Thursday, December 31, 2009
erysipelothrix-erysipelothrix rhusiopathie
erysipeloid ( a skin infection that resembles erysipelas caused by streptococci)
gardnerella vaginalis
1.bacterial vaginosis
2.preterm birth, premature rupture of membranes and chorioamnitis
3.postpartum@ postabortal fever
4.neonatal infections
2.preterm birth, premature rupture of membranes and chorioamnitis
3.postpartum@ postabortal fever
4.neonatal infections
corynebacterium diphtheriae
diphtheriae
-upper resp tract illness
- transmitted by droplets from case or carrier
- incubation period 5-6 days
- involve both local and systemi pathology
-upper resp tract illness
- transmitted by droplets from case or carrier
- incubation period 5-6 days
- involve both local and systemi pathology
moraxella catarrhalis
1.resp tract infection: bronchitis, pneumonia, otitis media and sinusitis
2.endocaridits
3.meningitis
2.endocaridits
3.meningitis
neisseria gonorrhoeae
1.gonorrhoea
2.neonatal conjunctivitis
3.vulvovaginitis
4.pelvic inflammatory diseases (PID)
5.Disseminated gonococcal infection (DGI) or gonococcaemia
2.neonatal conjunctivitis
3.vulvovaginitis
4.pelvic inflammatory diseases (PID)
5.Disseminated gonococcal infection (DGI) or gonococcaemia
enter0coccus
1.urinary tract infections
2.intra abdominal or pelvic wound infection
3.bacteraemia
4.endocarditis
5.abscessses,meningitis, peritonitis, osteomyelitis and wound infection
2.intra abdominal or pelvic wound infection
3.bacteraemia
4.endocarditis
5.abscessses,meningitis, peritonitis, osteomyelitis and wound infection
streptococcus pneumoniae (pneumococci)
1.penumonia, meningitis and otitis media
2.sinusitis and conjunctivitis
3.endocarditis and septic pericarditis
2.sinusitis and conjunctivitis
3.endocarditis and septic pericarditis
viridans streptococci
subacute bacterial endocarditis (SBE)
-they can adhere to cardiac valves, especially in people with underlying valvular disease.
-SBE may occur when dental manipulations of trauma to mucosa of upper resp tract
-the organism settled on the prosthetic valves
dental caries
-
-they can adhere to cardiac valves, especially in people with underlying valvular disease.
-SBE may occur when dental manipulations of trauma to mucosa of upper resp tract
-the organism settled on the prosthetic valves
dental caries
-
streptococcus agalacticae
1.neonatal sepsis manifest as pneumonia, septicaemia, meningitis,bone and joint infection...the baby who survives usually handicapped
2.serious infection in adults particularly in cancer and diabetec patients
2.serious infection in adults particularly in cancer and diabetec patients
streptococcus pyogenes
pyogenes infections
(a) pharyngitis ( sore throat,tonsilitis)
- transmitted by resp droplets
- character: pain, rdness and swelling of post pharynx
- accompanied by greyish white tonsillar exudate and fever.
(b) scarlet fever
-dev of scarlet red rash
(c) skin and soft tissue infections
-impetigo
-cellulitis and erysipelas
(d) invasive streptoccoccal infections
-puerperal fever
- acuute endocarditis
-necrotizing fasciitis
- toxic shock syndrome
post streptococcal sequelae
(a) acute rheumatic fever
(b) acute glomerulonephritis
(a) pharyngitis ( sore throat,tonsilitis)
- transmitted by resp droplets
- character: pain, rdness and swelling of post pharynx
- accompanied by greyish white tonsillar exudate and fever.
(b) scarlet fever
-dev of scarlet red rash
(c) skin and soft tissue infections
-impetigo
-cellulitis and erysipelas
(d) invasive streptoccoccal infections
-puerperal fever
- acuute endocarditis
-necrotizing fasciitis
- toxic shock syndrome
post streptococcal sequelae
(a) acute rheumatic fever
(b) acute glomerulonephritis
staphylococcus epidermidis
bacteraemia
native endocarditis
prosthetic valve endocarditis
infection of surgical wounds
infection of urinary tract
infection of prosthetic joint
native endocarditis
prosthetic valve endocarditis
infection of surgical wounds
infection of urinary tract
infection of prosthetic joint
staphylococcus aureus
pyogenic diseases
(a) localized skin infections-folliculitis, furuncles, carbuncles, abscesses
-posstoperative surgical wound infections (hospital acquired)
- traumatic wound infections following skin ijury and burns
(b) staphylococcal pneumonia
(c) invasive conditions-invasion of bloodstream (bacteraemia) and spread to numerous body sites lead to deep seate infections such as osteomyelitis, endocarditis and meningitis. A resulting septicaemia may be fatal.
toxin mediated diseases
(a) staphylococcal food poisoning
(b) toxic shock syndrome (TSS)
(c) Staphylococcal scalded skin syndrome-occurs in neonates
-
(a) localized skin infections-folliculitis, furuncles, carbuncles, abscesses
-posstoperative surgical wound infections (hospital acquired)
- traumatic wound infections following skin ijury and burns
(b) staphylococcal pneumonia
(c) invasive conditions-invasion of bloodstream (bacteraemia) and spread to numerous body sites lead to deep seate infections such as osteomyelitis, endocarditis and meningitis. A resulting septicaemia may be fatal.
toxin mediated diseases
(a) staphylococcal food poisoning
(b) toxic shock syndrome (TSS)
(c) Staphylococcal scalded skin syndrome-occurs in neonates
-
Thursday, December 17, 2009
Poxvirus-smallpox 54
Import features
1.They are brick-shape,dsDNA viruses.
2.They can be seen by the light microscope because of their large size
3.They contain a DNA-de
penndent RNA polymerase,not found in other DNA viruses because the virus replicates in the cytoplasm.
1.Smallpox (variola or alastrim ) virus.
