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
State the therapy for patients who had Vincent Angina
Leptotrichia -Penicillin
Borrelia - Penicillin
Treponema - Benzylpenicillins
State the condition and the most common affected site of Herpes Labialis
Condition : Herpes labialis
A) Painful vesicles near lips
B) Recurrent in nature
C) Vesicles may ulcerate and become secondarily infected.
Most common affected site - Buccal mucosa
Explain the properties of Herpes simplex virus
2 types
A) HSV type 1 ( human Herpes virus type 1 or HHV type 1)
- is transmitted by direct contact or droplets spread from cases or carries
B) HSV type 2 ( HHV type 2 )
- transmitted venereally
Explain the Pathogenesis of Herpes Viruses
At the site- The virus enters through defects in the skin or mucous membranes and multiplies locally, with cell-to-cell spread
Nerve fibers- The virus enters cutaneous nerve fibers and is transported intra-axonally to the where it replicates
Centrifugal migration of the virus- take place from the ganglia to the skin and mucosa to cause cutaneous and mucosal lesions
Latency- remains latent in the trigeminal ganglia (HSV ganglia type 1) and sacral (HSV type 2) nerves
reactivated periodically in some individuals causing recurrent oral and genital lesions to the skin and mucosa to cause cutaneous and mucosal lesions
Explain about the lab diagnosis of Herpes Virus ( microscopy,culture , serology , PCR )
Microscopy:
The Tzanck smear ( Multinucleated giant cell with faceted nuclei and homogenously stained “ ground glass” chromatin )
- Rapid , sensitive and inexpensive diagnostic method
- Specimen - smears are prepared from the lesions , preferably from the base of vesicles
- Stained with 1% aqueous solution of toluidine blue for 15 seconds .
Culture :
- Human diploid fibroblasts are preferred
- Virus produced cytoplasmic changes , well defined foci with heaped up round cells and syncytial or giant cell formation
Serology : useful in the diagnosis of primary infection
-demonstrated by ELISA , neutralisation or complement fixation tests
PCR : Detection of viral DNA and antigens
State chemotherapy of the Herpes Viruses
- Valaciclovir and famciclovir are more effective oral agents
- Acyclovir and Vidarabine provide effective management in case of serious and deep infections
Explain the life cycle of Cytomegalovirus (CMV )
1) Viruses attach to specific cell surface receptor via its glycoprotein surface antigens.
2) Replication of CMV DNA and morphogenetic of the virion capsid take place in nucleus
3) Following maturation of the capsid, newly synthesised viral DNA is cleaved by an enzyme that results in packaging of linear genomic DNA.
4) Subsequently, viral DNA containing capsids acquire an inner layer of tegument proteins during their egress from the nucleus.
5) This is the transported along the cytoskeleton until the particle is enveloped.
6) After this , the virus is released from the cell
Explain the transmission of CMV
- person to person
- Spread through placenta , blood transfusion , organ transplantation, breast milk , Sexual transmission.
- Congenital from a mother with acute infection during pregnancy is a significant of neurological abnormalities and deafness
-Individuals at an increased risk for CMV infection :
A) who works in daycare centre
B) who undergoes blood transfusion
C)who have multiple sex partners
D) recipient of CMV mismatched organ or bone marrow transplants
Explain the pathophysiology of CMV
-Lytic virus that cause cytopathic effect
- enlarged cell with viral intranuclear basophillic inclusion bodies with an “ owl eye” appearance
-immunomodulatory virus
- Largest number of genes dedicated to evading innate and adaptive immunity in the host
— CD4+ and CD 8 + lymphocytes play an important in immune protection after primary infection or reactivation of latent disease
- Patients deficient in cell mediated immunity are at greatest risk for CMV disease
Explain the lab diagnosis & treatment of CMV
A) Serology : positive IgM titer
B) Antigen testing : Detection of CMV pp65 antigen on leukocytes
C) Salivary gland biopsy specimens :
-Intracellular inclusions surrounded by clear halo
- *** Histopathological diagnosis is gold standard for diagnosis
D) Quantitive PCR assays
E) Shell vial assay ( Viral culture )
List the predisposing factor for Candidiasis
- patients on corticosteroids or cytotoxic drugs.
