Infectious and reactive arthritis: Flashcards
a. Infectious arthritides: bacterial (nongonococcal and gonococcal), mycobacterial, spirochetal (syphilis, Lyme), viral (HIV, hepatitis B, parvovirus, other), fungal, parasitic b. Whipple’s disease c. Reactive arthritides: acute rheumatic fever, arthritis associated with subacute bacterial endocarditis, intestinal bypass arthritis, post-dysenteric arthritides, postimmunization arthritis, other colitic-associated arthropathies (37 cards)
What interleukins are important in defense against hepatitis C?
IL-28 A and B and IL-29 are ~200aa, type III interferons that stimulate antiviral state by turning on Mx proteins (interferon induced GTP binding protein), 2’, 5’-oligo adenylate synthetase (results in latent RNase L activation), and interferon stimulated gene factor three (ISGF3G). Polymorphisms vary in ability to counteract hepatitis C.
What is the difference between NIs and NNIs in their actions inhibiting RNA polymerase?
RNA polymerase activity is inhibited by nucleotide analog inhibitors (NIs) which act at the active enzyme site and non-nucleotide analog inhibitors (NNIs) which act at allosteric sites.
What assessment is needed prior to hepatitis C treatment?
Prior to treatment, patients with hepatitis C need to be assessed for cirrhosis, hepatocellular carcinoma, esophageal and gastric varices. Progression to cirrhosis is higher if immunosuppressed, alcohol ingestion, schistosomiasis, hepatitis B, HIV, and male sex,
What are some extra hepatic complications of hepatitis C?
Extrahepatic complications of hepatitis C include mixed cryoglobulinemia, Sjogren’s syndrome, thrombocytopenia, liken planus, porphyria cutaneous tarda, insulin resistance, diabetes mellitus, diabetic neuropathy, autoimmune thyroiditis, B-cell lymphoproliferative disorder. Membranoproliferative glomerulonephritis, cardiomyopathy, central nervous system involvement can occur.
How is hepatitis C spread?
Hepatitis C exposure is high in intravenous drug abuse, intrauterine device users, and those with tattoos. The risk of a needlestick from a known carrier is 1.8%. Improper sterilization of medical and dental equipment in Egypt has led to the highest prevalence worldwide.
How does Trophorema whipplei cause disease?
Trophorema whipplei infection is a common cause of diarrhea in children and a very rare cause of systemic illness in adults.Trophorema whipplei causes Whipple’s disease by producing an overwhelming intracellular disseminated bacterial infection within macrophages. Gram staining reveals the organisms and PAS staining reveals carbohydrate deposits characteristic of the disease.The process is more akin to leprosy in terms of bacterial load and tempo.
What are the musculoskeletal and neurologic manifestations of Whipple’s disease?
Neurologic involvement in Whipple’s disease usually presents as dysarthria, myoclonus, or oculomasticatory myorhythmia.Musculoskeletal involvement usually starts as arthralgia progressing to intermittent tenderness and effusions then persistent arthritis over eight years.
When should the diagnosis of Whipple’s disease be a serious consideration?
Whipple’s disease should be considered in cases of joint pain with weight loss, diarrhea, and abdominal pain. Rare additional presentations include culture negative endocarditis, multiple sclerosis, maladsorption, and hypopituitarism.
How does syphilitic chronic meningitis present?
Syphilitic meningitis is usually asymptomatic, but may present with acutely with headache, confusion, nausea and vomiting, and stiff neck. Inflammatory vasculitis resulting in posterior uveitis and diminished visual acuity. Additional manifestations include optic neuropathy, interstitial keratitis, uveitis, chorioretinitis and retinal vasculitis. Facial and auditory nerves may also be involved.
What are the symptoms and initial laboratory findings indicative of Human Granulocytic Ehrlichiosis (HGE), Human Monocytic Ehrlichiosis (HME), or Human Granulocytic Anaplasmosis (HGA, anaplasmosis) due to Anaplasma phagocytophilum?
Ehrlichiosis is due to an obligate intracellular gram negative bacteria of the family Anaplasmataceae, genera Ehrlichia and Anaplasma. Symptoms usually include high fever, joint and muscle aches, and occur up to 14 days following a tick bite. Occasional rash occurs in HME. Leukopenia, thrombocytopenia, and elevated liver enzymes are common. Immunosuppression commonly follows. Death is usually due to respiratory distress syndrome, hepatitis, or opportunistic nosocomial infections. Doxycycline is recommended for all suggestive systemic illnesses if tick exposure is suspected. Tick bites should be watched and treated should fever develop.
What are the diagnostic methods used for Human Monocytic Ehrilichiosis (HME), and Human Granulocytic Anaplasmosis (HGA)?
Diagnosis can be made by a serology using indirect fluorescent antibody test, peripheral blood or Buffy coat examination for intraleukocytic morulae, PCR for HME and HGA, immunochemical staining of ehrlichial or anaplasmal antigens in tissue. Due to cross reactivity among species and non standard procedures definite cut off levels for positivity are impossible but increasing titer x4 is convincing. HGA is carried by Ixodes scapularis in the eastern United States and I. pacificus in the western United States. HME is carried by the Lone Star tick (Amblyomma americanum.
How are Human Granulocytic Ehrlichiosis (HGE), Human Monocytic Ehrlichiosis (HME), Human Granulocytic Anaplasmosis (HGA, anaplasmosis) due to Anaplasma phagocytophilum classified?