2.Vaccinia virus and cowpox virus belong to orthopoxvirus genus.Members of orthopoxvirus cross -react and elicit neutralizing antibodies . Therefore, vaccinia virus was used in imuunization against smallpox.
3. Molluscum contagiosum virus belongs to a different genus.
Smallpox
The last endemic case occured in 1977 and 1980 the WHO General Assembly certified that smallpox had been eradicated. The importance of smallpox should not be forgotten because:
1. It had a marked impact on the development of civilization.
2. It is the first disease to be controlled by immunization.
3. It is the first virus disease for which chemoprophylaxis (Methisazone) was available.
4. It is the first to be eradicated.
Prevention
The disease was eradicated by the global use of the live attenuated vaccinia virus caccine. The success of the vaccine in eradicating smallpox was dependent upon five critical factors:
1. Smaallpox has a single, stable serotype.
2. There is no animal reservoir, and humans are the only host.
3. The antibody response is prompt.
4. The disease is easily recognized clinically.
5. There is no carrier state or subclinical infection.
1.They are brick-shape,dsDNA viruses.
2.They can be seen by the light microscope because of their large size
3.They contain a DNA-de
penndent RNA polymerase,not found in other DNA viruses because the virus replicates in the cytoplasm.
1.Smallpox (variola or alastrim ) virus.
2.Vaccinia virus and cowpox virus belong to orthopoxvirus genus.Members of orthopoxvirus cross -react and elicit neutralizing antibodies . Therefore, vaccinia virus was used in imuunization against smallpox.
3. Molluscum contagiosum virus belongs to a different genus.
Smallpox
The last endemic case occured in 1977 and 1980 the WHO General Assembly certified that smallpox had been eradicated. The importance of smallpox should not be forgotten because:
1. It had a marked impact on the development of civilization.
2. It is the first disease to be controlled by immunization.
3. It is the first virus disease for which chemoprophylaxis (Methisazone) was available.
4. It is the first to be eradicated.
Prevention
The disease was eradicated by the global use of the live attenuated vaccinia virus caccine. The success of the vaccine in eradicating smallpox was dependent upon five critical factors:
1. Smaallpox has a single, stable serotype.
2. There is no animal reservoir, and humans are the only host.
3. The antibody response is prompt.
4. The disease is easily recognized clinically.
5. There is no carrier state or subclinical infection.
Polyomavirus 53
Plyomavirus are of 2 types,JC and BK. They frequently cause inapparent persistent infections, whichmay reactivate under immunosupression and then result in overt disease. JC virus causes a rare but serious demyelinating disease, progressive multifocal leukoencephalopathy (PML), whereas reactivation of BK virus may result in haemorrhagic urnary tract infections especiallyin transplant patients. BKV and JCV also induces tumours if inoculated into newborn hamsters.
Simian vaculating virus (SV40) is another polyoma virus that can replicate in monkey and human cells. It is highly tumourigenic expermientaly in hamsters and can transform tissue culture cells
Simian vaculating virus (SV40) is another polyoma virus that can replicate in monkey and human cells. It is highly tumourigenic expermientaly in hamsters and can transform tissue culture cells
Human papillomavirus53
Human papillomaviruses (HPVs) are non enveloped ds DNA viruses with icosahedral capsids, 45-55nm in diameter.
Pathogenesis
HPV s induce epithelial cell proliferation. Cutaneous HPV types are transmitted by direct contact or via fomites, while transmission of genital types is through sexual route.The majority of HPV infections are self limite, but certain genital HPV types result in malignant tumors and also certain types of HPV play a role in pathogenesis of non melanoma skin cancers.
Cutaneous infection with HPVs occurs usually during childhood and is usually self limited. It manifests as plantar warts in soles of the feet as well as common warts in hands and arms.These warts are benign. Flat warts and epidermodysplasia verruciforms are other skin lesions which may progress to carcinoma.
Mucosal HPVs primarily infect the anogenital tract epithelium. Genital tract HPV infection is the most common sexually transmitted viral infection. Infections manifest as genital warts (condyloma acuminata) on the vulva, vagina, cervix, penis and anus, and laryngeal papilloma.
Diagnosis
HPV ca not be cultivated and serologic tests are not yet available. So the following methods are used:
1.Histopathology examination
2.DNA detection by DNA hybridization or PCR.
Treatment and prevention
There is no specific antiviral therapy.
2 aprroved vaccines gardasil and cervarix
Pathogenesis
HPV s induce epithelial cell proliferation. Cutaneous HPV types are transmitted by direct contact or via fomites, while transmission of genital types is through sexual route.The majority of HPV infections are self limite, but certain genital HPV types result in malignant tumors and also certain types of HPV play a role in pathogenesis of non melanoma skin cancers.
Cutaneous infection with HPVs occurs usually during childhood and is usually self limited. It manifests as plantar warts in soles of the feet as well as common warts in hands and arms.These warts are benign. Flat warts and epidermodysplasia verruciforms are other skin lesions which may progress to carcinoma.
Mucosal HPVs primarily infect the anogenital tract epithelium. Genital tract HPV infection is the most common sexually transmitted viral infection. Infections manifest as genital warts (condyloma acuminata) on the vulva, vagina, cervix, penis and anus, and laryngeal papilloma.
Diagnosis
HPV ca not be cultivated and serologic tests are not yet available. So the following methods are used:
1.Histopathology examination
2.DNA detection by DNA hybridization or PCR.
Treatment and prevention
There is no specific antiviral therapy.
2 aprroved vaccines gardasil and cervarix
parvoviruses B19---52
The parvoviridae family contains, small, non-enveloped, ssDNA viruses with icosahedral capsids. Medically impotant genera are:
1.Dependovirus( e.g adeno-associated virus) is a defective virus and requires helper virus for its own replication. There is no specific disease caused by dependoviruses.
2. Erythrovirus ic capable of autonomous replication, which is independent of helper virus. Parvovirus B19 is the only member, and is the only parvovirus that is human pathogen. It is associated with several defined clinical syndromes. Human erythroid progenitor cells are the specific host cells, where the virus replicates inside the nucleus.
