Microbiology Flashcards
the species of orientia called?
O. tsutsugamushi
what different between orientia and rickettsia
in 16S rRNA sequence and cell wall structure
type of Rickettsia & Orientia
short bacilli
stain of Rickettsia & Orientia
Giemsa stain
culture of Rickettsia & Orientia and why this culture
tissue culture
embryonated eggs
experimental animals
because they are obligate intracellular
mode of transmission of Rickettsia & Orientia
by arthropods
ticks and mites inject bacteria to blood
lice and fleas in feces on skin
mention the Rickettsia & Orientia species and caused disease
R. prowazeki»>Epidemic typhus (man louse)
R. typhi»> Endemic typhus (rat flea)
O.tsutsugamushi»>Scrub typhus (rodents mites)
R. rickettsii»>Rockey mountain spotted fever (dogs and rodents tick)
symptoms of Epidemic typhus
prolonged fever
severe prostration
skin rash
enlargment of liver and spleen
mode of transmission and pathogenesis of Epidemic typhus
louse»feces>blood»capillary endothelium causing vasculitis in heart and brain» Disseminated intravascular coagulation and vascular occlusion
what is brill-zineser disease
It is caused when the rickettsia remains latent in lymph nodes for several years then activated due to lacking immunity to produce epidemic disease again
mode of transmission of R. typhi
is transmitted from rat to man by fleas
mode of trasmission of rocky mountain spotted fever
transovarian among ticks
Dogs and rodents are also resevoirs of infection
symptoms of rocky mountain spotted fever
non specific symptoms
The typical rash, which appears 2-6 days later, begins With macules that progress to petechiae that appear first on hands and feet then move to the trunk.
* CNS manifestations e.g. delirium, coma, D1C and circulatory collapse may occur in severe cases. It can be fatal if untreated.
diagnosis of rickettsial disease
-
Direct detection in blood and skin biopsy specimens from the rash; by immuno-histochemical methods and PCR
* 2. inoculation in pigs, mice, yolk sac of embryonated eggs which replaced by tissue culture
* 3. serologic diagnosis
causes Q fever
Coxietta burnetii
difference between rickettsia and coxiella
coxiella is being more resistant to drying, disinfectants and UV
form endospores and its function
coxiella burnetti which make coxiella able to survive for months (in dried animal discharges (placental tissues or aminiotic fluid)
faeces, urine or milk
which phase is a virulent phase of Coxiella Burnetii
Phase 1
mode of infection of Coxiella burnetti (Q fever)
- inhalation of dust or aerosols contaminated with infected animal discharge and excreta
- consumption of unpasteurized infected milk
it not detected in blood (has negative blood culture result)
Coxiella burnetii
pathogenesis and clinical picture of Q fever
- infection of alveolar macrophages and a brief rickettsemia due to inhalation of infected aerosols
- acute disease begins with fever and influenza-like symptoms
- pneumonia and hepatitis
- Chronic Q fever can make life threatening endocarditis in abnormal patients
Diagnosis of Coxiella burnetii
serologic detection of a rising antibody titre to phase I or II
Indirect immunofluorescence , e.g. ELISA
PCR is useful in diagnosing culture negative endocarditis
best way to diagnose culture negative(of what) endocarditis
PCR
vaccine of Q fever
A formalin-killed whole cell, phase I C. burnetii vaccine is available for those occupationally at risk
Morphology of actinomyctes
filamentous branching Gram positive bacilli
the two genera of actinomyctes
Actinomyces and Nocardia
the diseases caused by actinomyctes
actinomycosis, nocardiosis and actinomycetoma
pathogenesis of Actinomyces israelii
it invades the tissues after local trauma causing actinomycosis, which is a chronic inflammatory, granulomatous lesion that drains pus through sinus tracts which contains yellow “sulphur granules”.
produce sulfur granules
Actinomyces israelii
morphology of Actinomyces israeli
These are composed of a central mycelial mass with a
peripheral zone of swollen clubs
most lesions of Actinomyces israelii
Actinomyces israeliicervico-facial (associated with poor dental hygiene or tooth extraction), abdominal or thoracic.
Diagnosis of Actinomyces israelii
- Pus from lesions .
- sulphur granules are seen with radially arranged clubs.
