Micro written Flashcards
Give reason Staphylococcus aureus Is pathogenic bacteria
As it has extracellular protein -> convert plasma fibrinogen to fibrin -> fibrin barrier is formed
-> this leads to:
O Protection from phagocytic and immune defences
Give reason MSA is selective Protein (A) is anti-phagocytic virulence factor
As it binds to Fc-portion of IgG on surface of S. aureus -> inhibition of opsonization
Give reason Gram stained smear is not diagnostic in staph
Due to presence of S. epidermidis which have the same morphology and characters of S. aureus.
Give reason Most of staphylococcal Infections are localized while most of streptococcal Infections
ore diffuse
Because staphylococci have coagulase enzyme which leads to localization of infection, while
streptococci have hyaluronidase and nuclease enzymes together with streptokinase contribute
to the spreading nature of streptococcal infections.
Enumerate the mechanisms of resistance of Staphylococcus aureus to beta-
lactamase enzyme
Resistant strains remain susceptible to semi-synthetic penicillins (e.g. oxacillin & methicillin)
& to cephalosporins
® MRSA isolates are often multi-resistant to other antibiotics -> Vancomycin is used as the
drug of choice for treatment of MRSA infections.
© Some strains of MRSA displayed intermediate (VISA) or full resistance (VRSA) to vancomycin
new antibiotics linezolid and streptogramins are used for treatment of infections not
responding to vancomycin
Enumerate 4 most important virulence factors of S. Aureus
Staphylococcus-coagulase
Protein A
Hemolysin
Clumping factor
Disease of staphylococcus epidermidis
Device related infections
Urinary tract and surgical infection
Mention diseases caused bv staphylococcus saprophylcuss
Spread to urinary tract in young sexually active women -> urinary tract infections
(honeymoon cystitis) -> (endogenous infection) -> due to ability of organism to adhere to
uroepithelial cells
Give short account on Toxin-medicated diseases of Staphylococcus
Staphylococcal food poisoning
* The commonest food poisoning
* Incriminated foods: (containing preformed toxin)
D Protein-rich food -> mayonnaise, milk & its products (ice cream)
D Carbohydrate-rich food -> pasta, cake and koskosi.
* Six enterotoxins (A, B, C, D, E & G) produced by “50% of S. aureus strains -> heat-stable
toxin (for “30 min. of boiling) & do not change food characters (taste, colour or odour)
* I.P.: 1-6 hours
* Violent vomiting & diarrhoea, usually without fever -> self-limited
© ToxicShocksyndromeHSS);
* Caused by TSST-1 producing S. aureus
* Young menstruating females use vaginal tampons -> also occur in any individual
suffering from TSST-1 produdng 5. aureus infections anywhere in body
* High fever, diarrhoea, vomiting, red rash, hypotension with cardiac & renal failure
* Mortality rate may reach 10-15%
* Occurs in neonates & children under five years of age.
* Caused by 5. aureus that produces exfoliatin toxins.
* Large bullae -> rupture leaving moist, red, scalded dermis.
* Full recovery without scar formation.
Give reason gram-stained smears useful only in cases of skin and soft tissue infections
Since S. pyogenes cannot be visually distinguished from the normal oral streptococcal flora
Give reason long-acting penicillin used as chemoprophylactic agent against recurrent S. pyogenes infections
To prevent repeated rheumatic attacks
Give reason pregnant females colonized with Streptococcus agalactia at the end of the third trimester are given ampicillin during delivery
To reduce neonatal sepsis
Enumerate the most important virulence factors of Streptococcus pyogenes
M proteins: allows bacteria to colonize skin and escape phagocytosis
Protein F
Lipoteichoic acids
Invasins
Enumerate localized infections caused by streptococcus pyogenes
O Pharngynaitis
e Scariet.fe.yeG
* Caused by erythrogenic toxin*producing S. pyogenes
* Characterized by; scarlet red rash (sandpaper rash) & strawberry tongue
Skin^softtissueinfectionsi
D Impetigo infection of superficial skin layers with blisters & denudedsurface covered with crusts
□ Cellulitis: infection of deep layers of skin
Enumerate invasive infections caused by streptococcus pyogenes
Puerperal fever: life threatening infection of endometrium post birth can lead to septicemia and toxic shock syndrome
Acute endocarditis
Necrotizing fasciitis
Toxic shock syndrome
Enumerate the disease caused by Viridans Streptococcus
Dental caries
Subacute bacterial endocarditis —> dental manipulations or tonsillectomy —–> bacteria and adhere to cardiac valve
Enumerate 4 diseases caused by Streptococcus pneumoniae
Pneumonia, meningitis, otitis media, Sinusitis
Pregnant females colonized with Streptococcus agalactiae at the end of the third trimester are given ampicillin during delivery.