Pathogenesis of Parvovirus B19
Infection is transmiited by resp secretions and saliva, transplacental infection of the foetus, and blood transfusion or blood product therapy. Humans are the natural reservoir.
Most of the infections are asymptomatic. Human infection include :
1.Erythema infectiosum (slapped-cheeks syndrome, fifth disease).
2. Transient Aplastic Crisis (TAC)
3. Foetal infections leading to foetal hydrops and foetal loss.
4. Chronic B19 infections in the immunocompromised patients such as chronic anaemia, leukopenia, or thrombocytopenia.
Erythema infectiosum (EI) and transient aplastic crisis (TAC) are the commonest syndromes.
Anaemia is due to B19 infection of the red blood cell precursors. The rash associated with erythema infectiosum is due to infection of the endothelial cells as well as deposition of immune complexes. These immune complexes also contribute to the arthritis seen in adults. Infection provides lifelong immunity.
Lab Diagnosis
Cultivation of parvovirus B19 is difficult and not routinely used for diagnosis. Diagnosis is made either by direct detection of B19 antigen or DNA in clinical material, or by serologic tests.
Treatment and prevention
There is no antiviral therapy and no vaccine. Pooled immunoglobulins may be useful in chronic B19 infections in immunocompromised patients.
1.Dependovirus( e.g adeno-associated virus) is a defective virus and requires helper virus for its own replication. There is no specific disease caused by dependoviruses.
2. Erythrovirus ic capable of autonomous replication, which is independent of helper virus. Parvovirus B19 is the only member, and is the only parvovirus that is human pathogen. It is associated with several defined clinical syndromes. Human erythroid progenitor cells are the specific host cells, where the virus replicates inside the nucleus.
Pathogenesis of Parvovirus B19
Infection is transmiited by resp secretions and saliva, transplacental infection of the foetus, and blood transfusion or blood product therapy. Humans are the natural reservoir.
Most of the infections are asymptomatic. Human infection include :
1.Erythema infectiosum (slapped-cheeks syndrome, fifth disease).
2. Transient Aplastic Crisis (TAC)
3. Foetal infections leading to foetal hydrops and foetal loss.
4. Chronic B19 infections in the immunocompromised patients such as chronic anaemia, leukopenia, or thrombocytopenia.
Erythema infectiosum (EI) and transient aplastic crisis (TAC) are the commonest syndromes.
Anaemia is due to B19 infection of the red blood cell precursors. The rash associated with erythema infectiosum is due to infection of the endothelial cells as well as deposition of immune complexes. These immune complexes also contribute to the arthritis seen in adults. Infection provides lifelong immunity.
Lab Diagnosis
Cultivation of parvovirus B19 is difficult and not routinely used for diagnosis. Diagnosis is made either by direct detection of B19 antigen or DNA in clinical material, or by serologic tests.
Treatment and prevention
There is no antiviral therapy and no vaccine. Pooled immunoglobulins may be useful in chronic B19 infections in immunocompromised patients.
Adenoviruses 50
Charasteristic features
Morphology
Adenovirus Infection in human
Lab Diagnosis
Treatment
Prevention
Morphology
Adenovirus Infection in human
Lab Diagnosis
Treatment
Prevention
HHV6+7+8(49)
There are recently described viruses. HHV6 is the cause of a common disease of infancy called Exanthem subitum (roseola infantum or sixth disease), characterized by high fever and skin rash. HHV 7 is associated with persistent salivary glands infection.
Human Herpes Virus 8
(Kaposi's Sarcoma-Related Herpesvirus)
The new virus was identified in 1994 from tissue of Kaposi's sarcoma in patients with AIDS.
Human Herpes Virus 8
(Kaposi's Sarcoma-Related Herpesvirus)
The new virus was identified in 1994 from tissue of Kaposi's sarcoma in patients with AIDS.
Wednesday, December 16, 2009
Cytomegaloviruses49
The name cytomegalovirus was chosen on account of the swollen state of virus-infected cells. The virus is widespread.
Primary infections occur in 40-60% of individuals and the virus persists in the host for life (latent infection). Reactivation is common. Infection may be tranplacental (congenital) or by other methods as close contact, sexual intercourse, breast feeding, blood transfusion and organ transplantation.
Clinical features: Most infections are asymptomatic:
1. Congenital infection: It may cause still birth or abortion. In 5% of infected babies, congenital abnormalities occur "cytomegalic inclusion disease". The most common features of the syndrome are growth retardation, microcephaly, hepatosplenomegaly, thrombocytopenia and blindness.
2 Mononucleosis syndrome; similar to that caused by EBV. However, pharyngitis and lymphadenophaty are unusual and heterophil antibodies are not found.
3 Infection in immunocomproised patients; my manifest as pneumonitis, encephalitis, hepatitis, retinitis...etc.
Lab diagnosis
1. Isolation of the virus from throat washings or urine on tissue culture.
2. Detection of viral DNA by PCR or hybridization assay.
3. Detection of viral antigens in urine or saliva.
4. Serodiagnosis: Detection of CMV IgM or rising titre of IgG by EIA or latex agglutination assay.
Treatment
Ganiclovir has been used successfully in treatment of CMV infections in immunosuppressed patients.
Prevention and control
-Screening blood donors and organ donors and exclusion of seropositive ones.
- Vaccines are under trial.
Primary infections occur in 40-60% of individuals and the virus persists in the host for life (latent infection). Reactivation is common. Infection may be tranplacental (congenital) or by other methods as close contact, sexual intercourse, breast feeding, blood transfusion and organ transplantation.
Clinical features: Most infections are asymptomatic:
1. Congenital infection: It may cause still birth or abortion. In 5% of infected babies, congenital abnormalities occur "cytomegalic inclusion disease". The most common features of the syndrome are growth retardation, microcephaly, hepatosplenomegaly, thrombocytopenia and blindness.
