Hiv/aids

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Common effects of antibody deficiency

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Infection with pyogenic bacteria (pneumonia and ear infections) and Giardia

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Common effects of T cell deficiency

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Infection with viruses, fungi, protozoa, and intracellular bacteria

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Common effects of combined B and T cell defects

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Infections of all kinds

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Common effects of phagocytic cell dysfunction

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Recurrent pyogenic bacterial skin infections (boyles) and periodontitis

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Common effects of complement deficiencies

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Pyogenic bacteria, immune complex disease

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X-linked hypoagammaglobulinemia

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Brutons disease, presents about 6 months of age and results in very low B cell count and low serum IgG. Due to mutation on btk gene

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Common variable immunodeficiency

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variable inheritance, presents as an adult, normal B cell count but all have abnormal function.

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Treatment for primary antibody deficiency

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IV administration of human IgG monthly for life

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Hyper IgM syndrome

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Due to lack of CD40 ligand on T cells. Without CD40 interaction, there is no class switch to IgG. Results in recurrent bacterial infections

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Selective IgA deficiency

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Normal B cells but very low IgA levels. Anti-IgA found in some patients. Mostly asymptomatic, but can have some recurrent bacterial infections

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DiGeorge Syndrome

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Thymic aplasia due to deletion on chromosome 22. Effects 3rd and 4th pouches (thymus and parathyroids). Low T cells and deficient B cell function. Need thymus transplant

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Severe Combined Immune Deficeincy (SCID)

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Due to mutations, thymic aplasia and atrophy of lymphoid tissue. Low B and T cells. Need bone marrow graft or gene therapy

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Neutrophil dysfunction

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Periodontitis is a very common manifestation, as well as recurrent pyogenic infections and chronic granulomatous disease

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Compliment deficiencies

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C1 inhibitor results in angioedema, C1,2,4 results in immune complex disease, C3 bacterial infections, C5-9 Neisserial infections

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Most common cause of immune deficiency worldwide

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Malnutrition due to low protein and calorie. Results in reduced lymphocyte responsiveness

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一个星期

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yí ge xīngqī

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a week

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What cells in the body have the highest frequency of HIV infection?

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Memory CD4+ T cells in the gut (where most CD4 cells reside)

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Which non-CD4 cells can become infected by HIV?

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Mucosal epithelial cells. They are infected through a galactosylceramide receptor by CXCR4 tropic strains

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What is the major infected cell type in the CNS?

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Microglial cells that express CD4 and CCR5 (M-tropic HIV strains). Infected cells release neurotoxins that kill other cells.

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How long does it take for HIV viral loads to peak?

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There is only a 10 hour doubling time for viral load and peak viremia is at about 21 days.

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HIV reservoirs

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Resting memory T cells (months-years), macrophages (14 days), follicular dendritic cells (months-years), astrocytes and parenchymal microglia

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What is unique about follicular dendritic cells as HIV reservoirs?

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They trap virions of many different serotypes for a very long time. Looking at these is a good way to look at infection history.

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Humoral immune response to HIV

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Slow response (2-12 weeks), very innefective because HIV env proteins are heavily glycosylated and they are highly variable due to mutation

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Cell mediated response to HIV infection

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CD8+ cells release chemokines that block CXCR4 expression and help stop infection of new cells.

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What factor has the strongest correlation with HIV outcome?

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Activity of polyfunctional CD8+ T cells that produce a strong IFN-gamma response along with IL-2 and TNF

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HIV immune evasion

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Infection and depletion of effector T cells and macrophages. Glycosylation of gp120, high mutation rate, down-regulation of MHC-1, and ability to establish reservoirs.

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Mechanism of T cell depletion in AIDS

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Cell lysis, syncitia formation, CTL killing infected T cells, infection of T cell presursors.

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Polyclonal B cell activation in HIV

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gp120 binds to mannose C-type lectin receptors and B cells undergo class switching without CD40. Many different antibodies produced to all kinds of things

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Cell populations in HIV

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Total lymphocyte count down, T cell count down, CD4+ count down, B cell count normal or elevated

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Cell function in HIV

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DTH down (anergy), IL-2 production down, serum antibody will be high at first, then fall off.

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Lymph node pathology in AIDS

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Early on there will be follicular hyperplasia where the node will be stuffed full of follicles. Then there will be follicular involution and atrophy of the lymph node (also seen in spleen and thymus)

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AIDS defining criteria (in terms of T cell count)

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>500 is during acute infection period, 200-499 is symptomatic but not AIDS defining, <200 is definition of AIDS

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Predictors of control in "elite HIV controllers"

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HLA B27 and B57, CCR5-delta32 polymorphism, and good quality CTL response

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Herpes simplex virus in AIDS

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Recurrent infections with increased severity, often disseminated (encephalitis and esophagitis), which is unusual in healthy pts. DOC acyclovir

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HSV-2 and AIDS

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you have an increased susceptibility to HIV infection
and the HIV pos person has increased ability to give it to
you…bottom line, if you both have HSV-2 you're screwed

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CMV and AIDS

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Causes retinitis that can cause blindness. Also, pneumonia and sialadenitis. DOC is gancyclovir