To prevent transfer of bacteria during delivery to the infant. ampicillin is give for colonized mother
Give reason enterococcus faecalis used as indicator of faecal pollution of water
Constantly found in human & animal faeces and exclusively found in intestine
Enumerate 2 similarities between Enterococcus and Streptococcus
Gram positive
Facultative anaerobes
Disease caused by Enterococcus species
UTI
Intrabdominal infections
Bacteremia
Give reason Neisseria can survive intracellular
As it has porin proteins which prevents fusion of phagosomes & lysosomes
lgA protease is a colonizing factor
Because IgA protease inactivates secretory IgA -> more adherence & colonization of mucosa
Gonococci coni Infect vagina
Vagina is acidic medium which is not suitable for growth of gonococci
Gonococci can produce repeated infections
O High Ag variations of gonococcal pili
® Superficial nature of infection
- Production of IgA protease
Any newly born Infant should take early eve drops antibiotics as chemoprophylaxis
To prevent gonococcal neonatal conjunctivitis
Enumerate diseases caused by Neisseria Gonorrhoae
Gonorrhoae
Neonatal conjuctivits
Vulvovaginitis (due to secual abuse)
Enumerate the most important virulence factors of Neisseria
Pill for attachment
IgA protease
PS capsule (MOST IMPORTANT)
LPS endotoxin
Give a short account on meningococci treatment and prevention
Treatment: Penicillin G and 3rd generation cephalosporin
Prevention: Capsular vaccines (Bivalent and Quadrivalent) and Protein conjugate vaccines for children less than 2.
Antitoxin of Diphtheria should be given
Because antitoxin will not neutralize toxin that is already fixed to tissues, but will neutralize the circulating (unbound) toxin
Enumerate disease caused by Corynebacterium Diptheria
Pharyngeal diphtheria—> adheres to membrane of larynx causing airway obstruction
Cervical lymphadenitis
Toxemia which can lead to myocarditis
Write short account about treatment and prevention of DIptheria
Treatment: Immediate Diphtheria antitoxin, penicillin and respiratory support
Immunization: Diphtheria toxoid combined with tetanus toxoid, given at 2,4,6 and 8 months of age
Booster doses ore given every 10 veors to maintain Immunity
Because more frequent boosters are unnecessary & may cause hypersensitivity reactions
Botulism hot long Incubation period
As the toxin is absorbed in intestine & is transported systemically via bloodstream to reach peripheral neuromuscular synapses so It take to much time to make a disease
There Is no reason to give antibiotics except In In Infant botulism
As it is still effective if it binds to toxin before toxin binds neuromuscular junction
Although N. gonorrhoea is frequently resistant to tetracycline -> azithromycin
should be given
due to concurrent Chlamydia infection
The most important virulence factor of Clostridium tetani
Tetanospasmin toxin.
