle bacilli from infectious patients are inhaled.
B)Adhesion to macrophages: (LAM) binds to complements receptor leads to internalisation of bacilli.
C) Phagocytosis by macrophages : It is enhanced by complement (C3b) mediated opsonisation of bacilli.
D) Survival inside the macrophages : due to LAM which phagosome-lysosome fusion by inhibiting an increase in intracellular Ca2+ and phosphatidylinositol 3-phosphate.
E) Macrophages rupture and release its bacillary contents which infect other uninflected phagocytes and infection cycle continue.
Clinical manifestations & Complications
Infection by Mycobacterium tuberculosis - non immune host >primary tuberculosis >Ghon focus >
I) Heals by fibrosis > Delayed hypersensitivity > Tuberculin skin +
II) Progressive lung disease (HIV , malnutrition) > Death
III) Severe bacteremia > Miliary tuberculosis > Death
IV) Lymphatic / hematogenous dissemination > Dormant tubercle bacilli in several organs (Latent tuberculosis) > Reactivation in adult life > Extrapulmonary TB
Describe the lab diagnosis and immunoprophylaxis of tuberculosis.
Specimen : PTB : sputum & gastric aspirate ( children )
: EPTB ( depending site involved )
Digestion ( to liquefy the thick pus cell and homogenisation) , Decontamination ( to inhibit normal flora ) & Concentration ( increase yield )
A) Modified Petroff’s method( 4%NaOH) - recommended for LJ culture
B) NALC (N-acetyl- L -cysteine ) + 2%NaOH
C) Direct microscopy by acid fast staining :
-Ziehl-Nielsen( ZN) Technique : “ acid fast bacilli resembling M. tuberculosis are seen by smear microscopy by ZN stain”
D) Fluorescense Staining - Tubercle bacilli appear bright brilliant green/yellow against dark background
E) Culture Method (Gold standard method )
I) Conventional Solid Media ( Lowenstein- Jensen Medium) - Colonies : M. tuberculosis : typical rough , tough , & buff coloured colonies ;
M. Bovis : smooth, moist & white colonies that break up easily when touched
II) Automated Liquid Culture (BACTEC MGIT) - used liquid broth supplemented with enriched growth media and antibiotic mixture.
F)Serology - low sensitivity ( not recommended)
G) Molecular Methods - Automated NAA / RT- PCR - fast , sensitive , detect drug resistance gene.
Immunoprophylaxis Anti tuberculosis drugs for DS- TB( First line Agent) 1) Isoniazid (H) 2) Rifampicin (R) 3) Pyrazinamide ( Z) 4) Ethambutol (E)
Vaccine - Bacillus Calmette- Guerin Vaccine (BCG)
Explain the types of infective endocarditis with examples
A) Acute endocarditis
- Toxic presentation , caused by highly virulent invasive organisms
- Affect normal / progressive destruction in damaged valves
- Most commonly Staphylococcus Aureus
B) Subacute Endocarditis
- Mild toxicity
- Source of infection are periodontal infection ( dental treatment) , urinanry tract infection , GIT infection
- Occurs on damaged valves themselves or at sites where the endothelium is damaged by high pressure jet of blood.
- Most commonly Streptococcus viridans and enterococci
Explain the predisposing factors , clinical features of the infective endocarditis
Predisposing factors :
A) Dental procedure : Root canal treatment , dental extraction
B) Cardiac Conditions : Prosthetic valve implantation ,development of calcified valves
C) Intravenous drug abuse
Clinical features : Nonspecific symptoms - Fever, chills and sweats - Anorexia , murmurs Specific symptoms - Petechial & cutaneous manifestations (Osler’s nodes , Roth spots )
Complications : Embolism , Renal disease , infarction , Congestive heart failure
Explain the Pathogenesis of infective endocarditis.
A)Streptococcus viridans- S. mutans , S.sanguis
- Residents in mouth & URT , and typically producing greening ( alpha lysis) on blood agar.
- Streptococcus sanguis cause subacute bacterial endocarditis in person with pre-existing cardiac lesion.
- Following tooth extraction , they cause transient bacteremia and get implant on damaged or prosthetic valves and form vegetation.
**Strep.mutan - has a polysaccharide coat ( glycocalyx) that allows it to stick to teeth and to damaged heart valves ; it can invade the bloodstream.
- ***B)Endocardial injury and vegetation formation
- Injury by turbulent blood flow
- Injection drug user , direct injection of contaminating debris may damage tricuspid valve surface.
I) Endothelial damage triggers sterile thrombus formation , which occurs deposition of fibrin and platelets .
II) Once sterile thrombus is present , transient bacteremia can seed the thrombus.
III) once bacteria have attached to the endocardium, additional deposition of fibrin and bacterial proliferation leads to mature vegetation formation
List the prophylactic measures against infective endocarditis.
For oral procedure:
Antibiotics : ( Amoxycillin / Ampicillin )
- 30-60 mins before any oral procedure
What types of M protein commonly cause acute rheumatic fever.
Type 5
Explain the Pathogenesis of Acute rheumatic fever
A) Autoimmune theory : Molecular mimicry - antigens of S. pyogens are similar to that of those found on cardiac tissue -> antibodies cross react -> valvular damage
B) Streptococcal superantigens
- M- proteins fragments & pyrogenic exotoxin serves as superantigens -> stimulate activation of T - cells which release cytokines which become auto reactive
- B -lymphocytes also get stimulated producing auto reactive antibodies
C) Cytotoxic theory - streptococcal toxins are directly to cardiac tissue.
