56947428 hiv-aids

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HUMAN HUMAN IMMUNODEFICIENCY IMMUNODEFICIENCY VIRUS AND AIDS VIRUS AND AIDS

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Page 1: 56947428 hiv-aids

HUMAN HUMAN IMMUNODEFICIENCY IMMUNODEFICIENCY

VIRUS AND AIDS  VIRUS AND AIDS  

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Human immunodeficiency virus Human immunodeficiency virus (HIV) (HIV)

There are about 33.2 million There are about 33.2 million (estimate range: 30.6 million - 36.1 (estimate range: 30.6 million - 36.1 million) HIV-infected people in the million) HIV-infected people in the world of whom about 22.5 million world of whom about 22.5 million (range: 20.9 million - 24.3 million) (range: 20.9 million - 24.3 million) are in sub-Saharan Africa where the are in sub-Saharan Africa where the adult infection prevalence is about adult infection prevalence is about 6%.6%.

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Human immunodeficiency virus Human immunodeficiency virus (HIV) (HIV)

In October 2008, CDC released In October 2008, CDC released estimates of the extent of the estimates of the extent of the HIV/AIDS epidemic. These showed HIV/AIDS epidemic. These showed that 1,106,400 adults and that 1,106,400 adults and adolescents were living with HIV adolescents were living with HIV infection in the United States at the infection in the United States at the end of 2006 (95% Confidence end of 2006 (95% Confidence Interval: 1,056,400–1,156,400). Interval: 1,056,400–1,156,400).

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In sub-Saharan AfricaIn sub-Saharan Africa

ТТhere are an estimated 22.5 million here are an estimated 22.5 million (range: 20.9 million–24.3 million) (range: 20.9 million–24.3 million) people infected by HIV with over 2.8 people infected by HIV with over 2.8 million new infections in 2006. In this million new infections in 2006. In this region, there were 2.1 million deaths. region, there were 2.1 million deaths. Ten million young Africans between Ten million young Africans between the ages of 15 and 24 and 3 million the ages of 15 and 24 and 3 million children are infected.  children are infected. 

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Asia/PacificAsia/Pacific region region

In 2006, about 1 million people in the In 2006, about 1 million people in the Asia/Pacific region became infected by HIV Asia/Pacific region became infected by HIV and 630,000 people died. The total and 630,000 people died. The total infected population in this region is an infected population in this region is an estimated 4.9 million (range 3.7 million - estimated 4.9 million (range 3.7 million - 6.7 million) people; of these, 2.1 million 6.7 million) people; of these, 2.1 million are age 15 to 24 years and 2.4 million are are age 15 to 24 years and 2.4 million are women (up 21% since 2004). In this women (up 21% since 2004). In this region, HIV is increasing at a rate of 10% region, HIV is increasing at a rate of 10% per year. per year.

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HIVHIV

It is likely that HIV first appeared in It is likely that HIV first appeared in humans in Africa near the beginning humans in Africa near the beginning of the twentieth century of the twentieth century

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STRUCTURE OF THE VIRUSSTRUCTURE OF THE VIRUSCOMPONENTS OF HIVCOMPONENTS OF HIV

HIV is a retrovirus with a similar HIV is a retrovirus with a similar structure to other retroviruses. structure to other retroviruses. 

SURFACE STRUCTURESSURFACE STRUCTURES Viral membraneViral membrane The  membrane is host-derived as a result of The  membrane is host-derived as a result of

budding from the cell surface. Some host proteins budding from the cell surface. Some host proteins become incorporated into the viral membrane. become incorporated into the viral membrane. This lipid envelope make the virus susceptible to This lipid envelope make the virus susceptible to organic solvents.organic solvents.