2 Mononucleosis syndrome; similar to that caused by EBV. However, pharyngitis and lymphadenophaty are unusual and heterophil antibodies are not found.
3 Infection in immunocomproised patients; my manifest as pneumonitis, encephalitis, hepatitis, retinitis...etc.
Lab diagnosis
1. Isolation of the virus from throat washings or urine on tissue culture.
2. Detection of viral DNA by PCR or hybridization assay.
3. Detection of viral antigens in urine or saliva.
4. Serodiagnosis: Detection of CMV IgM or rising titre of IgG by EIA or latex agglutination assay.
Treatment
Ganiclovir has been used successfully in treatment of CMV infections in immunosuppressed patients.
Prevention and control
-Screening blood donors and organ donors and exclusion of seropositive ones.
- Vaccines are under trial.
Epstein Bar viruses (EBV)48
Infection with EBV is wide spread and most infections are asymptomatic. The link between EBV and a variety of lymphoproliferative disease is now clear.
1.EBV is the causative organism of the classical infectious mononucleosis (glandular fever)
2. Other EBV associated diseases are:
Nasopharyngeal carcinoma
Burkitt's lymphoma
Oral hairy leukoplakia (seen in AIDS patients)
Hodgkin's disease
T cell lymphoma
The virus is excreted and transmitted via the saliva and multiply in the oropharyngeal mucosa. EBV receptors are also present on B-lymphocytes
then about Infectious Mononucleosis ( Glandular Fever)
1.EBV is the causative organism of the classical infectious mononucleosis (glandular fever)
2. Other EBV associated diseases are:
Nasopharyngeal carcinoma
Burkitt's lymphoma
Oral hairy leukoplakia (seen in AIDS patients)
Hodgkin's disease
T cell lymphoma
The virus is excreted and transmitted via the saliva and multiply in the oropharyngeal mucosa. EBV receptors are also present on B-lymphocytes
then about Infectious Mononucleosis ( Glandular Fever)
VZV47
Infection with VZV presents in two clinical forms: The proary infection;varicella(or chickenpox) is a generalized eruption, whereas the reactivation; zozter (or shingles) is localized. There is only one antigenic type of VZV.
Pathogenesis and clinical picture
1. Varicella (chickenpox) : The virus is thought to enter, by droplet infection, through the upper respiratory tract. After an incubation period about 2 weeks, the typical rash of varicella appears first on the trunk then spread to the face and limbs. The skin rash is initially macular and rapidly evolves through papules to clear vesicles. The vesicles change to pustules which dry to form scabs which heal without scar formation.
The patient is usually a child 4-10 years old. Disease usually runs a benig course. Some cases are complicated by secondary infection of skin, pneumonia or cerebellar ataxia. Pregnant women infected in the first half of pregnancy may pass infection to the foetus which at birth may show foetal varicella syndrome with high mortality rate.
2. Zoster (shingles): It results from reactivation of latent varicella infection in the neurons. The virus reaches the ganglion from the periphery by travelling along nerve axons or by blood during viraemic stage of varicella infection during childhood.
The disease usually occurs in older people and manifests as painful vesicular eruption, unilateral and confined to one dermatome usually thoracic or lumbar. The condotion may follow trauma to the spinal cord or may be complicate lymphomas, leikaemia or immuno supression.
Treatment
Acyclovir givenI.V is effective in the treatment of varicella and zoster. It is not used for all cases, but indicated in the following conditions:
1. Immunocompromized patients
2. Ophthalmic zoster to avoid corneal scarring
3. Varicella complicated by pneumonia
4. Neonatal infection
Prevention and control
1. Acyclovir and interferon are given to immune deficient children.
2.VZ immune globulin (VZIG) of high antibody titre should be given to contacts of cases to prevent development of disease.
3. Live attenuated varicella vaccine( Varivax) is given as one dose for children1-12 years of age.
Pathogenesis and clinical picture
1. Varicella (chickenpox) : The virus is thought to enter, by droplet infection, through the upper respiratory tract. After an incubation period about 2 weeks, the typical rash of varicella appears first on the trunk then spread to the face and limbs. The skin rash is initially macular and rapidly evolves through papules to clear vesicles. The vesicles change to pustules which dry to form scabs which heal without scar formation.
The patient is usually a child 4-10 years old. Disease usually runs a benig course. Some cases are complicated by secondary infection of skin, pneumonia or cerebellar ataxia. Pregnant women infected in the first half of pregnancy may pass infection to the foetus which at birth may show foetal varicella syndrome with high mortality rate.
2. Zoster (shingles): It results from reactivation of latent varicella infection in the neurons. The virus reaches the ganglion from the periphery by travelling along nerve axons or by blood during viraemic stage of varicella infection during childhood.
The disease usually occurs in older people and manifests as painful vesicular eruption, unilateral and confined to one dermatome usually thoracic or lumbar. The condotion may follow trauma to the spinal cord or may be complicate lymphomas, leikaemia or immuno supression.
Treatment
Acyclovir givenI.V is effective in the treatment of varicella and zoster. It is not used for all cases, but indicated in the following conditions:
1. Immunocompromized patients
2. Ophthalmic zoster to avoid corneal scarring
3. Varicella complicated by pneumonia
4. Neonatal infection
Prevention and control
1. Acyclovir and interferon are given to immune deficient children.
2.VZ immune globulin (VZIG) of high antibody titre should be given to contacts of cases to prevent development of disease.
3. Live attenuated varicella vaccine( Varivax) is given as one dose for children1-12 years of age.
HSV45
HSV1 dan HSV2
Pathogenesis and clinical picture
Clinical types of HSV infection
Lab diagnosis of HSV infection
Treatment
Prevention
Pathogenesis and clinical picture
Clinical types of HSV infection
Lab diagnosis of HSV infection
Treatment
Prevention
Astroviruses 35
Astroviruses are about 30nm diameter and contain a positive-sense ssRNA. Thet exhibit a distinctive morphology in the electron microscope due to presence of pointed star shapes on the particles.