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EBV and AIDS

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Associated with primary CNS lymphoma (most common neoplasm in AIDS), and oral hairy leukoplakia. HAART has reduced incidence

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Herpes Zoster and AIDS

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More serious infection in AIDS and involves more than one dermatome and is bilateral(which never happens in healthy pts). May disseminate and cause encephalitis or ocular problems. DOC acyclovir and analgesia

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JC virus and AIDS

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Most people have this, but only causes problems in AIDS. Causes progressive multifocal leukoencephalopathy (PML). White matter in CNS degenerates and causes ataxia and dementia

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HPV and AIDS

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Causes oral warts (types 6 and 11) and cervical cancer (types 16 and 18). Cervical cancer in HIV pt is considered AIDS defining

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Hep B and AIDS

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Co-infection is common bacause risk factors are similar. HIV pts have increased risk of chronic hepatitis and serious liver disease. Also, they are more infectious (high HBe)

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Hep C and AIDS

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HIV infection appears to speed progression of HCV to end stage liver disease. 45% of HIV+ pts are HCV+ also

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Candida and AIDS

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Most common oral manifestation in AIDS. Can be esophageal, heart/lungs. Predictive for AIDS.

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DOC for candida

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nystatin for topical use, ketoconazole or fluconazole for oral, micafungin for esophageal, and amphotericin B via IV for systemic infection

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hyperplastic candida

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whitish plaques that can't be removed. May be confused with hairy leukoplakia. 9-40% of cases are associated with underlying oral cancer.

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Pneumocystis jirovecii and AIDS

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a ubiquitious fungus that is the most common AIDS defining opportunistic pathogen. Most common cause of pneumonia in AIDS. DOC is trimethoprim-sulfamethoxazole

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Cryptococcus neoformans

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Encapsulated yeast found in pigeon droppings. Most common manifestation is meningitis. DOC amphotericin B

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Bacterial respiratory diseases and AIDS

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S. pneumoniae and H. influenzae are the most common casue of bacterial pnuemonia in HIV pts and the most common cause of death from pneumonia

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tuberculosis and AIDS

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TB is the major OI in HIV/AIDS worldwide and 1 in 8 people with AIDS dies of TB. Higher risk of primary and reactivated disease than non-AIDS.

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Cryptosporidium parvum and AIDS

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animal reservoir, transmitted by contaminated water. Produces watery diarrhea in AIDS and DOC is paromomycin

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Microsporidia and AIDS

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Obligate intracellular parasite, causes diarrhea, but also can cause pulmonary problems, hepatitis, ocular infection, and encephalitis.

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Toxoplasma gondii

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Cats are the host. Causes dissemination of cysts in visceral organs, and eye (retinitis), and CNS (50% of all brain lesions in AIDS). Often fatal, DOC trimethoprim-sulfamethoxazole

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What are the most common oral manifestations in AIDS?

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80% of AIDS pts have oral manifestations. Candida is number one and hairy leukoplakia is number two.

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AIDS defining cancers

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Kaposi's sarcoma, non-Hodgkin lymphoma, including primary CNS brain lymphoma, and invasive cervical cancer

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Relative risk of Kaposi sarcoma in HIV pts

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HIV patients are 73,000 times more likely to get KS. It is the most common neoplasia in HIV. MSM is the greatest risk group

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Effects of Kaposi's sarcoma

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Proliferation of small, delicate capillaries within tumors that are very susceptible to bleeding. Common in GI tract, bronchial, and 22% occur as oral lesions (mostly on palate)

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Oral Kaposi's sarcoma

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>50% of pts with skin KS also have oral lesions. Primarily on hard and soft palate. Lesions are areas of purple discoloration that can become raised and/or blood-filled. There is a lot of variation in presentation, so it can be hard to recognize

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Treatment of Kaposi sarcoma

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Low-dose radiation, chemotherapy, and alpha-interferon. You can inject the drugs directly into the cancer and it works well. Painful mucositis can occur in AIDS pts

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Incidence of lymphomas in HIV pts

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Occurs in about 10% of HIV+ pts without HAART. Non-Hodgkin is much more common than Hodgkin.

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Non-Hodgkin lymphoma

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second most common neoplasm in AIDS (80% of all lymphomas), this is an AIDS defining condition. 5% are intraoral and 60% are extra-nodal, primarily in the brain and GI tract.

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Squamous cell carcinoma and AIDS

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The tongue is the most frequent site. Carcinogenic factors play a role, but HIV pts are 2-6 times more likely to develop this oral cancer. Rx is radiation and/or surgery

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Cancer in HIV/AIDS in the HAART era

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Both Kaposi sarcoma and non-hodgkin lymphoma have dropped in incidence since HAART era began

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Linear gingival erythema

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Only happens in AIDS pts, 2-3mm wide erythematous band along the gingival margin. Usually painless and often bleeds. Likely caused by fungus (Candida)

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Rx for linear gingival erythema

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Chlorhexidine or ketoconazole. If those don't work, metronidazole can be taken

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Necrotizing ulcerative gingivitis

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Results in rapid destruction of soft tissue, especially interdental papillae. No attachment loss, but bleeding, pain, and halitosis are common.