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Surface glycoproteinSurface glycoprotein

Gp160 is encoded by the env (envelope) gene. Gp160 is encoded by the env (envelope) gene. Gp160 is cleaved after translation by host Gp160 is cleaved after translation by host enzymes in the Golgi Body to form Gp120 (SU) enzymes in the Golgi Body to form Gp120 (SU) and Gp41 (TM). Gp 41 is embedded in the and Gp41 (TM). Gp 41 is embedded in the membrane, Gp120 is not but is held to Gp41 by membrane, Gp120 is not but is held to Gp41 by non-covalent interactions. It is easily shed from non-covalent interactions. It is easily shed from the virus particle. There is a large number of the virus particle. There is a large number of sugar chains on gp120 (which may pose a sugar chains on gp120 (which may pose a problem for a vaccine). Gp120 is the protein that problem for a vaccine). Gp120 is the protein that interacts with a receptor on the cell to be interacts with a receptor on the cell to be infected. Gp41 is the fusogen that is exposed infected. Gp41 is the fusogen that is exposed after Gp120 has bound to the cell.after Gp120 has bound to the cell.

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HIVHIV

Kaposi's sarcomaKaposi's sarcoma

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Cysts of Pneumocystis carinii in AIDS. Cysts of Pneumocystis carinii in AIDS.

Histopathology of lung shows characteristic cysts with cup forms and Histopathology of lung shows characteristic cysts with cup forms and dot-like cyst wall thickenings.dot-like cyst wall thickenings. Methenamine silver stain. Methenamine silver stain. Dr. Edwin P. Ewing, Jr.Dr. Edwin P. Ewing, Jr.

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Cryptococcosis of lung in patient with AIDS.Cryptococcosis of lung in patient with AIDS.

Methenamine silver stain. Histopathology of lung shows numerous extracellular Methenamine silver stain. Histopathology of lung shows numerous extracellular yeasts of Cryptococcus neoformans within an alveolar space. Yeasts show narrow-yeasts of Cryptococcus neoformans within an alveolar space. Yeasts show narrow-base budding and characteristic variation in size.base budding and characteristic variation in size. CDC/Dr. Edwin P. Ewing, Jr. CDC/Dr. Edwin P. Ewing, Jr. [email protected]

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No cases of diffuse, undifferentiated No cases of diffuse, undifferentiated non-Hodgkins lymphoma were reported non-Hodgkins lymphoma were reported in the young male (20 - 39 years old) in the young male (20 - 39 years old) population of the San Francisco area population of the San Francisco area during the period 1977-1980. However, during the period 1977-1980. However, from March 1981 to January 1982, the from March 1981 to January 1982, the unusual occurrence of four cases within unusual occurrence of four cases within 10 months was observed; again, these 10 months was observed; again, these were in the homosexual male were in the homosexual male population.population.

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The virus was isolated in 1984 by Luc The virus was isolated in 1984 by Luc Montanier (Pasteur Institute, Paris), Montanier (Pasteur Institute, Paris), who shared the Nobel Prize for his who shared the Nobel Prize for his discovery in 2008, and Robert Gallo discovery in 2008, and Robert Gallo (NIH, Bethesda, USA). (NIH, Bethesda, USA).

Human immunodeficiency virus Human immunodeficiency virus (HIV) (HIV)

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From the original infection, there is From the original infection, there is usually a period of 8 to 10 years usually a period of 8 to 10 years before the clinical manifestations of before the clinical manifestations of AIDS occur; however, this period may AIDS occur; however, this period may be two years or less. Approximately be two years or less. Approximately 10% of patients succumb to AIDS 10% of patients succumb to AIDS within 2 to 3 years.within 2 to 3 years.

Human immunodeficiency virus Human immunodeficiency virus (HIV) (HIV)

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Human immunodeficiency virus Human immunodeficiency virus (HIV) (HIV)

Dendritic cells in the mucosal linings bind the virus shed by Dendritic cells in the mucosal linings bind the virus shed by macrophages and carry it to the lymph nodes where CD4+ macrophages and carry it to the lymph nodes where CD4+ T4 cells become infected. T4 cells become infected.