- Germination of spores is favoured by presence of necrotic tissue & poor blood supply in wound
- Vegetative cells grow locally in necrotic tissue & release tetanospasmin toxin -> spreads by
retograde transport within axon & haematogenously until it reaches CNS
Blocks release of inhibitory mediators at spinal synapses==> causing flaccid paralysis
Enumerate the diseases of Clostridium botulinum
Botulinum toxin is most potent in existence: prevents release of ach resulting in flaccid paralysis
Classic botulism: difficulty speech and descending systemic flaccid paralysis
Infant botulism: flappy baby syndrome; due to germination of spores in GIT from raw honey and transfer to baby from mother
wound botulism: occurs in drug addicts
Compare between types of poising of Bacillus cereus
Emetic form: short, vomiting & cramps, heat-stable, Irritate gastric mucosa, found in fried rice
Diarrheal form: Long, diarrhea & abdominal cramps, heat-liable, intestinal fluid secretion, found in meat dishes
Prevention of Clostridium tetani
- The toxoid is given to:
O Infants - Triple vaccine (DPT) -> at age of 2,4 & 6 months by I.M. injection
- Booster doses are given at 18 months & upon school entry
- Booster doses (Td) are given every 10 years -> more frequent boosters are unnecessary & may cause hypersensitivity reactions
O People at high risk e.g. military personnel
© Pregnant females to prevent tetanus neonatorum
© Wounded individuals; postexposure prophylaxis against tetanus in wounded individuals
Discuss the treatment and prevention of Clostridium Botulinum
Potent trivalent (A, B, E) antitoxin -> only effective if it binds to toxin before toxin binds
neuromuscular junction (within 12 hours after ingestion)
a Serum sickness may occur
Prevention: proper sterilization of canned food, heating and swollen cans must be discarded
Shigella can be transmitted through person to person transmission
As the infection dose is ingestion of few organisms (100 organisms) is able to cause disease
Widal test is not good diagnostic test for E.coli
False positive: cross reacting antibodies, subclinical infection and vaccination
False negative: if performed during the first week of illness
Proteus incorporated in formation of stones (calculi)
As it contain urease hydrolyses urea in urine to form ammonia which raises pH increasing stone formation
Enumerate the most important virulence factors of E. Coli
Fimbrial adhesion: bind to urinary tract epithelium
Capsular antigens: interfere with phagocytosis
Enterotoxins
Shigatoxins
Enumerate the diseases caused by Klebsiella species
K. pneumoniae: UTI, pneumonia, neonatal sepsis
K.ozaenae: atrophic rhinitis
K. rhinoscleromatis: rhinoscleroma
Enumerate the most Important virulence factors of Shigella
Invasiveness: epithelium of terminal ileum and large intestine
Shiga toxin: acts as neurotoxin, cytotoxin and enterotoxin. May cause coma and hemorrhagic colitis
Enumerate the diseases caused by Proteus, Providencia and Morganella
UTI
RTI
Wound infection
Septicemia
Explain diseases caused by E. coli
UTI: some of own flora of colon goes on uro-genital area. Community-acquired UTI or Hospital-acquired UTI
Neonatal meningitis: from mother during birth
Pneumonia, sepsis, and septicemia
Diarrhea
Enumerate the types of diarrhoeagenic Escheria coli and give the mechanism of action of each type
Entero-pathogenic E.coli: adhere to mucosa—> interfere with water absorption
Entero-invasive E.coli: Invasion of mucosa without toxin production
Entero-toxigenic E.coli: Productions of enterotoxins
Enterohaemorrhagic E.coli: Production of shiga-like-toxin
Entero-aggregative E.coli: Adhere to mucosa by aggregative fimbria and production of enterotoxin
Antibiotics may be useful except in enterohaemorrhagic E.coli
Antibiotics may increase risk of developing HUS by increasing shiga toxin
Enumerate 3 complications of Typhoid fever
Perforation of bowel and hemorrhage from bowel ulceration
Explain the pathogenesis of Typhoid fever
- Organisms adhere to mucosa of small intestine -> invade to submucosal layer -> taken up by macrophages of Peyer’s patches -> transported to mesenteric lymph nodes -> via thoracic duct to bloodstream (transient bacteraemia)
- Organisms reach RES –> then re-invade blood causing 2ry heavier bacteremia
Give short account on Salmonella food poisoning (Gastroenteritis or Enterocolitis)
From raw eggs
Organism replicates in epithelial cells of small & large Intestines -> inflammatory lesions &
diarrhea
Self limited
Give short account on diseases caused by Yersinia pestis
Plague (Black death) —-> zoo tonic disease affecting rodents which acts as reservoirs
Man can be accidentally infected by:
Flea bite
Inhalations of droplets from animals
in either case, septicemic plague due to spread of organism to blood stream (can be used for bioterrorism)
Enumerate the most important virulence factor of Vibro cholera
Cholera toxins massive secretions of electrolytes and water into small intestine lumen
Why : Direct person-to-person transmission of Vibrio cholerae is not common.