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Necrotizing ulcerative periodontitis

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Marker of severe immunodeficiency (<100 T-cells). Preceeded by intense bone pain and is acute and rapidly progressive. There is attachment loss, but no pockets due to necrosis of tissue.

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Rx for necrotizing ulcerative periodontitis

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Debridement first, followed by chlorhexidine and antibiotics (metronidazole, amoxicillin, or clindamycin)

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Necrotizing stomatitis

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similar to NUP, rapid destruction of alveolar bone and gingiva w/severe pain. May involve palate, tongue, and buccal mucosa.

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Rx for necrotizing stomatitis

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same as NUP

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Periodontal abscess and AIDS

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Debride pocket and remove plaque, then do a culture. Consider systemic antibiotics and prophylactic antifungal

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Caries in AIDS pts

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Studies dhow increased risk of caries. Possibly due to xerostomia caused by HAART and sugar content of childrens medications.

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Oral lesions from M. tuberculosis

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May appear as painful, indurated ulcers. Probably caused by auto-innoculation from pts own infected sputum.

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Pseudomonas aeruginosa in AIDS pts

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Can cause necrotic gingiva

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Make-up of HAART meds

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Cocktail of 2 reverse transcriptase inhibitors and 1 protease inhibitor.

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Nucleoside reverse transcriptase inhibitors (NRTI)

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First generation not very specific, caused bone marrow suppression and liver toxicity. Azidothymidine (AZT) then Zidovudine (ZDV) which is more specific to RT

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Mechanism of action of NRTI

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Nucleoside analog that blocks active site of reverse transcriptase and terminates DNA synthesis

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Non-nucleoside reverse transcriptase inhibitors (NNRTI)

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Nevirapine (NVP), Efavirenz (EFV), Delavirdine (DLV), and Etravirine

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Mechanism of action of NNRTI

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These aren't nucleoside analogs, they bind allosterically and inhibit in a non-competitive way. These are less toxic and have less side effects

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Protease inhibitors

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Block the HIV protease from cleaving the polyprotein. Highly specific, blocks active site. DOC Ritonavir (RTV)

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Fusion inhibitors

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Binds to gp41 and prevents formation of viral entry pore. DOC is Enfuvirtide (INN)

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Entry inhibitor

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Blocks gp120 from binding CCR5 (M-tropic strains only). DOC is Maraviroc and it is a CCR5 antagonist

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Integrase inhibitors

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Approved for HAART resistant pts, prevents the integration of viral DNA into host genome. DOC is Raltegravir

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Indications for HAART therapy

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All HIV pts with AIDS-defining illness or CD4 count <350, all pregnant HIV pts, and HIV post-exposure prophylaxis (ie. needle stick)

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Which HIV pts would not receive HAART

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HAART is optional during the acute HIV infection stage

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HAART and pregnancy

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After 12 weeks gestation, mother should start 3-part ARV regimen that includes AZT. Newborn should be given AZT for first 6 weeks of life

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HIV post-exposure prophylaxis

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Either use a 2 drug regimen (2 NRTI's) or a 3 drug regimen (2 NRTI's and 1 protease inhibitor) for 4 weeks.

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What is the most common manifestation of immune restoration disease (IRD)?

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Flares of mycobacterial disease when immune system rebounds. There will be an overwhelming inflammatory response

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Side effects of protease inhibitors

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They cause lipodystrophy, which is an abnormal change in fat (either weird accumulations of losses). Women get buffalo hump and crixy belly. Usually accompanied by increase in fat levels in the blood.

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Ancillary therapies for AIDS

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Biological response modifiers: Erythropoietin for red cell dysplasia, GCSF for neutropenia, and Interferon-alpha for Kaposi's sarcoma

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What is the most common type of HIV?

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HIV-1 is the more common type. M group is the most common worldwide, B most commin in states and Europe.

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Symptoms of acute HIV infection

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Fever, pharyngitis, myalgias, headache, nausea, diarrhea, maculopapular rash, and oral ulcers (mononucleosis like illness)

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Asymptomatic HIV infection

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last 10 years on average, no symptoms aside from lymphadenopathy. Pt should be treated evaluated and treated for other diseases

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Early symptomatic HIV infection

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Diarrhea and weight loss (cryptosporidium), and candidiasis are common

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Late symptomatic and advanced HIV infection

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AIDS defining fungal, viral, bacterial infections and neoplams.

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AIDS defining fungal infections

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candidiasis, coccidioidomycosis, cryptococcis, histoplasmosis, pneumocystis jirovecci

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AIDS defining viral infections

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Cytomegalovirus, Herpes simplex, JC virus

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AIDS defining bacterial infections

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Mycobacterium avium and tuberculosis. Also, salmonella septicemia.

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AIDS defining parasitic infections

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Cryptosporidiosis and isosporosis

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AIDS defining neoplasias

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Cervical cancer, Kaposi's sarcoma, brain lymphoma, and non-Hodgkin lymphoma

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Diagnosis of HIV

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ELISA for HIV antibody, Western blot (gold standard) for proteins, or PCR for viral RNA.