HIV-1 budding from cultured lymphocyte. Transmission electron micrograph.

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Human immunodeficiency virus Human immunodeficiency virus (HIV) (HIV)

There is a "window period" of There is a "window period" of seronegativity during which an infected person does during which an infected person does not give a positive not give a positive western blot HIV test or HIV test or ELISA, even though the viral load is high , even though the viral load is high and the patient may exhibit some symptoms. This seronegative period can last for and the patient may exhibit some symptoms. This seronegative period can last for six months before six months before seroconversion although the latter usually occurs between one although the latter usually occurs between one and four weeks after infection. and four weeks after infection. 

Scanning electron micrograph of HIV-1 budding from cultured lymphocyte. Multiple round bumps on cell surface represent sites of assembly and budding of virions (CDC)

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During the course of infection, there is a During the course of infection, there is a profound loss of the specific immune profound loss of the specific immune

response to HIV because:response to HIV because: responding CD4+ cells become infected. Thus, there is responding CD4+ cells become infected. Thus, there is

clonal deletion leading to tolerance. The cells that clonal deletion leading to tolerance. The cells that proliferate to respond to the virus are infected and killed by proliferate to respond to the virus are infected and killed by itit

epitope variation can lead to escape of HIV from the epitope variation can lead to escape of HIV from the immune responseimmune response

activated T cells are susceptible to apoptosis. Spontaneous activated T cells are susceptible to apoptosis. Spontaneous apoptosis of uninfected CD4+ and CD8+ T cells occurs in apoptosis of uninfected CD4+ and CD8+ T cells occurs in HIV-infected patients. Also there appears to be specific HIV-infected patients. Also there appears to be specific apoptosis of HIV-specific CD8+ cellsapoptosis of HIV-specific CD8+ cells

the number of follicular dendritic cells falls over time, the number of follicular dendritic cells falls over time, resulting in diminished capacity to stimulate CD4+ cellsresulting in diminished capacity to stimulate CD4+ cells

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Onset of disease - AIDSOnset of disease - AIDS

The period of clinical latency varies The period of clinical latency varies in length from as little as 1 to 2 years in length from as little as 1 to 2 years to more than 15 years. to more than 15 years.

It is the onset of HIV-associated It is the onset of HIV-associated cancers and opportunistic infections cancers and opportunistic infections that defines AIDS proper. that defines AIDS proper.

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AIDSAIDS

AIDS is currently defined in persons AIDS is currently defined in persons older than 13 years as the presence older than 13 years as the presence of one of 25 conditions indicative of of one of 25 conditions indicative of severe immunosuppression or HIV severe immunosuppression or HIV infection in an individual with a infection in an individual with a CD4+ cell count of less than 200 CD4+ cell count of less than 200 cells per cubic mm of blood.cells per cubic mm of blood.

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AIDS. AIDS.

Candida and herpes simplex in AIDS Candida and herpes simplex in AIDS 

Bristol Biomedical Image Archive, University of Bristol. Used with permission Bristol Biomedical Image Archive, University of Bristol. Used with permission

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AIDS. AIDS.

Hairy leukoplakia of tongue in AIDSHairy leukoplakia of tongue in AIDS

Bristol Biomedical Image Archive, University of Bristol. Used with permission Bristol Biomedical Image Archive, University of Bristol. Used with permission

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Cysts of Pneumocystis carinii in AIDS. Cysts of Pneumocystis carinii in AIDS.

Histopathology of lung shows characteristic cysts with cup forms and Histopathology of lung shows characteristic cysts with cup forms and dot-like cyst wall thickenings.dot-like cyst wall thickenings. Methenamine silver stain. Methenamine silver stain. Dr. Edwin P. Ewing, Jr.Dr. Edwin P. Ewing, Jr.