- Prolonged antibiotics usage
- HIV patients
- Xerostomia
- Diabetes Mellitus
- Pregnancy
List the Pathogenesis of Candidiasis
A) When normal host immunity is disturbed , the organism may overgrow on the oral mucosa.
B) It leads to desquamation of epithelial cell and accumulation of keratin , bacteria and necrotic tissue.
C) This debris form a pseudo-membrane , which adheres closely to the mucosa.
D) This membrane may involve extensive areas of edema , ulceration and necrosis of under,ting mucosa.
E) This membrane may involve extensive areas of edema , ulceration , and necrosis of underlying mucosa.
F)Blood stream infection : break in gastrointestinal tract mucosal barrier ; intravascular catheter
Describe the laboratory diagnosis of Oral Candidiasis
Microscopy :
A) Gram stain : Dark Gram positive budding yeast cells with pseudo hyphae formation
B) Wet films : Abundant presence is significant
:Demonstration of mycelia forms indicates colonisation and tissue invasion
C) Germ tube test : (Reynolds- Braude phenomenon )
- Candida albicans produce germ tube when icubated in serum at 37C for 2-4 hrs
D) Culture :
- Growth on Sabouraud’s dextrose agar ( SDA) : White , smooth creamy colonies with yeasty odor.
- Growth on Corn Meals agar at 20C : Chlamydospores are formed
E) Biochemical Test :
- Sugar assimilation & fermentation tests for differentiating various Candida species
Explain about the development of dental plaque
Microorganism that form biofilm are anaerobes - mainly Streptococcus mutants and Fusobacterium.
- S. mutants and other anaerobes are the initial colonisers of tooth surface and play a major role in the establishment of early biofilm community
Steps of Plaque formation
A) Association : Dental pellicle forms on the tooth and provides bacteria surface to attach
B) Adhesion : Within hours, bacteria loosely bind to the pellicle.
C) Proliferation : Bacteria spreads throughout the mouth and begins to multiply
D) Microcolonies : Streptococci secrete protective layer ( slime layer )
E) Biofilm formation : Microcolonies form complex groups with metabolic advantages
F) Growth or maturation : The biofilm develops a primitive circulatory system
- S. mutans use the enzyme glucansucrase to convert sucrose into a sticky , dextran-based polysaccharides that allows the bacteria to cohere
Others factor that involved the plaque formation
- Salivary alpha- amylase plays a role in binding & adhesion.
-Proline- rich proteins ( PRP ) - Ecological factors :
A) pH : 6.7 and 8.3
B)saliva : acts as a buffer ( btw 6 and 7 )
C)temperature : 2 degree change drastically shifts the dominant species
D) redox reactions : carried out by aerobic bacteria keeps the O2 levels in the mouths at a semi-stable homeostatic condition allow bacteria to survive
Explain the Pathogenesis of dental caries
A) Acid demineralisation : Dissolution of tooth mineral ( primarily hydroxyapatite )by acids derived from bacterial fermentation of sucrose and other dietary carbohydrates
B) S.mutans is located on the enamel surface
C) Debriding procedure ( tooth brushing) do not remove bacteria firmly attached to the enamel surface & sequestered in defects in the enamel surface.
D)The incipient / white spot lesion occurs when the acidogenic activity of the cariogen cause cause the tooth mineral to be mobilised from the subsurface enamel to buffer the pH at the plaque-enamel interface
E) When lesion progresses to the stage of cavitation , the organism penetrate the enamel crystals.
F) Secondary cariogens ( lactobacilli ) appear as a result of the selection for aciduric organisms in the plaque.
G) In advanced clinical stage , S.mutans can no longer survive , only secondary cariogens -lactobacilli
H) White spot stages culture isolated S . Mutans , while in advanced stage , lactobacilli was isolated
Explain about Gingivitis
- Accumulation of supragingival plaque along the gingival margins
- Initial colonisers of teeth are Streptococci spp and later colonised by other bacteria present in saliva such as Actinomyces species and Veillonella spp.
-If plaque remain undisturbed , the flora gradually shifts toward an anaerobic, Gram negative flora , that includes black pigmented Bacteroides spp and several types of Spirochetes spp.
**Plaque in which Spirochetes spp and Actinomyces viscosus provoke bleeding gingivitis
Explain the types of E.Coli and theirs mechanism
A) ETEC - bind loosely via , secrete toxins ( like Cholera toxins ) into the gut that then gain entry into the cell without disruption of cytoskeleton.