Vibrios are sensitive to acid and most die in the stomach -> high infectivity dose is required
so direct person-to-person spread is not common
They cause massive watery diarrhea which may lead to hypovolemic shock
Enumerate the autoimmune diseases that may complicate Campylobacter enteritis
Guillain-Barre syndrome: antibodies against disease cross react with antigens on neurons
Reactive arthritis
Reiter’s disease: triad of arthritis, conjunctivitis and urethritis
Enumerate clinical outcomes of H.Pylori infection
Gastric ulcer
Chronic gastritis
Stomach cancer
Enumerate the most important virulence factors of H. Pylori
Urease -> “ammonium cloud” -> permits H. pylori to survive In acidic environment
- Corkscrew motility -> organism penetrate (pore) through the viscous gastric mucus
- Mucinase -> penetration of mucous layer -> reach stomach lining (where pH Is neutral)
Enumerate 4 diseases caused by pseudomonas aeruginosa
Wound infection
Folliculitis
External ear infection
Eye infection
Enumerate the most important virulence factor of Haemophilius infleunza
PS capsule
IgA protease
It Is not preferred to give pertussis toxin vaccine after age of 6 Years
Because in a very small number of cases, severe or irreversible brain damage may
occur especially if given after 6 years of age.
Give reason(s): Most Haemophilus influenzae infections occur in children between 6 months and 6 years.
decline of maternal IgG with
inability of child to generate antibodies against polysaccharide capsular (Tl) antigen
Cultivation of Brucella Is useless
There is high risk to laboratory personnel to acquire infection by Inhalation
* The culture requires long incubation (2-4 weeks)
O Being fastidious, the organism needs special growth requirements which are not always available
Enumerate the Modes of transmission of Malta fever.
O Ingestion of contaminated unpasteurized milk or milk products
® Direct contact through skin abrasions during handling of infected animals or their discharges
© Inhalation of infected aerosol during handling of Infected animals
The major virulence factor of Malta fever (Brucellosis)
Endotoxin (LPS)
Mycobacteria Is not stained by Gram stain / Mycobacteria Is acid fast bacteria
Because the organisms firmly retain dye used & resist decolorization even by acidic solutions
Prolonged therapy is indicated in TB (mycobacterium)
> The intracellular location of the organism
Blocking of drug penetration by caseous material
The slow rate of growth of the organism.
The presence of the persisters (metabolically inactive bacilli) within the lesion
Clinical disease of Leprosy may develop after years of initial contact
O Low infectivity of M. leprae
9 Long generation time (slow rate of growth)
Mention the Importance of lipids In the cell wall of M, tuberculosis
Lipids: are Mycolic acid and Mycobacterial sulfolipids (reason they’re called Mycobacterium)
a- Impermeability to stains and dyes
b- Resistance to many antibiotics
c- Resistance to killing by acidic and alkaline compounds
d- Resistance to osmotic lysis via complement deposition
e-Ability to survive inside macrophages and induce CMI response
Discuss the pathogenesis of TB and mode of transmission
■ The droplet nuclei reach the terminal alveoli where they are engulfed by alveolar macrophages.