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Pathology of Lung InfectionPathology of Lung InfectionPneumocystis carinii PneumoniaPneumocystis carinii Pneumonia

Pneumocystis carinii pneumonia. The alveoli are filled with a foamy exudate, and the interstitium is thickened and contains a chronic inflammatory infiltrate.

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Pathology of Lung InfectionPathology of Lung InfectionPneumocystis carinii PneumoniaPneumocystis carinii Pneumonia

A centrifuged bronchoalveolar lavage specimen impregnated with silver shows a cluster of Pneumocystis cysts.

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PNEUMOCYSTIS CARINIIPNEUMOCYSTIS CARINIIPneumoniaPneumonia

Pneumocystis carinii causes progressive, often fatal pneumonias in persons with severely impaired cell-mediated immunity and is the most common serious opportunistic pathogen in persons with AIDS.

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PNEUMOCYSTIS CARINIIPNEUMOCYSTIS CARINIIPneumoniaPneumonia

P. carinii is distributed worldwide, and because 75% of the population have acquired antibodies by 5 years of age, it is reasonable to assume the organisms are inhaled regularly by all. In persons with intact cell-mediated immunity, P. carinii infection is rapidly contained, without producing symptoms.

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PNEUMOCYSTIS CARINIIPNEUMOCYSTIS CARINIIPneumoniaPneumonia

However, 80% of all patients with AIDS develop P. carinii pneumonia during the course of their illness.

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PNEUMOCYSTIS CARINIIPNEUMOCYSTIS CARINIIPneumoniaPneumonia

Pathogenesis: P. carinii reproduces in intimate association with alveolar type 1 lining cells, and active disease is confined to the lungs. Infection begins with attachment of the Pneumocystis trophozoite to the alveolar lining cell.

Pathogenesis

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PNEUMOCYSTIS CARINIIPNEUMOCYSTIS CARINIIPneumoniaPneumonia

The trophozoite feeds on the host cell, enlarges, and transforms into the cyst form, which contains daughter organisms. The cyst then ruptures to release new trophozoites, which, in turn, attach to additional alveolar lining cells. If the process is not checked by the host immune system or antibiotic therapy, the infected alveoli eventually fill with organisms and pro-teinaceous fluid.

Pathogenesis

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PNEUMOCYSTIS CARINIIPNEUMOCYSTIS CARINIIPneumoniaPneumonia

The progressive filling of alveoli prevents adequate gas exchange, and the patient slowly suffocates. The pathology of P. carinii pneumonia is discussed.

Pathogenesis

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Pathology of Lung InfectionPathology of Lung Infection

Pneumocystis carinii PneumoniaPneumocystis carinii Pneumonia

Clinical Features: Clinical Features: The presentation of Pneumocystis pneumonia is variable. At one extreme, symptoms are minimal, whereas at the other, there is rapidly progressive respiratory failure. Treatment is with trimethoprim-sulfisoxazoleor pentamidine.

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Cryptococcosis of lung in patient with AIDS.Cryptococcosis of lung in patient with AIDS.

Methenamine silver stain. Histopathology of lung shows numerous extracellular Methenamine silver stain. Histopathology of lung shows numerous extracellular yeasts of Cryptococcus neoformans within an alveolar space. Yeasts show narrow-yeasts of Cryptococcus neoformans within an alveolar space. Yeasts show narrow-base budding and characteristic variation in size.base budding and characteristic variation in size. CDC/Dr. Edwin P. Ewing, Jr. CDC/Dr. Edwin P. Ewing, Jr. [email protected]

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Pathology of Lung InfectionPathology of Lung Infection

Fungal InfectionsFungal Infections

CryptococcosisCryptococcosis

Cryptococcosis results from inhalation of the Cryptococcosis results from inhalation of the spores of spores of Cryptococcus neoformans, Cryptococcus neoformans, an an organism that is frequently encountered in organism that is frequently encountered in pigeon droppings. The pulmonary lesions pigeon droppings. The pulmonary lesions range from small parenchymal granulomas to range from small parenchymal granulomas to several large, granulomatous nodules, several large, granulomatous nodules, pneumonic consolidation, and even pneumonic consolidation, and even cavitation. Most serious cases of pulmonary cavitation. Most serious cases of pulmonary cryptococcosis occur in those who are cryptococcosis occur in those who are immunocompromised.immunocompromised.