B) EPEC destroys the brush border microvilli , and becomes firmly attached through a pedestal consisting of actin and actin binding proteins .
C) EIEC - gains entry into the cell , escaping from the immune system by digesting phagolyosome. They can grow and divide in cytoplasm and gain entry to neighbouring cells by bursting through and digesting membranes.
D) EHEC - like EPEC but in addition of Shiga toxins
State the important feature in Vibrio Cholerae
- comma-shaped Gram-negative bacilli
- Single polar flagellum
- Darting motility
Explain the Pathogenesis of vibrio cholerae
- Inactivates GTPase function of G -protein in intestinal cells
- G proteins stuck in “On” position
- 100 fold increase in cAMP
- Activation of ion channels
- Ions flow out and water follows
Explain about the Laboratory Diagnosis about the vibrio cholera
A) Direct microscopy
B) Culture :
- Selective media
-Bile salt agar
- Monsur’s GTTA ( Gelatin Tauocholate Tryticase Tellurite agar )
- *** TCBS ( Thiosulphate Citrate Bile salts Sucrose ) medium [V.cholerae with yellow colonies due to sucrose fermentation]
State the identification of Vibrio cholerae
Gram stain : Curved GNB
Hanging drop preparation : darting motility
Biochemical test : oxidase positive
: String test positive ( One drop of Na deoxycholate added to emulsified overnight culture of V.c becomes viscous)
Agglutination test
State 4 serogroups of Shigella species
Serogroups A : S. dysenteriae ( 12 serotypes )
Serogroups B : S. flexneri (6)
Serogroups C : S . boydii ( 23)
Serogroups D : S. sonnei (1)
Explain the uses of Type III secretion system & abbreviated TTSS or T3SS ( called Injectisome or Injectosome) Shigellosis
- Used as sensory probe to detect the presence of host cell.
- Secrete proteins that help the bacteria infect them.
- creating a pore in the host cell membrane
- Induces apoptosis in macrophages
Explain the Pathogenesis of Shigella
A) Uptake by M cell
-Taken up by specialised epithelial cells of the small intestine known as Microfold cell
B) Apoptosis of Macrophges
In the macrophages , the bacteria disrupt the phagosomes vacuole and moves into cytosine and cause death of the cell.
C) Invade epithelial cell , multiply.
Shigella cells start releasing T3SS effectors that are involved in cell invasion. They activate their own internalisation into the cells through the production of type III secretion system (T3SS)
D) Toxin production - causes cell death
E) Dysentry
State the Lab Diagnosis for Shigellosis
A) Transport medium : Sachs buffered glycerol saline
B) Culture : MacConkey agar
C) Hanging drop preparation : Non motile bacilli
D) Biochemical test : Indole and MR positive
: Urease , citrate & H2S negative
E) *** All the serogroups except S .soneii do not ferment lactose and sucrose
Explain the Pathogenesis of the salmonella typhoid
1 week - rising fever ( step ladder pyrexia )
-Blood ( negative in Wiesel test or other serology tests at this stages)
2 week - rose coloured spots , abdominal pain and splenomegaly ( Serology Widal positive )
3 week - abdominal complications of haemorrhage or perforation ( forms ulcers in peyer’s patches )
- stool common
4 weeks - recovery
State the result widal test for Salmonella typhoid
STO ( O - group specific Ag )
STH ( H - species specific Ag )
SPAH ( S.paratyphi A )
SPBH ( S.paratyphi B)
Explain the Pathogenesis & Transmission of Rotavirus
Transmission - Feco-oral transmission
Pathogenesis - Rotavirus produces an enterotoxin
I) Decreased Brush Border enzymes ( Decrease Sucrase , Maltase and lactase ) —> Osmotic Diarrhea
II) Rotavirus Enterotoxin NSP4 —> Toxic Effects
III) Enteric Nervous system overactivation —> watery diarrhea
Explain the Pathogenesis and clinical features of Entamoeba histolytica
Entamoeba histolytica - human colon
- Infection restricted to the lumen of the intestine (“luminal amebiasis” ) are asymptomatic
- Amebic colitis occurs when intestinal amebiasis occurs when the mucosa is invaded. Symptoms : severe dysentry
- Severe chronic infections may lead to further complications: formation of amebic granulomas ( ameboma)
-Extraintestinal amebiasis
: Amoebic liver abscesses -** most common manifestation
: Pleuropulmonanry abscess , brain abscess
Explain the Pathogenesis and Clinical Features of Giardia lamblia
Habitat - duodenum and upper jejunum
Pathogenesis & Clinical features
: Trophozoites does not invade the tissue but remain adhered to intestinal epithelium by means of the sucking disc causing stunting and shortening of the villi
: Patients are usually asymptomatic , but in some cases , Giardiasis may causes diarrhoea , fat malabsorption, dull Epigastric pain , & flatulence
- Children may develop chronic diarrhoea , malabsorption of fat and vitamin A and weight loss
Explain about the habitat and morphology of Taenia solium ( pork tapeworm)
Habitat : in small intestine of human
Morphology:
Adult : comprise head / scolex , neck and a body divided into several proglottids
Egg : contains embryo that contain 3 pair of booklets surround by embryophore
Larvae : called cysticercus cellulose
Explain the Haibitat and Morphology of Taenia saginata.