■ Cell-mediated immune response, which is the main immune mechanism against mycobacteria, is
initiated about 4-6 weeks after infection resulting in granuloma (tubercle) formation
■ Its capacity to multiply both inside and outside cells, makes M. tuberculosis a facultative
intracellular pathogen
■ The majority of these Bacilli are destroyed or inhibited but the remaining bacilli are able to survive
and multiply intracellularly by inhibiting fusion of phagosomes and lysosomes allowing
intracellular survival (even if fusion occurs, the fatty nature of cell wall reduces killing effect).
* Within the granuloma, M. tuberculosis can survive in small numbers in a relatively dormant state
(latent tuberculosis infection), & this situation is due to balanced state of host-parasite relationship
Under certain conditions primary TB Infection may be activated …. Explain
■ Under certain conditions, e.g. immunosuppression, disturbance of the host-parasite balance may
lead to reactivation of latent tuberculosis infection and development of tuberculosis disease.
* Reactivation usually occurs within 2 years after initial infection in about 5% of individuals with
latent TB infection.
* The most common site of reactivation is the apex of the lung
Pathogenesis of leprosy appears to derive from:
O Ability of M. leprae to survive & replicate within macrophages, nerve cells & other host cells
* The consequent immune response to organism
Clinical disease mov develop years after Initial contact with organism -> this is due to:
Low infectivity of M. leprae
© Long generation time (slow rate of growth)
Compare between tuberculoid leprosy and lepromatous leprosy
tuberculoid leprosy: macular skin lesions, slow disease progress and good prognosis
lepromatous leprosy: nodular skin lesions, aggressive disease progression and very poor prognosis.
Although spirochaetes have no flagella but is motile
Due to presence of axial filaments (endoflagella) which give it characteristic corkscrew motility
Syphilis cant be transmitted by stored blood
because it dies when stored at 4*C within 3-5 days.
Give the clinical manifestation of primary syphilis
□Hard painless genital or oral ulcer (chancre)
-Contagious (infectious)
-Heals spontaneously (within 3-6 months)
Give 4 cardinal features of secondary syphilis
1- Generalized maculopapular skin rash
2- Mucous patches in mouth
3- Chondyloma lata around the genitals
or anus
4- Generalized lymphadenopathy
Give an account on Fusospirochaetal disease
the normal spirochaetes of the mouth, together with
anaerobic fusiform bacilli (fusobacteria) find suitable conditions for multiplication -> They increase in
numbers causing;
Vincent’s angina: fusospirochaetal infection of the pharynx with pseudomembrane formation
Enumerate the most important species and their disease
Mycoplasma pneumoniae: atypical pneumonia
Genital mycoplasmas: Non-gonococcal urethritis, PID, post abortal fever
Mention the causative organism and the mode of transmission of chancer
Causative organism: syphilis
mode of transmission: sexually and transplacentaly
Give reason the genus Mycoplasma is resistant to beta-lactam antibiotics
Mycoplasmas are bacteria without cell wall -> lack of cell wall renders these organisms:
O Resistant to antibiotics which inhibit cell wall synthesis (e.g. beta-lactam antibiotics)
8 Unstainable by Gram stain
© Variable in shape (pleomorphic)
Enumerate and discuss the important diseases caused by Chlamydia trachomattis
Non-gonococcal urethritis: can become prostatitis in males and PID in females. Females are asymptomatic because similar to normal discharge and pain
Lymphogranuloma venereum: inguinal lymphadenopathy
Trachoma which can lead to chronic keratoconjucutivis can lead to blindness
Inclusion conjunctivitis: most common cause of neonatal conjunctivitis
Neonatal pneumonia
Give short account on the pathogenesis and clinical manifestations of Rickettsia
- Rickettsia infect the endothelial lining of the blood vessels *■> leading to vasculitis
- Damage to vessels of skin results in characteristic rash & in oedema & haemorrhage
- Rickettsial disease is usually accompanied by fever, headache & skin rash
- In severe cases, rickettsial encephalitis with coma, convulsions & pulmonary oedema are grave
conditions that are often fatal
Explain why Coxiella is not classified as rickettsia
Not transmitted to humans by arthropods
Extremally resistant to heat so can live outside host for long time
Development of antibodies to HAV confers lifelong Immunity.