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HIV. Kaposi's sarcoma.HIV. Kaposi's sarcoma.

Kaposi's sarcoma (skin). Kaposi's sarcoma (skin). Bristol Biomedical Image Archive, University of Bristol. Used with permissionBristol Biomedical Image Archive, University of Bristol. Used with permission

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HIV. Kaposi's sarcoma.HIV. Kaposi's sarcoma.

Skin showing AIDS-associated Skin showing AIDS-associated Kaposi's sarcoma    Kaposi's sarcoma   

Bristol Biomedical Image Archive, University of Bristol. Used with permissionBristol Biomedical Image Archive, University of Bristol. Used with permission

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HIV. Kaposi's sarcoma.HIV. Kaposi's sarcoma.

The perivenular infiltrate of Kaposi sarcoma shows a mixture The perivenular infiltrate of Kaposi sarcoma shows a mixture of  spindle cells, inflammatory cells, and ectatic vascular of  spindle cells, inflammatory cells, and ectatic vascular spaces.  spaces.  The Johns Hopkins Autopsy Resource (JHAR). Image Archive. The Johns Hopkins Autopsy Resource (JHAR). Image Archive. 

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HIV. Kaposi's sarcoma.HIV. Kaposi's sarcoma.

Lesions on the stomach of a Lesions on the stomach of a patient with Kaposi's sarcoma patient with Kaposi's sarcoma 

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Kaposi's sarcoma microscopically produces slit-Kaposi's sarcoma microscopically produces slit-like vascular spaces in the dermis of the skin, like vascular spaces in the dermis of the skin, seen here as a nodule.seen here as a nodule.

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Kaposi's sarcoma characteristically has Kaposi's sarcoma characteristically has deposits of hemosiderin granules and faint, deposits of hemosiderin granules and faint, pale pink hyaline globules, as seen here.pale pink hyaline globules, as seen here.

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AIDS. AIDS.

CandidaCandida, , herpes simplexherpes simplex

Bristol Biomedical Image Archive, University of Bristol. Used with Bristol Biomedical Image Archive, University of Bristol. Used with permission permission

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herpes simplexherpes simplex

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СПИДСПИД. .

Лейкоплакия языкаЛейкоплакия языка

Bristol Biomedical Image Archive, University of Bristol. Used with Bristol Biomedical Image Archive, University of Bristol. Used with permission permission

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AIDS. AIDS.

Leukoplakia of tongue.Leukoplakia of tongue.

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Patients with AIDS Patients with AIDS

In 2006, the estimated number of In 2006, the estimated number of persons living with AIDS (i.e. overt persons living with AIDS (i.e. overt disease rather than infection by the disease rather than infection by the virus) in the United States and virus) in the United States and dependent areas was 448,871. In the dependent areas was 448,871. In the 50 states and the District of 50 states and the District of Columbia, this included 432,915 Columbia, this included 432,915 adults and adolescents, and 3,775 adults and adolescents, and 3,775 children under age 13 years. children under age 13 years.

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Note: As more and more people Note: As more and more people survive with an HIV infection because survive with an HIV infection because of successful chemotherapeutic of successful chemotherapeutic intervention, the number of intervention, the number of infectious people in the population is infectious people in the population is rising even though fewer people are rising even though fewer people are dying of AIDSdying of AIDS

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CD8+ cells are only infected by HIV CD8+ cells are only infected by HIV in small numbers and their levels in small numbers and their levels remain high during the course of the remain high during the course of the disease for many years. And then, disease for many years. And then, until recently inexplicably, they until recently inexplicably, they rapidly die off.  It appears that some rapidly die off.  It appears that some of the HIV subtypes that occur late in of the HIV subtypes that occur late in infection prompt a mass apoptosis of infection prompt a mass apoptosis of CD8 cells. CD8 cells.