- Gram staining will reveal filamentous branching Gram positive bacilli with bacillary and coccoid forms
- Culture anaerobically on thioglycolate broth and brainheart infusion blood agar. Colonies are identified by morphology and immunofluorescent staining.
culture of A. israelii
thioglycolate broth and brainheart infusion blood agar
causes nocardiosis
Nocardia asteroides
pathogenesis of N.asteroides
Inhalation of the organism causing chronic pulmonary infections and brain and skin abscesses
diganosis of N. asteroides
detection of Gram positive bacilli, coccobacillary cells and branching filaments
culture of N. asteroides
brain-heart infusion agar
difference between actinomycotic and Eumycotic mycetoma in
- causative agent
- Granules
- Microscopic examination
- culture
- treatment
P. 37 Lecture 1
morphology of Listeria monocytogenes
small gram positive, non-spore forming bacilli
characterized by tumbling movement
Listeria monocytogenes
the tumbling movement of Listeria monocytogenes is at which temp
22-28 C
what distinguishes Listeria monocytogenes from corynebacterium
tumbling movement of Listeria monocytogenes
catalase test of Listeria Monocytogenes
catalase positive
mode of transmission of Listeria monocytogenes to humans
1- Contact with domestic farm animals or their faeces, by ingestion of
contaminated unpasteurized milk or cheese and contaminated vegetables (i.e. food borne).
2- Vertical transmission can also occur transplacentally or during delivery
type of haemolysis of Listeria
Beta haemolysis
pathogenesis of listeria
- has ability to invade mononuclear phagocytic cells. After internalization a listeriolysin O enzyme lyses the membrane of the phagolysosome and they escape destruction
- It can move from cell to cell by means of actin rockets
- Since it grows intracellularly, cell mediated immunity (CMI) is a
more important host defense than humoral immunity
how Listeria move from cell to cell
by actin rockets
type of immunity initiated in Listeria infection
cell mediated immunity because Listeria grows intracellulary
diseases caused by listeria
1- Infection of pregnant women passes to the foetus transplacentally
causing granulomatosis infantiseptica characterized by pustular skin
lesions and intrauterine sepsis leading to abortion, still-birth or
premature labour.
2-Newborns infected during delivery from infected mothers, develop
neonatal meningitis.
3-Infection in immunosuppressed adults causes meningoencephalitis
and bacteraemia, specially in renal transplant patients.
4-Gastroenteritis which is characterized by watery diarrhoea, fever,
headache, myalgia and abdominal cramps but little vomiting.
Outbreaks are usually caused by contaminated dairy products.
Undercooked meats such as chicken and hot dogs have also been
involved.
Diagnosis of Listeria
- Isolation from blood by blood culture and from CSF on blood
agar and from stools on listeria selective media. - Isolation is enhanced if specimens are refrigerated for few
days before inoculation “cold enhancement”. - Identification is done by gram stain and detection of tumbling
motility and positive catalase. - It produces Beta- haemolysis, on sheep blood agar, which is
enhanced in the vicinity of a streak of Staph, aureus, i.e. CAMP
test positive
how listeria passes to fetus
transplacentally
what causes granulomatosis infantiseptica
Listeria
what causes neonatal meningits in newborns
listeria monocytogenes
what listeria do in immunosupressed patients
meningoencephalitis and bacteraemia
has tumbling motility
L. monocytogenes
causing undulant fever
Brucella
causing malta fever
Brucella
other names of brucellosis
undulant or Malta fever
Brucella
causing infection in goats and sheep
Br. melitensis
causing abortion of cattle
Br. abortus
Brucella causing infection in pigs
Br. suis
Borrelia causes infection in dogs
Br. canis
Morphology of Brucella
Gram negative short cocco-bacilli, non-motile, nonsporing and non-capsulated
media of brucella for growth
brucella agar,
brain heart infusion,
trypticase soy agar,
chocolate agar
which type of brucella require CO2 for growth
Br. Abortus
which brucella species produce H2S
Br. abortus and Br. suis
virulence and immunity of brucella
- A lipopolysaccharide (LPS) is the major virulence factor as well
as the major cell wall antigen. The LPS has endotoxic activity
and elicits an antibody response (IgG, IgM, IgA) which may be
protective. - Brucella can survive and multiply within host cell phagocytes
i.e. facultative intracellular parasite, so immunity is mainly
cell mediated
immunity triggered in brucella
cell mediated because brucella is facultative intracellular parasite
antibodies elicted in response to the LPS virulence factor of brucella
IgG, IgM, IgA
incubation period of brucella
1-6 weeks
brucella is found in
uterine discharges and milk of infected animals
mode of transmission of brucella
1- Ingestion of contaminated unpasteurized milk or milk products.