Astroviruses cause sporadic gastroenteritis in infants, children, elderly and immunocompromised people. Astroviruses are transmitted from person to person by the fecal oral route through contaminated food, water, person-to-person contact, or contaminated surfaces.
Astroviruses cause sporadic gastroenteritis in infants, children, elderly and immunocompromised people. Astroviruses are transmitted from person to person by the fecal oral route through contaminated food, water, person-to-person contact, or contaminated surfaces.
norwalk viruses34
The best known of the human caliciviruses is Norwalk virus, which is the most important cause of epidemic viral (non bacterial) gastroenteritis in school children and adults.Norwalk virus was first discovered during an epidemic of gastroenteritis that occur in Norwalk, Ohio, in 1968.
Characteristic Features
- Caliciviruses are small( 27-nm) , round nonenveloped positive sense ssRNA viruses.
-They have a single structural protein.
-They have cup-shaped depressions on their capsid surface (hence their name which is derived from calyx). These identification give the virion a 'Star of David" appearance in the electron microscope.
-Human caliciviruses have not been cultivated in vitro
Epidemiology
About half of the outbreaks of acute infectious non bacterial gastroenteritis are due to Norwalk virus. The disease occurs worldwide ad is common in older children and adults. Out breaks occur in such settings as camps, retaurants, cruise ships and schools. Out breaks are associated with contaminated food, water, or by raw or undercooked shellfish, particulrly oysters, Norwalk virus has a low infectious dose (10 virus particles) and relative stability in the environment (resists chlorine)
Pathogenesis
The virus can be transmitted from person to person by the faeco oral route. Viruses grow in the small intestine, causing transient lesions of the intestinal mucosa, and are shed in faeces.
Diagnosis
The diagnosis is suggested by acute gastroenteritis in an outbreak setting. It may beconfirmed by antigen detection or observation of an antibody rise.
Control
No specific antiviral therapy or vaccine is available for Norwalk or other human calicivirus gastroenteritits. Hand washing and careful monitoring of water purification are the most important measures in the control of infection.
Characteristic Features
- Caliciviruses are small( 27-nm) , round nonenveloped positive sense ssRNA viruses.
-They have a single structural protein.
-They have cup-shaped depressions on their capsid surface (hence their name which is derived from calyx). These identification give the virion a 'Star of David" appearance in the electron microscope.
-Human caliciviruses have not been cultivated in vitro
Epidemiology
About half of the outbreaks of acute infectious non bacterial gastroenteritis are due to Norwalk virus. The disease occurs worldwide ad is common in older children and adults. Out breaks occur in such settings as camps, retaurants, cruise ships and schools. Out breaks are associated with contaminated food, water, or by raw or undercooked shellfish, particulrly oysters, Norwalk virus has a low infectious dose (10 virus particles) and relative stability in the environment (resists chlorine)
Pathogenesis
The virus can be transmitted from person to person by the faeco oral route. Viruses grow in the small intestine, causing transient lesions of the intestinal mucosa, and are shed in faeces.
Diagnosis
The diagnosis is suggested by acute gastroenteritis in an outbreak setting. It may beconfirmed by antigen detection or observation of an antibody rise.
Control
No specific antiviral therapy or vaccine is available for Norwalk or other human calicivirus gastroenteritits. Hand washing and careful monitoring of water purification are the most important measures in the control of infection.
Tuesday, December 15, 2009
Rotavirus 34
Reoviruses are medium sized viruses with a segmented dsRNA genome. The family includes the human rotaviruses, the most important causes of infantile gastroenteritis around the world.
Rotavirus genome is surrounded with a double-layered protein coat giving the wheel appearance by electron microscope (Rota=wheel). It is transmitted via faeco-oral route. Incubation period is 1-4 days.
Lab Diagnosis
1 Exam of stools by electron microscope to detect the wheel like viral particles.
2 Detection of viral antigen in stools by serological tests.
3 Using rotavirus specific nuclei acid probe to detect virus particles in stools ( dot hybridization)
4 Demonstration rising titres of the serum antibodies by ELISA.
Treatment
By restoring fluid and electrolyte balance.
Prophylaxis
-Hygienic measures to control faeco-oral infections
-Living attenuated accine is now available.
Rotavirus genome is surrounded with a double-layered protein coat giving the wheel appearance by electron microscope (Rota=wheel). It is transmitted via faeco-oral route. Incubation period is 1-4 days.
Lab Diagnosis
1 Exam of stools by electron microscope to detect the wheel like viral particles.
2 Detection of viral antigen in stools by serological tests.
3 Using rotavirus specific nuclei acid probe to detect virus particles in stools ( dot hybridization)
4 Demonstration rising titres of the serum antibodies by ELISA.
Treatment
By restoring fluid and electrolyte balance.
Prophylaxis
-Hygienic measures to control faeco-oral infections
-Living attenuated accine is now available.
coronaviruses33
Large, enveloped, positive sense stranded RNA viruses. They have the largest RNA genome.
Coronaviridae family was distinguished on basis of its distinctive morphology and received the name corona because of the crown like appearance of the surface projections.
The human coronaviruses(CoVs) are responsibe for about 30% of mild upper repiratory tract illnesses, ( common cold). Recentyly, CoVs have received the newly emerged SARS-CoV which causes the severe acute respiratory syndrome (SARS) that has been recently reported in Asia, North America and Europe.
Clinical aspects of SARS
- After an incubation period of 2-10 days, onset of the disease is characterized by fever, chills/rigors, headache, myalgia and malaise.
- Respiratory symptoms often begin 3-7 days ater symptom onset and peak in the second wee.
- Diarrhoea has been a prominent feature of early illness in some cases.
SARS transmission
Droplet s and contact of the skin or fomites that are contaminated with infectious dropekrs and then touchinh the eyes, nose or mouth.
