Y2 2013 Spring Microbiology Block II – Flashcards
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| What is the primary causative agent of tooth decay? |
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| Streptococcus mutans |
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| What causes cariogenic dental plaques? |
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| Mouth acidity |
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| What is periodontal disease? |
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| Inflammation of the gums in response to plaque bacteria such as in dental calculus or gingivitis Responsible for tooth loss in the elderly |
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| What causes gingivitis? |
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| Porphyromonas gingivalis |
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| What causes trench mouth? |
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| Synergistic infection of spirochetes (oral spirochete of Treponema genus; T. pallidum is the cause of syphilis) and anaerobic bacteria |
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| What causes watery diarrhea? |
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| Pathogenic mechanisms that attack the proximal small intestine (more than 90% of physiologic net fluid absorption occurs) |
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| What organisms cause the purest form of watery diarrhea? |
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| Enterotoxin-secreting bacteria such as Vibrio cholerae and enterotoxigenic Escherichia coli (ETEC), which cause fluid loss without cellular injury |
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| Which causes of watery diarrhea are uniquely not self limiting to 1-3 days? |
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| V. cholerae, which usually produces a more severe illness Giardia lamblia, which produces a watery diarrhea that may last for weeks |
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| What is dysentery? |
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| Rapid onset of frequent intestinal evacuations, but the stools are of smaller volume than in watery diarrhea and contain blood and pus |
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| What causes dysentery? |
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| Inflammatory and/or destructive changes in the colonic mucosa either by direct invasion or by production of cytotoxins |
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| What causes enteric fever? |
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| Penetration by the organism of the cells of the distal small bowel with subsequent spread outside the bowel to the biliary tract, liver, mesentery, or reticuloendothelial organs |
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| What is the only infection causing enteric fever that is well studied? |
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| Typhoid fever caused by Salmonella enterica serotype Typhi |
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| What are the most common causes of traveler's diarrhea? |
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| 50% caused by ETEC 10%-20% by Shigella species Ingestion of uncooked or incompletely cooked foods is the most likely source of infection |
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| What are the most common causes of food poisoning? |
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| Salmonella, Clostridium perfringens, and S. aureus Most often due to improper storage temperature |
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| What are the most common causes of hospital associated diarrhea? |
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| E. coli (in infants) C. difficile (patients on antibiotics) |
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| Which hepatitis virus is "silent" and often goes undetected? |
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| Hep C |
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| How is liver cell damage present? |
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| Hepatic cell degeneration and necrosis, cell dropout, ballooning of cells, acidophilic degeneration of hepatocytes forming Councilman or apoptotic bodies |
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| What are the unique features of Hep A? |
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| Single stranded RNA picornavirus Resists inactivation and is stale at -20C with low pH Never becomes chronic, has only one serotype, no animal reserve, vaccine existence is leading to eradication of the virus |
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| What kind of abnormal liver cells are characteristic of liver disease? |
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| Kupffer cells |
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| What are the symptoms of Hep A? |
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| Fever, anorexia, nausea, pain in upper right abd, jaundice, dark urine and clay-colored stool, enlarged, tender liver, elevated serum aminotransferase and bilirubin Will never cause cancer or progress to chronic liver disease |
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| How is Hep A treated? |
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| Almost all are self limiting to a few weeks-months |
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| How is Hep A detected in serology studies? |
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| Fecal HAV detected 4-6 weks IgM Anti-HAV detected early on but then drops IgG is inclusive because it increases over time, needs to see the trend |
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| How long in advance must immune serum globulin be given to confer temporary immunity to Hep A? |
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| Protective if given before or during the incubation period of the disease Not indicated once symptoms have appeared |
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| What are the unique features of Hep B? |
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| Member of hepadnaviridae family Smallest DNA virus known All newborns become chronic, 50% of children become chronic |
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| What is present in the nuclei of cells infected with Hep B? |
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| HBcAg, HBeAg, and hepatitis B DNA |
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| What is present in the cytoplasm of cells infected with Hep B? |
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| HBsAg |
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| The HBV S gene codes for what? |
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| The "major" envelope protein HBsAg |
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| What does the HBV P gene code for? |
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| Largest gene, codes for DNA polymerase |
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| What does the HBV C gene code for? |
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| Two nucleocapsid proteins, HBeAg, a soluble, secreted protein and HBcAg, the intracellular core protein |
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| What does the HBV X gene code for? |
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| HBxAg, which can transactivate the transcription of cellular and viral genes; its clinical relevance is not known, but it may contribute to carcinogenesis by binding to p53 |
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| How do infants acquire HBV from their mother? |
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| Not vertically, accquired intrauterally via ingestions or abrasions during birth |
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| What are the consequences of chronic HBV infection? |
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| Necrosis of hepatocytes, Collapse of the reticular framework of liver Progressive fibrosis Leads to syndrome of postnecrotic hepatic cirrhosis |
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| What causes extrahepatic manifestations of HBV? |
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| Deposition of HBsAg-anti-HBs circulating immune complexes in tissue blood vessel walls results in prodromal serum sickness-like syndrome, glomerulonephritis, and nephritic syndrome |
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| Polyarteritis nodosa is associated with which Hep virus? |
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| HBV Develops in considerably fewer than 1% of patients with chronic HBV infection However, 20 to 30% of patients with PAN have HBsAg in serum |
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| Essential mixed cryoglobulinemia is associated with which Hep virus? What are its features? |