2- Direct through skin abrasions during handling of infected animals or their discharges.
Therefore brucellosis is an occupational disease affecting mostly butchers, farmers and veterinarians
3- inhalation of infected aerosol during handling of infected animals or their cultures in the
laboratories
what is undulant fever
disease caused by brucella characterized by an accute bacteraemic phase followed by chronic stage
what the brucella invade
The organism localizes in the reticulo-endothelial system; lymph nodes, liver, spleen and bone marrow.
undulant fever complicated by
osteomyelitis, meningitis or cholecystitis
which brucella biovar is more acute and which is more chronic
Br. melitensis infection is more acute and severe. Br. suis infection is more chronic
Blood cultures of brucella should not be discarded as negative before how many weeks
4 weeks
blood culture of brucella
brain heart infusion broth
diagnosis of brucella
Blood, bone marrow and lymph node biopsy for culture
1. blood culture: in brain heart infusion broth
2. serologic diagnosis:
Standard tube agglutination test (STAT)
A rapid slide agglutination test
ELISA for detection of IgG, IgM or IgA
**3. PCR: **
4. Brucellin test:
causes of false negative results of serologic tests of brucella
- prozone phenomenon
- presence of non-agglutinating IgA “blocking antibodies”
how to deal with prozone phenomnon
wide range of serum dilutions (up to 1/5120) shoud be done.
how to deal with the blocking antibodies IgA
Coomb’s antiglobulin method
What diseases caused by Borrelia
Relapsing fever and Lyme disease
has endoflagella
borrelia
culture of borrelia
Barbour-Stoenner-Kelly (BSK-II)
microaerophilic environment
a disease characterized by repeated bouts of fever alternating
with periods of apyrexia
Relapsing fever
Epidemic relapsing fever is caused by …… and transmitted by ….
B. recurrentis
lice
endemic relapsing fever is caused by ….. and transmitted by ……
B. duttoni and B. hermsii
ticks
Man is the only host for which species of Borrelia
B. recurrentis and B. duttoni
incubation period of Borrelia
3-10 days last for 4 days
then 3-10 days of afebrile period
which 3-10 relapses may occur
death in cases of borrelia due to
the spirochaetes invade many organs (heart, spleen, liver and kidney) with death generally due to myocarditis
diagnosis of Borrelia
1- During the febrile stage:
* Blood films stained with Leishman, Wright or Giemsa stains reveal large numbers of
spirochaetes.
2- During afebrile stage :
* Cultivation and mouse enrichment must be done as the organism is scanty in the
blood and blood films are negative.
* Diagnosis is done by injecting white mice intraperitoneally with the patient’s blood.
* After 2-4 days, films from tail blood are stained and examined for presence of
Borreliae.
* Mice blood is inoculated on BSKII medium.
3- DNA probes may be used for identification.
lyme disease is caused by
Borrelia burgdorferi
and is transmitted by ticks
the main animal reservoir for lyme disease (Borrelia burgdorferi)
Rodents and deer
the early and late manifestation of Lyme disease
- The early stages are characterized by a distinctive skin lesion
called “erythema migrans” associated with fever, chills, muscle
pain and headache. - Late manifestations arthritis, myocarditis and neurologic manifestations e.g.
meningitis.
causes Erythema migrans
Borrelia burgdorferi
morphology of Yersinia
gram negative bacilli
causes plague in man
Yersinia pestis
causes of human diarrhoeal diseases
Yersinia enterocolitica and Yersinia pseudotuberculosis
How Yersinia pestis is transmitted
transmitted to man by the rat flea Xenopsylla cheopis
Morphology of Yersinia pestis
Gram negative short ovoid, non-motile bacilli. In tissue, they form a
capsule-like outer envelope
they show marked bipolar staining “safety pin appearance
Yersinia pestis
staining of Yersinia pestis
Geimsa or methylene blue
gram negative
Cultural characters of Yersinai pestis
- Facultative anaerobes.