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Pathology of Lung InfectionPathology of Lung Infection

Viral PneumoniaViral PneumoniaCytomegalovirus produces a characteristic interstitial pneumonia. Initially described in infants, it is now well recognized in immunocompromised persons. This viral pneumonia features an intense, interstitial infiltrate of lymphocytes. The alveoli are lined by type II cells that have regenerated to cover the epithelial defect left by the necrosis of type I cells. The infected alveolar cells are very large and display the typical dark-blue nuclear inclusions.

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Cytomegalovirus x40 Cytomegalovirus x40 ••Classic CMV intranuclear inclusions are Classic CMV intranuclear inclusions are

deep purple, occupy >50% of the nuclear deep purple, occupy >50% of the nuclear diameter, have a clear perinuclear zone diameter, have a clear perinuclear zone and a rim of condensed nuclear chromatin and a rim of condensed nuclear chromatin

••In this case the perinuclear clear zone is In this case the perinuclear clear zone is obliterated by the large size of the CMV obliterated by the large size of the CMV inclusion inclusion

••Intracytoplasmic CMV inclusions can be Intracytoplasmic CMV inclusions can be present as small punctate dots(nicely seen present as small punctate dots(nicely seen in this case) in this case)

(Description By:Martin Nadel, M.D. ) (Description By:Martin Nadel, M.D. ) (Image Contrib. by:Martin Nadel, M.D. UCHC )(Image Contrib. by:Martin Nadel, M.D. UCHC )

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In order to find the mycobacteria in a tissue section, a stain for acid fast bacilli is done (AFB stain). The mycobacteria stain as red rods, as seen here at high magnification.

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ГриппГрипп

Грипп (от франц. Грипп (от франц. grippegrippe —  — схватывать) — острое схватывать) — острое высококонтагиозное заболевание, высококонтагиозное заболевание, вызываемое РНК-вирусом вызываемое РНК-вирусом (семейство (семейство OrthomyxoviridaeOrthomyxoviridae), ), имеющим сродство к эпителию имеющим сродство к эпителию дыхательных путей. Заболевание дыхательных путей. Заболевание возникает обычно в холодное возникает обычно в холодное время года.время года.

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ЭпидемиологияЭпидемиология..

Болезнь может быть вызвана одним Болезнь может быть вызвана одним из трёх вирусов гриппа: А, В, С. из трёх вирусов гриппа: А, В, С. Серотип А наиболее эпидемически Серотип А наиболее эпидемически опасен, он заражает человека, опасен, он заражает человека, свиней, лошадей и птиц. Серотип В свиней, лошадей и птиц. Серотип В вызывает спорадические вспышки и вызывает спорадические вспышки и эпидемии, а серотип С приводит эпидемии, а серотип С приводит лишь к спорадическим вспышкам лишь к спорадическим вспышкам гриппа, преимущественно у детей.гриппа, преимущественно у детей.

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Заболевший человек заразен за Заболевший человек заразен за 24 ч до появления клинических 24 ч до появления клинических симптомов и в течение двух суток симптомов и в течение двух суток после клинического после клинического выздоровлениявыздоровления

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ПатогенезПатогенез гриппа гриппа

● ● Внедрение и первичная репродукция вируса в Внедрение и первичная репродукция вируса в эпителии дыхательных путей соответствуют эпителии дыхательных путей соответствуют инкубационному периоду болезни. инкубационному периоду болезни. Длительность — от нескольких часов до 2–4 сут.Длительность — от нескольких часов до 2–4 сут.