N.B Causative agents of common cold include:
1.Rhinovirus causes about 50% of cases.
2. Human coronaviruses; are responsible for about 30% of cases.
Coronaviridae family was distinguished on basis of its distinctive morphology and received the name corona because of the crown like appearance of the surface projections.
The human coronaviruses(CoVs) are responsibe for about 30% of mild upper repiratory tract illnesses, ( common cold). Recentyly, CoVs have received the newly emerged SARS-CoV which causes the severe acute respiratory syndrome (SARS) that has been recently reported in Asia, North America and Europe.
Clinical aspects of SARS
- After an incubation period of 2-10 days, onset of the disease is characterized by fever, chills/rigors, headache, myalgia and malaise.
- Respiratory symptoms often begin 3-7 days ater symptom onset and peak in the second wee.
- Diarrhoea has been a prominent feature of early illness in some cases.
SARS transmission
Droplet s and contact of the skin or fomites that are contaminated with infectious dropekrs and then touchinh the eyes, nose or mouth.
N.B Causative agents of common cold include:
1.Rhinovirus causes about 50% of cases.
2. Human coronaviruses; are responsible for about 30% of cases.
rubella(german measles)32
properties of virus
pathogenesis and clinical findings
infection during pregnancy
lab diagnosis
prevention and control
pathogenesis and clinical findings
infection during pregnancy
lab diagnosis
prevention and control
Respiratory Syncytial Virus (RSV)
-RSV ia an important cause of olower resp tract disease in infants and young children, underf one year of age.
-No viraemia.
-Most cases are asymptomatic.
-The disease range from common cold-like illness inadults to febrile bronchiolitis, ronchitis and pneumonia in infants and young children.
Diagnosis
Antigen detection in resp secretions.
Treatment
Ribavirin aerosol
Prophylaxis
No specific prophylaxis is available
-No viraemia.
-Most cases are asymptomatic.
-The disease range from common cold-like illness inadults to febrile bronchiolitis, ronchitis and pneumonia in infants and young children.
Diagnosis
Antigen detection in resp secretions.
Treatment
Ribavirin aerosol
Prophylaxis
No specific prophylaxis is available
measles and rubeola virus30
Measles is an acute highly infectious disease of children and no immune adults.
The virus has only one stable antigenic type.
Pathogenesis and clinical findings
-Man is the olny natural host for the virus
- Transmission is by aerosol
- Incubation period is 8-12 days.
- The virus replicates locally in the mucosa and regional lymph nodes of the upper repiratory tract followed by viraemia and localization of virus in and mucous membranes.
- After a prodrome of 2-4 days, a viraemic phase starts that manifests bu high fever, sneezing, coughing, eye pains and as "Koplik's spots" on the inside of the cheeks. The eruptivepase follows and is characterized by maculopapular pink skin rash mainly on the trunk region.
-Complication may occur in debilitated children as penumonia, otitis media, and post-measles encephalitis.
Treatment
-No specific antiviral drug is effective.
-Early administration of human globulins may be effective in modifying the disease.
-Bacterial superinfections are to be treated by antibiotics.
Prophylaxis
Active immunization by a living attenuated vaccine. It is usually available in combination with mumps and rubella (MMR). It is better given in two doses,the first at 15 months and the second at school age.
Passive Immunization: Human globulins are given to protect susceptible contacts.
Immunity: Life-long immunity is gained after a single infection. This is due to :
-Measles virus is of only one stable antigenic type.
-There is a stage of viraemia, so circulating antibodies are protective.
The virus has only one stable antigenic type.
Pathogenesis and clinical findings
-Man is the olny natural host for the virus
- Transmission is by aerosol
- Incubation period is 8-12 days.
- The virus replicates locally in the mucosa and regional lymph nodes of the upper repiratory tract followed by viraemia and localization of virus in and mucous membranes.
- After a prodrome of 2-4 days, a viraemic phase starts that manifests bu high fever, sneezing, coughing, eye pains and as "Koplik's spots" on the inside of the cheeks. The eruptivepase follows and is characterized by maculopapular pink skin rash mainly on the trunk region.
-Complication may occur in debilitated children as penumonia, otitis media, and post-measles encephalitis.
Treatment
-No specific antiviral drug is effective.
-Early administration of human globulins may be effective in modifying the disease.
-Bacterial superinfections are to be treated by antibiotics.
Prophylaxis
Active immunization by a living attenuated vaccine. It is usually available in combination with mumps and rubella (MMR). It is better given in two doses,the first at 15 months and the second at school age.
Passive Immunization: Human globulins are given to protect susceptible contacts.
Immunity: Life-long immunity is gained after a single infection. This is due to :
-Measles virus is of only one stable antigenic type.
-There is a stage of viraemia, so circulating antibodies are protective.
Mumps 30
-Mumps is an acute contagious disease of children characterized by nonsupurativeenlargement of one both parotid glands (parotitis).
-Mumps virus mostly causes a mild childhood disease, but in adults it may be complicated with meningitis and orchitis.
-At least 1/3 of infections are asymptomatic.
Pathogenesis and clinical findings
- Man is the only host for mumps virus.
-Transmission is by droplets.
-The virus replicates locally in the resp mucosa and regional lymph nodes, followed by viraemia and localization of the virus in salivary glands especially the parotid glands. The virusmay also disseminate into testes, ovaries, pancreas and brain.
-After an incubation period of 2-3 weeks, the disease manifests as fever and painful swelling of the parotid glands.
Prevention and control
1.Living attenuated vaccine for children over 1 year. It is given in a single IM dose.
2. Mumps vaccine is available in combination with other 2 living attenuated virus vaccines, measles and rubella (MMR vaccine).
Immunity is life-lasting immunity after a single infection. This is because:
-Only one stable antigenic type exists.
- There is a stage of viraemia, so circulating virus neutralizing antibodies (IgM and IgG) are protective.