- They grow on blood agar and MacConkey producing non-lactose fermenting colonies
- rats die within few days when injected subcutaneosly
Virulence factors of Yersinia pestis
1- A lipopolysaccharide endotoxin that causes endotoxic shock.
2- F1 antigen is antiphagocytic and induces protective antibodies.
3-V-W antigens are present in virulent strains and are encoded by genes on plasmids. They are antiphagocytic.
4-Yops (Yersinia outer proteins) have a variety of activities, including inhibiting phagocytosis, inhibiting platelet aggregation and preventing an effective inflammatory response.
5- Plasminogen activator protease degrades fibrin and extracellular proteins and facilitates systemic spread from the inoculation site.
6- An exotoxin lethal to mice
pathogenesis of Yersinia plague
bubonic plague in lymph nodes
pneumonic plague or meningitis
septicaemic plagu: Dissemination is associated with endotoxic shock, DIC and cutaneous haemorrhages
can be uesd in bioterrorism
Yersinia pestis
cause of Primary pneumonic plague
due to inhalation of infected droplets from a patient.
Haemorrhagic consolidation, sepsis and death may occur
diseases caused by Y. enterocolitica and Y. pseudotuberculosis
- enterocolitis
- mesenteric adenitis
- bacteraemia and abscesses in liver or spleen
- Immunologic sequelae e.g. reactive arthritis and erythema nodosum
mode of transmission of Y. enterocolitica and Y. pseudotuberculosis
transmitted to humans by contamination of food with the excreta of domestic animals
charachterized by peripheral zone of swollen club
Actinomyces israelii
causing vasculitis in heart and brain
R. Prowazeki
Epidemic typhus
causing DIC and vascular occlusion
- R. Prowazeki Epidemic typhus
- R. ricketsii rocky mountain spotted fever
causes mesenteric adenitis
Y. enterocolitica and Y. pseudotuberculosis
cause infection of alveolar macrophages
coxiella burnetti (Q fever)
coxiella burnetti is transmitted between goats, sheep, cattle by
ticks
incubation period of coxiella burnetti
2 weeks
best method to diagnose coxiella burnetii
Indirect immunofluorescence
pelvic actinomycosis due to
infection with women keeping an intrauterine device for a long period
three different families of arbovirus
- Togaviruses
- Flaviviruses
- Bunyaviruses
Transmission of arboviruses by
blood-sucking arthropods e.g. mosquitoes, ticks,
or sandflies
Common clinical pictures of arboviruses
Encephalitis, hemorrhagic fevers, myalgias, arthralgias, non hemorrhagic rash, lymphadenopathy
Causes arbovirus encephalitis
togavirus and flavivirus groups are endemic
Culture of arbovirus encephalitis
tissue culture
chick embryo
in mouse brain by intracerebral inoculation
Pathogenesis of Arbovirus encephalitis
Infection is transmitted by a bite of the infective arthropod»>the virus multiplies in local lymphoid tissue then reaches the blood stream»> causing viraemia in same time with fever» leads to general lymphadenopathy and maculopapular rash» then it invaded the CNS causes encephalitis,
meningitis and myelitis
Arboviruses causes cause mild meningitis disease
West Nile and Sindbis
Fever characterized by jaundice and albuminuria
Yellow fever
Causative organism and reservoir of yellow fever
Causative organism: flavivirus
Reservoir: monkeys
Monkey to monkey transmission of yellow fever by
mosquito Aedes africanus in Africa and Haemagogus in South America
Urban yellow fever is transmitted from man to man by
Aedes aegypti
Can infected with it when you visit the jungle
Yellow fever
Hematemesis is picture of what?
Yellow fever
Vaccine of yellow fever
live attenuated vaccine called 17-D vaccine
Contraindication of 17 D vaccine of yellow fever
Contraindicated for
* Infants less than 9 months
* Pregnancy
* persons with
* altered immune systems e.g. HIV or organ transplant patients
Dengue viruses are transmitted principally between humans by the
Aedes aegypti
How many antigenic types of Dengue viruses
Four
The two types of dengue fever
Classic dengue (rarely fatal) and dengue hemorrhagic fever (fatal)
Clinical picture of dengue hemorrhagic fever
Shock and hemorrhage
Pathogenesis of Dengue virus
Forms virus-antibody complexes results in increasing virus permeability and thrombocytopenia
the antibodies increase the entry of virus into monocytes and macrophages with the consequent release of large amounts of cytokines vasoactive mediators causing DIC, haemorrhages and shock
what listeria cause in renal transplant patients
meningoencephalitis and bacteraemia
Which disease that its vaccine is given to animal
Rift valley fever
Complications of Rift valley fever
retinitis, encephalitis and haemorrhagic
fever. Permanent loss of vision may occur.