Habitat : Live in the small intestine of human
Morphology
- Adult : consist of head / scolex , neck and body that divided into several proglottids
- Egg : contain embryo which contains 3 pairs of hooklets
- Larvae : is called cysticercus bovis = infective stage to human
State the Pathogenesis & clinical features of intestinal Taeniasis
Intestinal taeniasis
- mostly asymptomatic
- in symptomatic patient mostly vague abdominal discomfort , nausea
- cases of acute intestinal obstruction & acute appendicitis
- Cysticercosis : caused by larval stage ( cysticercus cellulosae ) T.solium
: Most common organ be involved is ** ( subcutaneous tissue , brain & eye )
: Neurocysticercosis ( cysticercosis of the brain ) = most common and most serious form of cysticercosis.
: In ocular cysticercosis : patient present with blurred vision or loss of vision
Explain the Pathogenesis and clinical features of Ascaris lumbricoides
Pathogenesis contributed to
- host immune response
- migration of larvae
- mechanical obstruction by adult worm
- nutritional deficiencies
A) Pulmonary phase : migrating larvae in the lungs , which provoke an immune mediated hypersensitivity response
: cause cough , chest discomfort
***: Eosinophilic pneumonia (Loefflers syndrome) : In severe cases , patients develop dyspnoea and transient patchy infiltrates in the chest X-ray along with transient peripheral eosinophilia.
B) Intestinal phase : results due to effect of adult worm in intestine \:Malnutrition and growth retardation \: Intestinal complications \: Allergic \:
Explain the Pathogenesis & clinical features Ancylostoma duodenale( egg with many blastomere)
-suck blood from intestinal vessel by
A) attaching and making cuts in intestinal wall by buccal capsule and teeth followed by sucking the blood through contraction of their muscular esophagus.
B)secreting hydrolytic enzymes
C)releasing anticoagulants which help to makntimg continuous oozing of blood from the attachment sites
Affect due to Migrating Larva
- cutaneous lesions : “ground itch” at the skin penetration ; Serpiginous track ( subcutaneous migration of the larva )
- Mild transient pneumonitis - Migrating larvae through the lungs
Affect due to adult worm in intestine
- depends upon worm load , mostly asymptomatic
A) Early intestinal phase ( less worm load ) - Epigastric pain , inflammatory diarrhea
B) Late intestinal phase ( chronic infection with heavy worm load ) - iron deficiency anemia & protein energy malnutrition resulting from blood loss
C) Wakana disease : When L3 larvae of A.duodenale are ingested by oral route , they either migrate to pharynx or develop to adult worm in the intestine - both gastrointestinal & pulmonary symptoms are observed
List the hepatitis virus
- Hepatitis A (HAV) : Hepatovirus : ssRNA : Faecal-oral : No carrier state
- Hepatitis B : Hepadnavirus : dsDNA** : Blood-borne, sexual : Carriage associated with liver cancer
- Hepatitis C : Flavivirus :ssRNA : Blood borne : Carrier associated with liver cancer
- Hepatitis D : Deltavirus : ssRNA : From blood : Needs concurrent hepatitis B virus infection
- Hepatitis E : Calicivirus : ssRNA : Faecal oral : Common in Far East
- Yellow fever : Flavivirus : ssRNA :Mosquito : No person to person spread
Which hepatitis virus has replication defective
Hepatitis D
Which Hepatitis have DNA Polymerase in Virion
HBV
Which hepatitis virus only able to infect inviduals with concomitant hBV
HDV
Explain the Pathogenesis of Hepatits Virus
A) Infection with a virus that targets the liver ( HAV , HBV , HCV , HDV , HEV)
B) Attack of hepatocytes