-Mumps virus mostly causes a mild childhood disease, but in adults it may be complicated with meningitis and orchitis.
-At least 1/3 of infections are asymptomatic.
Pathogenesis and clinical findings
- Man is the only host for mumps virus.
-Transmission is by droplets.
-The virus replicates locally in the resp mucosa and regional lymph nodes, followed by viraemia and localization of the virus in salivary glands especially the parotid glands. The virusmay also disseminate into testes, ovaries, pancreas and brain.
-After an incubation period of 2-3 weeks, the disease manifests as fever and painful swelling of the parotid glands.
Prevention and control
1.Living attenuated vaccine for children over 1 year. It is given in a single IM dose.
2. Mumps vaccine is available in combination with other 2 living attenuated virus vaccines, measles and rubella (MMR vaccine).
Immunity is life-lasting immunity after a single infection. This is because:
-Only one stable antigenic type exists.
- There is a stage of viraemia, so circulating virus neutralizing antibodies (IgM and IgG) are protective.
parainfluenza viruses29
They cause severe lower respiratory tract disease particularly in infants and young children.
After an incubation period of 2-6 days, the disease manifests as mild fever, rhinitis and bronchitis.
Spasmodic laryngotracheitis (croup) and pneumonia may occur in severe cases.
After an incubation period of 2-6 days, the disease manifests as mild fever, rhinitis and bronchitis.
Spasmodic laryngotracheitis (croup) and pneumonia may occur in severe cases.
influenza viruses 27
classification , antigenic types and host range
morphology and structure
gene reassortment
antigenic change of the influenza virus and its impact on influenza epidemics and vaccine
preparation
pathogenesis andclinical picture
prevention
morphology and structure
gene reassortment
antigenic change of the influenza virus and its impact on influenza epidemics and vaccine
preparation
pathogenesis andclinical picture
prevention
Monday, December 14, 2009
Rhinoviruses
The rhinoirus group derives its name from predominant site of replication (the nose). The rhinovirus group is the commonest cause of the acute resp illness known as common cold.Over 100 serotypes of rhinoviruses are currently recognized.
Pathogenesis and clinical significance
Transmission is through drolet and hand to hand contact followed by self inoculation of virus into the nose and conjunctiva.
Incubation period is 2-3 days.
The virus multiplies locqally without blood invasion.
Peak of virus shedding coincides with acute rhinitiss, and virus becomes usually undetectable after 4 or 5 days.
Type specific immunity that correlates best with the local production of IgA.
2ry bacterial infection may cause otitis media, sinusitis, bronchitis or bronchopneumonia especially in children.
Repeated infection of common cold could be explained by :
1. Multiplicity of antigenic types ( over 100)
2. Being a superficial infection, serum antibodies plays no signigficance role in immunity
3. Immunity is mainly superficial by IgA and interferon (short term immunity)
Vaccine produce is not practical.
Pathogenesis and clinical significance
Transmission is through drolet and hand to hand contact followed by self inoculation of virus into the nose and conjunctiva.
Incubation period is 2-3 days.
The virus multiplies locqally without blood invasion.
Peak of virus shedding coincides with acute rhinitiss, and virus becomes usually undetectable after 4 or 5 days.
Type specific immunity that correlates best with the local production of IgA.
2ry bacterial infection may cause otitis media, sinusitis, bronchitis or bronchopneumonia especially in children.
Repeated infection of common cold could be explained by :
1. Multiplicity of antigenic types ( over 100)
2. Being a superficial infection, serum antibodies plays no signigficance role in immunity
3. Immunity is mainly superficial by IgA and interferon (short term immunity)
Vaccine produce is not practical.
HIV
MUKE 16
grup dan subtype
morphology dan truktur
HIV antigen
pathogenesis of HIV infection
HIV transmission
Disinfection
Clinical background
Diagnosis
Rawatan
Monitoring antiHIV therapy
Post exposure chemoprophylaxis
grup dan subtype
morphology dan truktur
HIV antigen
pathogenesis of HIV infection
HIV transmission
Disinfection
Clinical background
Diagnosis
Rawatan
Monitoring antiHIV therapy
Post exposure chemoprophylaxis
Hepatitis G
HGV is also known as GBV-C virus. It is a blood borne virus. Most patient show evidence of co-infection with other viruses such as HV or HCV.
Diagnosis
a) Anti-HGV antibodies in the serum can be detected.
b) Viral RNA can also be detected in bood by PCR.
Diagnosis
a) Anti-HGV antibodies in the serum can be detected.
b) Viral RNA can also be detected in bood by PCR.
Hepatitis E Virus (HEV)
It is a distinctive form of NANB hepatitis, characterized by faeco-oral transmission and a short incubation period of about 6 weeks.
Disease is of self limited natureoccuring either sporadic or n the form of epidemics. It affects mainly young adults.
There is little riskof development of chronic hepatitis, but there is high mortality rate due to disseminated intravascular coagulation especially in pregnant females.
Diagnosis
a)PCR is used to detect viral RNA in stools.
b) Detection of anti-hepatitis E virus IgM and IgG by ELISA.
Disease is of self limited natureoccuring either sporadic or n the form of epidemics. It affects mainly young adults.
There is little riskof development of chronic hepatitis, but there is high mortality rate due to disseminated intravascular coagulation especially in pregnant females.
Diagnosis
a)PCR is used to detect viral RNA in stools.
b) Detection of anti-hepatitis E virus IgM and IgG by ELISA.
Hepatitis Delta Virus (HDV)
The hepatitis delta virus is a unique defective spherical 36 nm virus, composed of a core containing a circular, ss-RNA genome, surrounded by HB surface antigen. HDV can only replicate in patients with HBV infection.
Infection is either a coinfection where the patient acquires both viruses at the same time or a superinfection.
As HDV is dependent on HBV it follows a similar epidemiology. It can be controlled through control of hepatitis B infection.
Diagnosis
By detection of anti HDV antibodies.
Infection is either a coinfection where the patient acquires both viruses at the same time or a superinfection.