● ● Вирусемия, сопровождается продромами и Вирусемия, сопровождается продромами и соответствует продромальной стадии болезни.соответствует продромальной стадии болезни.

● ● Вторичная репродукция вируса в Вторичная репродукция вируса в эпителиальных клетках, приводящая к эпителиальных клетках, приводящая к генерализации инфекции, соответствующая генерализации инфекции, соответствующая разгару болезни. Клинически характерны разгару болезни. Клинически характерны повышение температуры, головная боль, повышение температуры, головная боль, катаральный ринит, кашель, конъюнктивит, катаральный ринит, кашель, конъюнктивит, нередко суставные и мышечные боли.нередко суставные и мышечные боли.

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Патогенез и морфогенез гриппа Патогенез и морфогенез гриппа объясняют следующие свойства вируса:объясняют следующие свойства вируса:

  цитопатическое, приводящее к баллонной цитопатическое, приводящее к баллонной дистрофии эпителия дыхательных путей, его дистрофии эпителия дыхательных путей, его слущиванию и лизису, нарушению дренажной слущиванию и лизису, нарушению дренажной функции бронхов;функции бронхов;

  иммунодепрессивное, способствующее развитию иммунодепрессивное, способствующее развитию иммунодефицита (снижение хемотаксиса, иммунодефицита (снижение хемотаксиса, фагоцитарной активности макрофагов и фагоцитарной активности макрофагов и нейтрофилов, появление циркулирующих нейтрофилов, появление циркулирующих иммунных комплексов);иммунных комплексов);

  вазопатическое (вазопаралитическое), вазопатическое (вазопаралитическое), вызывающее гиперемию, стаз, плазматическое вызывающее гиперемию, стаз, плазматическое пропитывание стенок сосудов, периваскулярный пропитывание стенок сосудов, периваскулярный отёк и диапедезные кровоизлияния.отёк и диапедезные кровоизлияния.

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Различают лёгкую, средней Различают лёгкую, средней тяжести и тяжёлую формы гриппа.тяжести и тяжёлую формы гриппа.

● ● Лёгкая форма гриппа Лёгкая форма гриппа встречается наиболее часто. встречается наиболее часто. Характерны острый катаральный Характерны острый катаральный риноларингит или риноларингит или риноларинготрахеобронхит.риноларинготрахеобронхит.

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ГриппГрипп

Катаральное воспаление при гриппе

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Фуксинофильные включения в клетках Фуксинофильные включения в клетках респираторного эпителия при гриппереспираторного эпителия при гриппе

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● ● Грипп средней степени тяжести.Грипп средней степени тяжести. Характерно распространение Характерно распространение воспаления на все отделы воспаления на все отделы бронхиального дерева, иногда до бронхиального дерева, иногда до альвеол. Воспаление серозно-альвеол. Воспаление серозно-геморрагическое или фибринозно-геморрагическое или фибринозно-геморрагическое, с инфильтрацией геморрагическое, с инфильтрацией лимфоцитами, макрофагами, лимфоцитами, макрофагами, единичными нейтрофильными единичными нейтрофильными лейкоцитами, с участками некроза.лейкоцитами, с участками некроза.

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Цитопатические эффекты вируса гриппа Цитопатические эффекты вируса гриппа AA22

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Фибринозно-геморрагический ляринготрахеобронхит

Гнойный бронхит

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● ● Тяжёлый грипп протекает в двух Тяжёлый грипп протекает в двух вариантах: токсический грипп и грипп вариантах: токсический грипп и грипп с лёгочными осложнениями.с лёгочными осложнениями.

◊ ◊ Токсический грипп. Характерны Токсический грипп. Характерны тяжёлые общие изменения и тяжёлые общие изменения и усиление серозно-геморрагического усиление серозно-геморрагического воспаления с нарастанием воспаления с нарастанием геморрагического и некротического геморрагического и некротического компонентов воспалительной компонентов воспалительной реакции. реакции.