Causes sandfly fever
Bunyavirus transmitted by sandfly Phlebotomus papatasii
Transmitted by culex
West Nile fever
Fever that has no vaccine
West Nile fever
The main reservoir of west Nile fever
Wild birds
Mode of transmission of west nile fever
by culex mosquito from infected bird, infected traveller, infected mosquito in airplanes, or by blood transfusion or organ transplantation
Screening of the donated blood by PCR in which fever
Wild Nile fever
Infection that considered as endogenous
Brill Zinsser disease
Most cases of rocky mountain spotted fever occur in which generation
In children
Only rickettsia disease that man to man
R. prowazekii epidemic typhus
We use immunohistochemistry in diagnosis of what
Rickettsial disease
Type of HIV virus genome
diploid single stranded positive sense RNA
gene encodes the core proteins
gene encodes the enzymes of HIV
gene encodes the envelope proteins of HIV
Gag gene
Pol gene
Env gene
Surface glycoproteins of envelope of HIV
Internal structure proteins (core) of HIV
Gp120 & Gp41
P24 & P17
Proteins (enzymes) of HIV
Reverse transcriptase, integrase, Protease
Interacts with CD4 receptors on the cell surface
Gp120
Gp protrudes from the surface
Gp120
Mediates fusion between virus envelope and cell membrane of infected cells.
Gp41
appears in the serum early after infection by HIV and is a serologic marker for virus replication
P24
The most importance core protein of HIV
P24
Matrix protein surrounds p24
P17
Proteins encoded by pol gene:
Reverse transcriptase.
Integrase.
Polymerase.
Function of pol gene proteins
After viral fusion with cell, RT transcribes the genome RNA into double stranded DNA (provirus), which integrates into the host cell DNA by the action of the integrase enzyme. Viral mRNA is transcribed from the proviral DNA and transported to the cytoplasm, where it is translated into large polyproteins. These are cleaved by the protease enzyme to produce the different viral structures and enzymes
Mode of transmission of HIV
Sexual, blood, perinatal (trans-placentally, during delivery, breast feeding)
What is Initial infection of HIV
The initial infection of the genital tract occurs in dendritic cells that line the mucosa, these migrate to local lymph nodes where helper T cells become infected by attachment to CD4
A protein coreceptor on T cells that is required for infection of these cells.
CXCR4
A coreceptor on macrophages, monocytes, dendritic cells is required for their infection
CCR5
What cells response in the acute stage of HIV infection
cytotoxic CD8 lymphocytes (CTLs) and antibodies (humoral immunity) dramatically reduce HIV levels
Viral mechanisms in the latent infection
a- Latent infection of host cells as a provirus.
b- Rapid genetic mutation.
c- Trapping of infectious virus in lymphoid tissues in and on the surface of follicular dendritic
cells, which act as reservoirs.
II-Suppression of immune mechanisms which are more evident during late stages of infection of HIV
a-Deletion of CD4 T cells,
b-Deletion of HIV-specific CTL clones,
c- Dysfunction of CTLs due to; decreased production of IL-2, and decreased expression of
MHC-I by the action of viral genes, leading to decreased recognition of virus infected cells by
CTLs.
d- Impaired functions of APC.
e- Interference with humoral response which are T cell dependent
Clinical picture of acute stage of HIV infection
begins 2-4 weeks after infection with a
mononucleosis-like picture of generalized
lymphadenopathy, fever, sore throat and a
maculopapular rash.
fatigue, wasting, fever, chronic diarrhoea, and
persistent lymphadenopathy
AIDS Related Complex (ARC)
The latent stage of HIV infection are clinically called as
AIDS Related Complex (ARC)
Consequences of the late stage of HIV infections is AIDS
- The most characteristic are Kaposi’s sarcoma and
Pneumocystis jiroveci pneumonia. - Others are viral infections e.g. CMV, disseminated
herpes simplex and herpes zoster infections; fungal
infections such as C. albicans, cryptococcal
meningitis; bacterial infections such as, M avium
intracellular, M. tuberculosis; - protozoal infections such as toxoplasmosis
- and cancer e.g.. non-hodgkin’s lymphoma and
cervical cancer. - Many patients have neurologic problems e.g.
dementia and neuropathy.