As HDV is dependent on HBV it follows a similar epidemiology. It can be controlled through control of hepatitis B infection.
Diagnosis
By detection of anti HDV antibodies.
Hepatitis C
HCV is a member of the Hepacivirus genus in Flaviviridae family that causes over 90% of NANB (non-A, non-B) transfusion-transmitted hepatitis. HCV has a small positive single stranded RNA genome (++ssRNA). There are 6 genotypes.
Epidemiology
1.HCV has a worldwide distribution and is particularly prevalent in the Middle East.
2. Similar toHBV, HCV is transmitted mainly pareterally through skin and mucous membranes. Also there is perinatal transmision.
3.Still 40% of cases shows no definable source or route of infection.
4.50% of HCV infections are associated with development of chronic active hepatitis that ends in cirrhosis o hepatocellular carcinoma.
Lab Diagnosis
1. Detection of anti-HCV antibodies by ELISA, or the more specific RIBA test (recombinant immunoblotting assay). Seroconversion may take up to 6 months.
2. PCR for detection of viral RNA in blood. This useful in:
a) Diagnosis of early cases before seroconversion.
b) Serologically confirmed cases to demonstrate active viral replication and, thus the need for therapy.
c) Follow up the response of treatment.
d) Genotyping of HCV.
Control
No specific vaccine is available. Prevention is mainly directed at minimizing exposure as that of preventing HBV infection.
Treatment
A combnation of alpha-interferon and antiviral chemotherapy (ribavirin)
Epidemiology
1.HCV has a worldwide distribution and is particularly prevalent in the Middle East.
2. Similar toHBV, HCV is transmitted mainly pareterally through skin and mucous membranes. Also there is perinatal transmision.
3.Still 40% of cases shows no definable source or route of infection.
4.50% of HCV infections are associated with development of chronic active hepatitis that ends in cirrhosis o hepatocellular carcinoma.
Lab Diagnosis
1. Detection of anti-HCV antibodies by ELISA, or the more specific RIBA test (recombinant immunoblotting assay). Seroconversion may take up to 6 months.
2. PCR for detection of viral RNA in blood. This useful in:
a) Diagnosis of early cases before seroconversion.
b) Serologically confirmed cases to demonstrate active viral replication and, thus the need for therapy.
c) Follow up the response of treatment.
d) Genotyping of HCV.
Control
No specific vaccine is available. Prevention is mainly directed at minimizing exposure as that of preventing HBV infection.
Treatment
A combnation of alpha-interferon and antiviral chemotherapy (ribavirin)
Sunday, December 13, 2009
Hepatitis A
HAV, originally classified as Enterovirus type 72, is now considered to be the prototype of Hepatovirus genus in the Picornaviridae family. HAV is a non enveloped virus with a genome composed of positive-sense ssRNA, measuring 27nm in diameter. Thereis only one serotype. It is destroyed by boiling for 5 min and by treatment with chlorine.
HAV causes hepatitis A which has been called infectious hepatitis in the past. The disease occurs in sporadic or epidemic forms.
Pathogenesis
The host range for this virus is limited to humans and a few other primates. The virus is transmitted mainly by faeco-oralroute usually through ingestion of contaminated fooa and water. It affects children and young adults. Increased risk of transmission is due to decreased sanitary hygienic factors.
Clinical features
The incubation period is 2-6 weeks. Asymptomatic and subclinical infections are common in children. Viral hepatitis may be preceded by generalized gastrointestinal symptoms and fever. Nausea, vomiting, and anorexia are common symptoms. Many cases are wothout jaundice. Hepatitis A infection is usually mild, self limited and does not progress to chronic hepatitis.
Laboratory diagnosis
1 Marked elevation of liver transaminase and bilirubin.
2Detection of anti-HAV IgM (by RIA or ELISA) is diagnostic of acute phase.
3Detection of anti-HAV IgG during convalescnece. It indicates immunity and may persist for decades.
4Detection of HAV particles in stools or blood by RIA,PCR, genetic probes, or electron microscope.
Prevention and control
1Proper hand washing, chlorination or boiling of drinking water.
2 Careful disposal of sewage and avoiding contamination of fod and water.
3 An intactivated vaccine (Havrix) can be given intramuscularly (IM) as two doses above 2 years of age who live in endemic countries.
4HAV immune globulin for post exposure prophylaxis to prevent disease in the immunodeficient.
5Proper cooking.
HAV causes hepatitis A which has been called infectious hepatitis in the past. The disease occurs in sporadic or epidemic forms.
Pathogenesis
The host range for this virus is limited to humans and a few other primates. The virus is transmitted mainly by faeco-oralroute usually through ingestion of contaminated fooa and water. It affects children and young adults. Increased risk of transmission is due to decreased sanitary hygienic factors.
Clinical features
The incubation period is 2-6 weeks. Asymptomatic and subclinical infections are common in children. Viral hepatitis may be preceded by generalized gastrointestinal symptoms and fever. Nausea, vomiting, and anorexia are common symptoms. Many cases are wothout jaundice. Hepatitis A infection is usually mild, self limited and does not progress to chronic hepatitis.
Laboratory diagnosis
1 Marked elevation of liver transaminase and bilirubin.
2Detection of anti-HAV IgM (by RIA or ELISA) is diagnostic of acute phase.
3Detection of anti-HAV IgG during convalescnece. It indicates immunity and may persist for decades.
4Detection of HAV particles in stools or blood by RIA,PCR, genetic probes, or electron microscope.
Prevention and control
1Proper hand washing, chlorination or boiling of drinking water.
2 Careful disposal of sewage and avoiding contamination of fod and water.
3 An intactivated vaccine (Havrix) can be given intramuscularly (IM) as two doses above 2 years of age who live in endemic countries.
4HAV immune globulin for post exposure prophylaxis to prevent disease in the immunodeficient.
5Proper cooking.
Subscribe to:
Posts (Atom)