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Вирусная энцефалопатия при токсической Вирусная энцефалопатия при токсической форме инфекцииформе инфекции

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  Грипп с лёгочными Грипп с лёгочными осложнениями осложнениями

◊◊возникает при присоединении вторичной бактериальной возникает при присоединении вторичной бактериальной инфекции с развитием тяжёлой очагово-сливной инфекции с развитием тяжёлой очагово-сливной бронхопневмонии, обычно через неделю после начала бронхопневмонии, обычно через неделю после начала заболевания. Для бактериальной инфекции характерно гнойное заболевания. Для бактериальной инфекции характерно гнойное воспаление, вначале серозно-геморрагическое, затем гнойно-воспаление, вначале серозно-геморрагическое, затем гнойно-геморрагическое с некрозом и расплавлением лёгочной ткани. В геморрагическое с некрозом и расплавлением лёгочной ткани. В гортани и трахее — фибринозно-геморрагический (иногда гортани и трахее — фибринозно-геморрагический (иногда некротический) ларинготрахеит, в бронхах — серозно-гнойный некротический) ларинготрахеит, в бронхах — серозно-гнойный или геморрагически-гнойный бронхит с поражением всех слоёв или геморрагически-гнойный бронхит с поражением всех слоёв стенки бронха, нередко с расплавлением её участка стенки бронха, нередко с расплавлением её участка (сегментарный деструктивный панбронхит). Поражённое лёгкое (сегментарный деструктивный панбронхит). Поражённое лёгкое резко увеличено, неравномерной воздушности и плотности за счёт резко увеличено, неравномерной воздушности и плотности за счёт чередования красно-серых выбухающих и западающих синеватых чередования красно-серых выбухающих и западающих синеватых или красно-серых участков ателектазов, вздутых светло-серых или красно-серых участков ателектазов, вздутых светло-серых участков эмфиземы, грязно-серых абсцессов, тёмно-красных участков эмфиземы, грязно-серых абсцессов, тёмно-красных кровоизлияний . Такое лёгкое называют «большое пёстрое кровоизлияний . Такое лёгкое называют «большое пёстрое лёгкое». Селезёнка увеличена незначительно, даёт лишь лёгкое». Селезёнка увеличена незначительно, даёт лишь небольшой соскоб пульпы, лимфаденит выражен слабо.небольшой соскоб пульпы, лимфаденит выражен слабо.

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Множественные очаговые кровоизлияния и очаговые ателектазы

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Пневмония при гриппеПневмония при гриппе

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Гриппозная очагово-Гриппозная очагово-сливная пневмониясливная пневмония

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ИсходыИсходы.. Грипп лёгкой и средней тяжести протекает Грипп лёгкой и средней тяжести протекает

благоприятно, исход (через 5–7 и 20–25 дней благоприятно, исход (через 5–7 и 20–25 дней соответственно) — полное выздоровление. При соответственно) — полное выздоровление. При тяжёлых и осложнённых формах гриппа возможна тяжёлых и осложнённых формах гриппа возможна смерть на 4–5 день от сердечно-лёгочной смерть на 4–5 день от сердечно-лёгочной недостаточности на фоне прогрессирования недостаточности на фоне прогрессирования пневмонии и её осложнений, кровоизлияний, пневмонии и её осложнений, кровоизлияний, интоксикации, геморрагического отёка лёгких. интоксикации, геморрагического отёка лёгких. Наиболее опасен грипп для детей раннего Наиболее опасен грипп для детей раннего возраста, пожилых лиц, пациентов, страдающих возраста, пожилых лиц, пациентов, страдающих сердечно-сосудистыми заболеваниями. У детей сердечно-сосудистыми заболеваниями. У детей возможно развитие ложного крупа и смерть от возможно развитие ложного крупа и смерть от асфиксии, у пожилых — обострение хронических асфиксии, у пожилых — обострение хронических заболеваний.заболеваний.