Consequence of pediatric AIDS
Poor prognosis, present with clinical symptoms by 2 years of age; death follows in another 2 years from opportunistic infections,
Laboratory diagnosis of HIV infection
1- Decreased CD4 cells count and inversion of the CD4/CD8 ratio.
2- Detection of HIV antibodies which appear 6-12 weeks after infection.
3- Detection of viral nucleic acid by PCR to know virus load
4-Virus isolation
5- Detection of viral antigens p24 by ELISA
The antibody detection of HIV infection is confirmed by
the Western blot technique
What is the Western blot technique
is more specific technique and it detects antibodies against viral core protein p24 or envelope glycoproteins gp 41, gp 120 or gpl60
Diagnosis during the acute stage or pediatric AIDS of HIV infection
Diagnosis is made by viral isolation or by detection of viral RNA by PCR assay or by detection of p24
antigen
treatment of choice for acute HIV infections
2 nucleoside analogues (reverse transcriptase inhibitors) in addition to a protease inhibitor
Measures to reduce transmission of HIV infection from infected mothers to foetus
Screening of pregnant mothers for HIV,
those infected should receive treatment during pregnancy and delivery.
Neonates should receive the same drugs.
Delivery by cesarean section is recommended.
Infected mothers should not breast feed their infants
Mechanism of cell transformation by tumor viruses
- Introduction of newtransforming genes i.e.
“viral oncogenes” - Activation or over expression of preexisting cellular genes “proto-oncogenes”
- Inactivation of a tumour suppressor gene
What is the evidence of association between some viruses and human tumors?
a- Detection of virus nucleic acid integrated in the tumor cell chromosome or free in the
cytoplasm as in EB virus.
b- Detection of viral antigens in or on tumor cells.
c- The ability of viruses isolated from human tumors to cause transformation of cells in vitro e.g.
EBV, or to induce tumors in experimental animals.
d- The most definitive proof of a causal relationship is decreased tumor incidence by prevention
of viral infection e.g. HBV and HPV vaccination.
Structure of Human papillomavirus HPV
dsDNA non-enveloped virus
Mode of transmission of Human papillomavirus HPV
It is transmitted by direct and sexual contact
Diseases caused by HPV
Types 6 and 11 cause anogenital warts; types 16 and 18, are implicated as the cause of carcinoma of the cervix
Mechanism of oncogenesis of HPV
viral DNA integrated into host cell DNA leads to over-expressed E6 and E7 genes with
overproduction of E6 and E7 proteins which are HPV transforming proteins, which inactivates tumor suppressor proteins encoded by p35 and Rb genes and induce abnormal mitosis
Prevention vaccine of HPV
HPV quadrivalent recombinant vaccine
What is HPV quadrivalent recombinant vaccine
is composed of HPV LI proteins of types 6, 11, 16 and 18. It protects against cancer cervix and anogenital warts
Way of given HPV vaccine and times
I.M. injections in three doses at a schedule of 0,1-2 and 6 months
Vaccine of HPV for females
A bivalent vaccine containing types 16 and 18 is used for females only
Diseases caused by Human T cell lymphotropic retrovirus (HTLV)
cutaneous T cell lymphomas and leukemias as well as tropical spastic paraparesis
Mode of transmission of Human T cell lymphotropic retrovirus (HTLV)
blood transfusion, I.V. drug users, sexually in semen and from mother to infant in breast milk
Causes cutaneous T cell lymphomas and leukemiasblood transfusion, I.V. drug users, sexually in semen and from mother to infant in breast milk
Human T cell lymphotropic retrovirus (HTLV)
Causes nasopharyngeal carcinoma
Epstein-Barr
Diseases caused by Epstein Barr
nasopharyngeal carcinoma, Burkitt’s lymphoma,
Hodgkins, non Hodgkins lymphomas and gastric cancer.