Current taxonomy has reclassified ehrlichea by ribosomal DNA into 3 genera-ehrlichia - E. chaffeensis Etc., anaplasma-phagocytophilum, previously known as E. phagocytophilia, E. muris, and neorickettsia previously known as E.sennetsu. Most such organisms have complex genomes with multiple tandem repeats and frequent mutations. They affect animals-horses, deer; only three affect humans. Major target of HGA is the neutrophil, and HME use the mononuclear phagocytic cell and macrophages.
How does Anaplasmosis cause disease?
A. Phagocytophilum binds neutrophils that express CD15s (sialyated glycoprotein) by a specific platelet selection ligand. A phagocytophilum can evade oxidative killing by neutrophils but not monocytes. It also can prevent fusion of neutrophil cytochrome b558 granules, and delay apoptosis. At least 100 different surface proteins are available for switching expression, thus evading host defenses, causing chronic disease. Although antibody development does not correlate with resolution of infection, they can passively protect SCID mice, and complement receptor deficiency increases mortality.
How do Ehrlichia cause disease
Ehrlichia does not produce vasculitis, thrombosis, or acute or chronic endothelial cell injury as richettsial diseases do. Non-follicular lymphadenopathy with disappearance of follicles and lymphocytes is common. A phagocytophilum infection in humans may cause parenchymal and perivascular lymphohistiocytic infiltrates and hematologic abnormalities are due to macrophage destruction rather than bone marrow suppression.
How is hepatitis B excluded when considering immunosuppressive treatment?
Hepatitis B may flare when immunosuppression is started in tolerant patients, or when stopped if immunosuppression is controlling the hepatitis. Reactivated cytotoxic CD8+ T cell may induce more hepatic inflammation. During immunosuppression hepatitis is suppressed but viral production is not. Hepatitis B treatment may include pegylated interferon alpha, Lamivudine, Adefovir, Entecavir, Telbivudine, and Tenofovir and requires at least 1 year duration. GI consult help is necessary.
What is the best screening test for hepatitis B?
Test for surface antigen (small medium large in lipid envelope HBsAg) and antibody (anti-HBs), and anti-core antibody (anti-HBc), e antigen (between nucleocapsid and envelope HBeAg) and antibody (anti-HBe) may be positive during ongoing hepatitis B infection. Hepatitis B DNA testing is done to help with treatment more than for screening. Hepatitis B core antigen (nucleocapsid protein HBcAg) stays in the nucleus and may be demonstrated via liver biopsy.
What is the usual course of antigen/antibody changes during infection with hepatitis B?
During the initial course of hepatitis B Infection in adults, HBV DNA appears followed by hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg). Hepatitis core antigen develops in hepatocytes but is not secreted but the e antigen (a secretory protein processed from the precore protein) does. All 3 appear prior to symptoms. IgM anti-HBc appears at the onset of symptoms. At the time of recovery HBV DNA disappears first, then anti-HBe replaces HBeAg and anti-HBs replaces HBsAg, and HBV decreases.
What countries have a high incidence of hepatitis B (>8%) ?
All of Asia, South Pacific islands, and Africa, Middle East except Cyprus and Israel, Eastern Mediterranean-Malta and Spain, indigenous populations of Alaska, Canada, Greenland, South America-Ecuador, Venezuela and Amazon regions Bolivia, Brazil, Colombia, and Peru. All of Eastern Europe save Hungary, most of the Caribbean and in Central America Guatemala and Honduras.
Who is at risk for infection by hepatitis B?
Other people at risk for hepatitis B include infants of parents with hepatitis B, household contacts of HsAg positive parents, sexual partners of HBsAG positive patient, people with multiple sexual partners, men who have sex with men, inmates, those with chronically elevated ALT or AST, infected with HCV or HIV, renal dialysis, all pregnant women, prior to immunosuppressive therapy.
What determines prognosis during acute hepatitis B infection?
Prognosis is worse initially in severe cases with prolonged PT and encephalopathy. Those with chronic or intermittent ALT elevation are at risk for cirrhosis or HCC (hepatocellular carcinoma).
What antiviral medication is available to treat hepatitis B?
Antiviral treatment Telbivudine (synthetic thymidine nucleoside analog, lamivudine (cytosine analog), adefovir (acyclic nucleotide reverse transcriptase inhibitor), Entecavir (hepatitis B viral nucleotide reverse polymerase inhibitor), or tenofovir (a nucleotide reverse transcriptase inhibitor).
How is the hepatitis B virus genome organized?
The hepatitis B virus consists of a partially double-stranded DNA chains (~3000 nucleotides) that partially overlap forming a discontinuous circle. 4 proteins are produced, S producing HBsAg, with three sites of origin; the viral DNA polymerase, C producing HBcAg, alternate start site produces HBeAg, and X gene which is important in inducing hepatocellular carcinoma. The DNA produced is circular as part of each RNA chain is trimmed or elongated.
What can cause a flare during the course of hepatitis B infection?
Hepatitis B disease flare occurs in those treated with rituximab, hematologic malignancies, and preparative therapy for bone marrow transplant. Reactivation in HBsAg positive or those with high levels of HBV DNA and anti-HBc positive, flares occur more often if male sex, or use of glucocorticoids.
Why do steroids increased risk of flare of hepatitis B?
HBV DNA replication is increased during glucocorticoid treatment due to a steroid promoter in the viral genome.