As There is only one serotype of HAV.
The presence extra-hepatic manifestation In HBV Infection.
Due to deposition of the immune complexes mainly in the skin, joints and glomeruli.
Presence at HBcAb at the lgG form is Indicator of past Infection.
HBcAb of the IgG form is detected and persists for life whether the patient recovers from acute infection or develops chronic hepatitis.
The difference between hepatitis viruses and viral hepatitis.
- In hepatitis viruses the main site of infection is the liver.
- In viral hepatitis the viruses infect the liver but also infect other sites in the body -> and therefore are not exclusively hepatitis viruses.
The causes of fulminant hepatitis in HBV,
a) It may be due to massive lysis of hepatocytes by vigorous immune response
b) highly virulent strain of HBV
c) co-infection with another hepatitis virus
Pathogenesis of HAV.
a) Humans are the reservoir for HAV.
b) Virus is transmitted mainly by the faeco-oral route usually through ingestion of contaminated food or water.
c) The virus replicates in the GIT and spreads via the blood to the liver, where it replicates in the hepatocytes and is then shed in bile resulting in excretion or large amounts of the virus in faeces.
HBV treatment.
a) Specific treatment for acute HB Illness Is usually not needed .
b) Goal for treatment In patients with chronic hepatitis B Is to reduce risk of progressive liver disease & complications.
c) The most commonly used drugs are Interferon-a or a nucleoside analogue
Treatment of HCV
a. Combination of alpha-interferon and antiviral chemotherapy has been used -> Response depends upon the virus genotype.
b. Sofosbuvir (Sovaldi) is a nudeotide analogue inhibitor
Compare active hepatitis patients and chronic carriers in HBV infection
Chronic hepatitis: Elevated liver enzymes, HBeAg present, severe inflammation/necrosis, may end in cirrhosis
Chronic carriers: Normal liver enzymes, HBeAg is absent, no inflammation, may end in chronic hepatitis
Mention The primary cause of hepatic ceil destruction In HBV.
The primary cause of hepatic cell destruction appears to be Immune-mediated by cytotoxic T- cells which react specifically with viral antigens displayed on the surface of Infected hepatocytes.
Mention the difference! In mode of transmission between HBV L HCV
Unlike HBV, HCV transmission is uncommon vertically (from infected mother to infants) & sexually and HCV route of transmission is unknown in up to 40% of infected individuals.
The difference between hepatitis virus and viral hepatitis
- In hepatitis viruses the main site of infection is the liver.
- In viral hepatitis the viruses infect the liver but also infect other sites in the body -> and therefore are not exclusively hepatitis viruses.
PossibffitY of HBV transmission mov be very high compered to blood-borne Viruses
Because the viral load may reach very high levels (up to 10 10 copies/ml serum).
The presence extra-hepatic manifestation in HBV infections
Due to deposition of the immune complexes mainly in the skin, joints and glomeruli
HDV replicates only In the presence of HBV.
As HBV provides HDV with the envelope protein
HBV treatment and prevention
No specific treatment, reduce risk of progressive liver disease in chronic cases
Prevention: screen blood, apply infection control practices. Active immunization for health workers, medical students. Passive immunization neonates born to HBsAg positive mothers and unvaccinated individuals
Mention The primary cause of hepatic cell destruction In HBV
The primary cause of hepatic cell destruction appears to be immune-mediated by cytotoxic T-cells which react specifically with viral antigens displayed on the surface of infected hepatocytes
Genetic deficiency of chemokine receptor results In toll of binding to the Infected cell and causes resistance to HIV Infection
As the Viral gp120 bind to CD4 molecules -> followed by binding to chemokine receptor on cell surface.
HIV virus Is able to avoid the Immune response in spite of the virus is slowly dividing.
a) High rate of viral mutation
b) Integration of virus in chromosome of Infected cells shielded from recognition by immune system.
c) Down regulation of MHCI expression by the virus.
d) Loss of CD4 T cell responses.
detection of antibodies by ELISA In HIV diagnosis Is not a sure sign
As false positive results may occur in certain conditions (e.g. SLE & syphilis).