C) Liver inflammation
D) Lysis of hepatocytes ( increase in serum ALT , AST )
E) Resolution of infection ( caused by Acute Hepatitis ( Hep A & E ) )
F)( Chronic Hepatitis (Hep B and Hep C ) Decrease Hepatic metabolic activity , decrease plasma protein synthesis , decrease bilirubin clearance from blood
G) Progressive deterioration in liver function
Describe the clinical findings of viral hepatitis
1) Upper right quadrant pain
2) Hepatomegaly
3) Nausea
5) Elevated liver enzymes (AST , ALT , ALP )
6) Elevated bilirubin and jaundice
7) Decrease Serum glucose
8) Decrease albumin
Which Hep virus is dangerous and can result in fulminating hepatitis which can lead to death of the fetus.
Hep E
State the methods of transmission of viral hepatitis
A) Oro-fecal via contaminated food & water
- Hep A and Hep E
B) Blood- borne , puncture wounds , sexual transmission , IV drug use.
Hep B
Hep c
Hep D h only occurs when there is concurrent Hep B infection
State the prophylactic measure for viral hepatits
Vaccines only available for Hep A & Hep B
Eat & drink properly boiled food & water
Use protection during sexual intercourse
Describe the morphology of Hepatitis virus ( viral symmetry , type of genome , presence of envelope )
- All are icosahedral
- all are ssRNA , except Hep B ( ssDNA)
- only A & E are non-enveloped
In Hep B virus infection , 3 other particles are seen in plasma of infectious patient
I) Dane particles
II) Spherical particles
III) Filamentous particles
Describe the HÁČEK group of bacteria
A group of highly fastidius , slow growing , capnophilic , gram negative bacteria involve in development of infective endocarditis.
Haemophilias parainfluenzae
Aggregatibacter actinomycetemcomitans ( most chances causes endocarditis)
Cardiobacterium hominis
Describe the preventive strategies of acute rheumatic fever.
Treatment - Penicillin is the drug of choice. ( can be given orally ) \: Penicillin V or amoxicillin for 10 days ( Intramuscularly as single dose ) \: benzathine penicillin Supportive treatment : aspirin
Prevention :
: complete treatment of Grp A streptococcal sore throat
Influenza A is more likely to cause pandemics than influenza B or C because it has a ( ………) and also because it can undergo ( ……)
Influenza A is more likely to cause pandemics than influenza B or C because it has a ( wide host range of humans , pigs , horses , birds and marine mammals ) and also because it can undergo ( both antigenic shift and drift )
Which influenza virus has 7 gene segments
Influenza C
Describe the morphology of influenza virus
1) RNA virus
2) Segmented ( 7-8 gene segments )
3) Negative strand
4) Family : orthomyxoviridae , genus : Influenza A, B, C
5) Covered by projection of 3 proteins
I) Neuraminidase ( NA)
II) Hemagglutinin ( HA)
III) Matrix 2 ( M2) protein
Bacteria such as Spirochetes and black pigmented Bacteroides species like ( …….) and (……..) are implicated in periodontitis
(……) is most often associated with early onset periodontitis ( EOP) while ( …….) is found in both EOP and AP ( adult periodontitis)
Bacteria such as Spirochetes and black pigmented Bacteroides species like ( Prevotella intermedia) and (Porphyromonas gingivalis ) are implicated in periodontitis
(P. Gingivalis) is most often associated with early onset periodontitis ( EOP) while ( Prevotella intermedia ) is found in both EOP and AP ( adult periodontitis j
State the clinical manifestations of Acute Rheumatic fever
A) Migratory polyarthritis
B) Pancarditis
C) Subcutaneous nodules
D) Chorea : abnormal involuntary movement disorder
E) Erythema marginatum