Causes hepatocellular carcinoma (HCC)
Hepatitis B and C virus
Causes Kaposi sarcoma
Human Herpesvirus 8
What west nile virus and sindbis virus cause
mild meningitic disease
What are the flaviviruses
YDW yellow fever, dengue fever, west nile fever
Main reservoir of the yellow fever
monkeys
Pathogenesis and clinical picture of
Yellow fever
- The virus is introduced by the bite of an infective
mosquito. - It multiphes in the local lymph nodes and spreads to
the blood this coincides with sudden onset of fever,
headache, myalgias and photophobia; some patients
recover at this point. - The virus may reach the liver, spleen, kidney and bone
marrow leading to their destruction. - This results in jaundice, haemorrhages and proteinuria.
It may affect the heart or GIT leading to shock,
prostration haematemesis (black vomit). - Death may result from kidney or liver failure.
What are the bunya viruses
Rift valley fever and sandfly fever
Man is infected with rift valley fever by
epizootic in domestic animals by coming in contact with infected animal body fluids or mosquito
bites.
Animals infected with rift valley fever and how they infected
sheep and domestic animals infected with Aedes mosquito
Person to person transmission of west nile fever by
Blood transfusion or organ transplantation
grows on the chorioallantoic membrane of
chick embryo producing characteristic lesions
called “pocks”
Small pox virus
What growing culture of small pox virus
grows on the chorioallantoic membrane of
chick embryo producing characteristic lesions
called “pocks”
is the first disease to be controlled by
immunization
Small pox virus
Reintroduced as biologic weapon
Yersinia pestis
Small pox virus
Producing pocks lesions
Small pox virus
Is the agent used for preparation of smallpox vaccine
Vaccinia virus
Mode of transmission of small pox virus
The virus was transmitted by respiratory aerosol or by direct contact with skin lesions or contaminated fomites
Vaccination of small pox virus
live vaccinia virus
Clinical picture of small pox
- It is a systemic disease with a viraemic stage and final localization in the skin causing the rash
- The rash started on the face and extremities then appeared on the trunk.
- The rash evolved through stages from macules to papules, vesicles, pustules and finally crusts in 2-3 weeks.
- Crusts fell off leaving scarred area.
Immunity followed the smallpox vaccine (vaccinia virus)
humoral and cell mediated immunity
How small pox vaccine prepared
The vaccine is prepared from vesicular lesions (lymph) produced on shaved skin of calves or from virus grown on chick embryo; the final vaccine contains glycerol to stabilize the virus and phenol to destroy bacteria.
Causes of successful eradication of
small pox
1- Man is the only host, and there is no animal
reservoir of infection
2- There is only one stable serotype of the virus
3- There is no carrier state or subclinical infection
4- Effective vaccine that is highly immunogenic and was used world wide
5- A surveillance-containment program was used by the WHO.
Smallpox cases are easily recognized clinically. Cases were traced and all susceptible contacts were
identified and vaccinated. The vaccine is protective if given within 4 days after exposure
virus acquired by contact with wild animals killed for food or for their skins
Monkey pox
Clinical picture of monkeypox
Symptoms are similar to smallpox, but differ in
occurrence of lymphadenopathy
Causes pulmonary distress syndrome
Monkey pox
How to differentiate monkeypox from smallpox
Monkeypox is antigenically distinct and produces
different lesions on the chorioallantoic
membrane of chick embryo
Causes human warts (benign skin nodules)
Molluscum contagiosum
How Molluscum contagiosum is transmitted
close contact and sexually
Diseases caused by coxsackieviruses A
Herpangina
Acute hemorrhagic conjunctivitis
Handfoot and mouth disease
Diseases caused by coxsackieviruses B
Pleurodynia
Myocarditis and pericarditis
Diabetes mellitus
Diseases caused by coxsackieviruses A and B
Aseptic meningitis
Minor febrile illness
Diarrhea and hepatitis
What causes Pleurodynia
What causes Acute hemorrhagic conjunctivitis
What causes Minor febrile illness
B Coxsackie
A Coxsackie
A&B Coxsackie
What causes COX Diarrhea and hepatitis
What causes COX Diabetes mellitus
What causes Herpangina
A&B Coxsackie
B Coxsackie
A Coxsackie
What causes COX Aseptic meningitis
What causes COX Myocarditis and pericarditis
What causes Handfoot and mouth disease
A&B Coxsackie
B Coxsackie
A Coxsackie