State the clinical manifestation and complications of mumps
Clinical manifestation
A) Parotid gland swelling
B) High fever
C) Local pain
Complication
A)Epididymis-orchitis in post pubertal males
B) meningitis , meningoencephalitism
State how mumps, rubella & measles are spread
Via respiratory droplets , enters into upper respiratory tract -> regional lymph nodes to cause viremia
Describe the phases and clinical manifestations of measles
- highly contagious childhood disease
- incubation period -10D
I) prodromal stage
- 4 days
- characterised by fever , Kopliks spot , respiratory symptoms ( cough)
II) eruptive stages
After 4 days of fever , maculopapular rashes appear (first behind the ears then -> face , arm , trunk & legs )
III) post measles stages
- weight loss ,weakness
States some complications which may arise from measles
***A) Giant- cell pneumonia ( Hecht’s pneumonia)
**B) Subacute sclerosis panencephalitis (SSPE)
C) Otitis media & bronchopneumonia due to secondary bacterial infection
Describe postnatal rubella ( clinical manifestations
Rubella that occurs during neonatal age, childhood or adult life.
Clinical manifestations
- generalised maculopapular rashes
- Forchheimer spot : small , red spot on soft palate
- lymphadenopathy
Complication
I) Joint symptoms ( arthritis)
II) thrombocytopenia
III) encephalitis
Describe the congenital rubella syndrome
A) most serious consequence of rubella virus infection
B) rubella virus is highly teratogenic
C) occurs when rubella is transmitted from mother to fetus ( transplacental , airborne droplets)
D) Affects the ear ( deafness) , eyes (cataracts) & heart (patent ductus arteriosus)
Describe the Pathogenesis of influenza
- transmitted via respiratory droplets infection, aerosols suspended in the air .
- neuraminidase degrades mucus to allow access of the virus to respiratory epithelial cells
- Hemagglutinin of influenza virus binds to sialic acid receptors on host cells , initiating infection in the upper respiratory tract , trachea & bronchi.
- virus replicates in the nucleus & exits the host cells via budding
- cell death occurs , leading to sloughing of cells & release of breakdown products into bloodstream.
- systemic symptoms appears ( fever , shivers , sore throat)
- secondary bacterial infection due to decreased immune response can lead to death
Describe the transmission & Pathogenesis of respiratory syncytial virus ( RSV)
- transmission occurs via inoculation of nose or eyes via aerosols or direct contact.
- RSV infects the ciliates epithelial cells of URT & LRT, including type 1 pneumocytes & intraepithelial dendritic cells m
- widespread inflammation occurs w/ monocytes & T-cells infiltration, epithelial necrosis , sub-mucosal edema and mucus -overproduction
- airway obstruction occurs due to sloughing of epithelial cells & accumulation of mucus & inflammatory cells
Describe the clinical manifestation of RSV
URT symptoms / tracheobronchitis
- Coryza
- cough
- sore throat
LRT symptoms
- bronchiolitis : rhinorrhea
- bronchopneumonia
-presence of inclusion bodies -> multinucleated , eosinophilia giant cells — viral envelopes fuses w/ host cells membrane w/ help of viral at proteins
Explain about Vincent’s Angina
- Acute bacteria infection of gingiva caused by spirochetes such as Borrelia Vincentii , fusiform bacilli
- known as Acute necrotizing ulcerative gingivitis , Trench mouth
Explain about Borrelia vincentii
- motile spirochete with 3-8 coils of variable size
- Gram negative
- Normal mouth commensalism give rise to ulcerative gingivostimatitis or oropharyngitis ( Vincent’ angina
- always associated with fusiform bacilli.
What is Leptotrichia bucchalis ( Fusobacterium fusiforme )
Gram stained smear show very large gram negative long , straight spindle -shaped bacilli often with pointed end
- part of oral flora
What is Treponema denticole ( non- pathogenic treponema )
- ten regular spiral
- thin , delicate spirochete with tapering ends , about 10 micrometer long
- actively motile
Explain the Pathogenesis of Vincent angina
A) Starting with a shallow ulcerated area of gingival oral mucosa and interdental papillae
B) Tissue is erythematous and edematous with characteristic grey appearance
C) Without treatment , the gingival may become necrotic.
Initial signs
- Ulceration
- blackening of gums
- bleeding
- exudates
State the specimens , transport and method of anaerobiosis of Vincent angina
Specimens : Tissue bits , necrotic materials , pus , exudates .
Transport : Specimens should be immediately put into RCM broth or other anaerobic transport media and brought to the laboratory as soon as possible
Method of Anaerobiosis :
- Pus and other fluids may be collected in sealed vials with airtight seals gassed out with CO2 transported quickly
- Robertson’s cooked meat medium ( RCM)
- PRAS ( pre-reduced anaerobic sterilised) transport medium is a commercially available transport system. These contain tubes gassed out with nitrogen and fitted tightly with butyl stoppers
Explain the result of lab diagnosis of Vincent Angina ( microscopy , culture)
A) Microscopy : Gram stained smear showing long , straight gram negative bacilli with pointed ends.
OR
Dark ground or phase contrast microscopy for spirochetes ( definitive diagnosis )
B) Culture : for anaerobe Leptotrichia ( Fusobacterium ) :
- Freshly prepared blood agar with neomycin , yeast extract , hemin and vitamin K is adequate for routine diagnostic work,
- Plates are incubated at 37 C in an anaerobic jar with 10% CO2
- GASPAK system provides a convenient method of routine anaerobic culture
Borrelia : may be made by demonstrating spirochetes and fusiform bacilli in stained smears of exudates from the lesions
- Cultivated with difficulty anaerobic all in enriched media
- Fusiform bacilli also grow in the culture and it is very difficult to obtain a pure growth.
Treponema : Laboratory diagnosis consists of demonstration of spirochetes under the microscope and of antibodies in the serum.
Culture - inability to grow most pathogenic treponemes in vitro