In HIV infection No vaccine for human use Is available.
As rapid appearance of gp120 genetic variants -> makes the production of effective vaccine difficult
Enumerate 4 immunity cells which become infected by HIV
Follicular dendritic cells
Cells of nervous system
Macrophages
Monocytes
Discuss the results of T helper cells depletion
a) Loss of cell-mediated immunity.
b) Increased susceptibility to Infections & malignancies.
c) Eventually death.
The cases of HIV Infection In which using Serological fests are not useful
During the acute stage, as antibodies to HIV are not detectable except 3-4 weeks after infection
Newborns of Infected mothers due to presence of passively acquired maternal IgG
The stages of HIV clinical picture.
a) Acute (earty) stage: After incubation period of 2-4 weeks-> HIV-Infected individuals suffer acute flue-like or Infectious mononudeosis-like illness
b) Latent (middle) stage: Acute infection Is followed by extended period of clinical latency.
c) Immunodeficiency (late) stage: Viral replication & gradual depletion of CD4 T cells continue until finally, some years after initial infection, full-blown AIDS develops.
The Immunodeficlency (late) slope of HIV Infection,
b) Number of malignancies commonly arises in AIDS patients
c) The infected person becomes particularly susceptible to opportunistic infections.
d) Patients suffer from: (Debilitating weight loss- Neurologic manifestations).
e) Infections are the major cause of death in AIDS patients.
The antigenic drill results In mild epidemics.
Due to that the Antibodies produced against the previous variant of the virus can still cross-react with the new one and, therefore, most of the populations have some level of immunity. As a result, the new variant may cause and epidemic that is relatively mild.
In influenza virus, pigs play a major role in genetic reassortment
As their cells have receptors for both avian and human influenza strains and can be co-infected by more than one strain.
Gene reassortment doesn’t take place In type B influenza.
As they no animal host
Compare between antigenic drift and antigenic shift
Antigenic drift: refers to minor antigenic changes in HA and NA proteins. Results in mutation in viral RNA which can cross-react. Occurs yearly
Antigenic shift: refers to major antigenic changes in HA and NA proteins. It is the result of gene reassortment. Occurs less frequently
Compare killed (formalin-inactivated) vaccine and live attenuated vaccine
Killed (formalin-inactivated): Given intramuscularly, not good immunizing vaccine because leads to little secretary IgA
Live attenuated vaccine: It is given intranasally, provides good protective immune response mediated by secretory IgA
Measles vaccine gives life-long immunity
Measles virus has only 1 stable antigenic type.
There Is stage of viraemia 4 allowing circulating Abs (IgM and IgG) to neutralize virus.
Enumerate the complications of measles:
2ry bacterial infections
1ry measles virus pneumonia
Encephalitis
Abortion, premature labor
Enumerate complications of mumps
Orchitis—-> if bilateral can result in sterility
Pancreatitis
Meningitis
Complications of rubella virus in pregnancy
Abortion
Congenital malformations
Intrauterine foetal death
Enumerate disease which emerged due to corona virus
Common Cold
Severe Acute Respiratory Syndrome
Middle East Respiratory Syndrome
Coronavirus disease (COVID-19)
In rabies Infection there Is no delectable antibody or cell-mediated immune response
As the virus transport within nerves, virus is sequestered from Immune system.
Human rabies Immune qlobuln (HRIG) Is given of the bite site.
To neutralize the virus and to give time for vaccine to stimulate active Immunity before the virus reaches CNS.
HRIG & rabies vaccine should be given at different sites
To prevent neutralization of virus in vaccine by antibody in HRIG
Enumerate Factors that determine the duration of incubation period of rabies virus
a) Distance of site of bite from CNS -> (the further the bite from the CNS, the longer the I.P).
b) Severity of bite & amount of inoculated virus
c) Immune status of host
Indications for post-exposure prophylaxis
If animal is not available (act as rabies patient)
If animal is available -> animal should be observed for 10 days:
If no symptoms appear within this period -> diagnosis of rabies Is excluded & PEP is not indicated.
If animal dies or symptoms appear—> animal is sacrificed & brain tissue is examined for rabies -> PEP is indicated if diagnosis of rabies is established.
* After bites with expected short I.P. as in children or bites In head & neck (even if animal is available) -> PEP should be started immediately -> to be discontinued if animal proves not to be rabid.
- Bite or non-bite exposure to bats necessitates PEP
Rabies pathogenesis
a) Virus replicates at bite site -> then travels along peripheral nerves to CNS (no viraemia).
b) Virus multiplies in nerve cells forming characteristic intra-cytoplasmic inclusion bodies known as ‘Negri bodies”.
c) Virus then travels down peripheral nerves to salivary glands to be excreted in saliva.
Give short account on Rotavirus
- Rotavirus is the most important cause of gastroenteritis in infants and young children
- The disease manifests as watery non-bloody diarrhoea which may be fatal if untreated
- The incubation period is 1-4 days
- The virus is transmitted Faeco-orally following ingestion of contaminated food or water
Give reason high Incidence of rotavirus infection
- Low infectivity dose (10 ingested viral particles)
- Shedding of large number of virus particles in stools
- Relative stability of the virus allowing it to survive for extended periods on surfaces
Compare HSV-1 and HSV-2 in clinical manifestations
HSV-1: Encephalitis, Acute gingivostomatitis, herpes labials ( By saliva, trigeminal ganglion)
HSV-2: Herpes genitalia, neonatal herpes and aseptic meningitis ( sexual transmission, vertical during birth and found in sacral ganglia)
Compare between varicella (chickenpox and Zoster (shingles)
Varicella (chickenpox): Vesicular lesions dry to crust forming. occurs mainly in children and is more severe and likely to cause complications. Rash appears first on trunk and spreads to head and extremities.
Zoster (shingles): in older people. Results in latent varicella infection in immunosuppressive stress conditions. Painful vesicular eruption around one dermatome
Give Clinical manifestations of CMV
Mental retardation
Microcephaly
Blindness
Stillbirth
Compare between poxvirus and other DNA virus
Brick-shaped
replicate in cytoplasm
Only virus which can be seen with light microscope
Give reason successful eradication of smallpox
- Global use of highly effective vaccine by WHO -> vaccine contains vaccinia virus which is naturally attenuated for man
- Smallpox virus has single, stable serotype
- There is no animal reservoir -> & humans are the only host
- Disease is easily recognized clinically
- There is no carrier state or subdinical infection
Give reason widespread nature of the virus
As they are resistant to drying, detergents and mild chlorine treatment
4 other childhood diseases associated with fever and skin rash are
Scarlet fever
Varicella
Rubella
Measles
enumerate the integrated viral genes then cause transformation through:
Introduction of new “transforming gene” into cell
Activating of pre-existing cellular gene
Inactivation of tumor suppressor genes
Prevention of transmission of prion infections by usual infection control procedures is ineffective
As they are composed entirely of proteins —> they are devoid of any nucleic acid. They are also extremely resistance of prions to heat, disinfectants and irradiation.
Compare between Prions and Conventional viruses
Prions: no nucleic acid, non-cultivable, no immune response and no inflammatory response
Conventional viruses: Nucleic acid is present, Cultivatable, there is immune response, there is inflammatory response
Enumerate 5 predisposing factors to candiasis
Diabetes
Broad-spectrum antibiotic treatment
Steroid therapy
Immunosuppression
Old age
Give clinical features of candidiasis
Oral thrush
Vulvovaginitis
Interdigital
Intertrigo
Compare between Eumycotic mycetoma and Actinomycotic mycetoma
Eumycotic mycetoma: fungal, mainly black and white in color, poor response to chemotherapy (needs surgery)
Actinomycotic mycetoma: Bacterial, mainly yellow in color, chemotherapy is effective