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| HBV, HCV Precipitates at cold temp Arthritis Cutaneous vasculitis (palpable purpura) Glomerulonephritis (occasional) Circulating cryoprecipitable immune complexes (more than one immunoglobulin class) |
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| What are the characteristics of HBsAg? |
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| HBV surface antigen formed in excess and seen in serum |
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| What are the characteristics of HBcAg |
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| HBV core antigen found in nucleus of infected hepatocytes by immunofluorescence |
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| What are the characteristics of HBeAg |
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| HBV glycoprotein associated with the core antigen, used as a marker of potential virus activity, only seen when HBsAg is also present |
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| What are the characteristics of Anti-HBs |
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| Ab to HBsAg, correlates with past infection or immunization |
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| What are the characteristics of Anti-HBc |
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| Ab to HBcAg, seen in acute infection and chronic carriers, can be either IgM or IgG (acute vs. chronic) |
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| Anti-HBc IgM indicates what? |
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| Acute HBV infection |
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| Anti-HBc IgG indicates what? |
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| Chronic HBV infection |
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| Presence of Anti-HBe indicates what? |
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| Virus is not actively reacting and is in recession |
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| What is the best diagnostic measure for HBV detection? |
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| IgM antibody to HBcAg along with or without HBsAg in the serum |
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| How is vertical transmission of HBV to newborns prevented? |
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| Use of combined HBIG and HBV vaccine |
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| How do you treat chronic HBV? |
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| Interferon-alpha, Lamivudin, Adefovir |
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| What is the leading cause for liver transplants in the US? |
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| Liver failure due to Hep C |
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| How is HCV contracted? |
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| Commonly transmitted through blood contact (blood transfusion or needle sharing) than through transfer of body fluids; vertical transmission is possible |
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| What is the most common complication of HCV? |
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| Chronic liver disease (80% of cases with a course of intermittent inflammation and normality) 10-20% of chronic patients develop cirrhosis or cancer in the long run |
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| What is the average time from infection to the development of chronic hepatitis in HCV patients? |
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| 10-18 years Often asymptomatic |
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| What are the extra-hepatic manifestations of HCV? |
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| Essential mixed cryoglobulinemia (EMC) Circulating immune complexes containing HCV RNA Immune-complex glomerulonephritis |
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| How is HCV diagnosed? |
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| Detection of HCV antibody May remain negative for 1-3 weeks after clinical onset May never become positive in up to 20% of patients with acute, resolving disease |
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| How is HCV treated? |
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| Combination treatment with interferon-a and ribavirin |
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| The protein-RNA complex of Hep D is surrounded by what? |
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| HBsAg |
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| How is Hep D diagnosed? |
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| IgM or IgG antibodies or both to the delta antigen in serum IgM antibodies appear within 3 weeks of infection and persist for several weeks IgG antibodies persist for years |
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| How is Hep D prevented? |
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| By preventing Hep B |
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| How is Hep D treated? |
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| Interferon alpha Response to treatment in patients with delta hepatitis (and hepatitis B) is less than in those with hepatitis B alone |
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| The majority of GI pathogenic bacteria grow on what medias? |
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| Majority are gram-neg and grow on MacConkey agar which inhibits gram-pos growth |
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| How is Hektoen agar used to diagnostically distinguish GI pathogenic bacteria? |
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| Inhibits common colon flora Selective to recover Salmonella and Shigella spp. Indicators to detect H2S production (black centers to colony) |
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| What does Campylobacter spp. grow on? |
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| Enriched blood agar |
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| What is acute diarrhea and what are its causes? |
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| Diarrhea lasting 7-14 days caused by: Drugs Infectious Agents (Virus, Bacteria, Parasite) Feeding after a long fasting Fecal Impaction |
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| Which GI bacteria have vaccines? |
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| Most don't |
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| What makes distinguishing E. coli so difficult? |
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| Many strains are a part of the normal GI flora and basic diagnostics will not discriminate between normal and pathogenic E. coli |
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| What are the most common causes of Enterotoxigenic E. coli (ETEC)? |
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| Ingestion of contaminated water or food Major cause of travelers diarrhea |
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| What is the most common progression of a GI infection? |
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| Bacteria pass through to intestines Attachment to mucous layer or intestinal epithelia Secretion of toxins Induction of diarrhea and potentially other symptoms Clearance by host immune system |
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| What are the symptoms of an Enterotoxigenic E. coli (ETEC) infection? |
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| Watery diarrhea, cramps, vomiting, malaise, fever More severe symptoms if the infecting ETEC strain secretes both types of toxins |
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| What toxins are secreted by Enterotoxigenic E. coli (ETEC)? |
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| Either one or both: ST (small toxin) LT (heat labile toxin pierces the membrane of target cell) |
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| How is Enterotoxigenic E. coli (ETEC) diagnosed? |
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| Characteristic symptoms with ONLY lactose fermenting organisms on differential media ELISA for toxins |
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| How is Enteropathogenic E. coli (EPEC) contracted? |
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| Lack of good hygienic practices: fecal oral contamination Most often in infants (1 year old or less usually) with adults as carriers |
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| How is the progression of Enteropathogenic E. coli (EPEC) unique? |
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| Secretes of factors that alter the “host” cells (Type III secretion) Changes epithelial cell cytoskeleton to create a “pedestal” for the bacterial cell |
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| What are the symptoms of an Enteropathogenic E. coli (EPEC) infection? |
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| Fever, vomiting, watery diarrhea that may contain large amounts of mucus Associated with clusters in the US such as daycare, hospitals, nursery |
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| How is Enterohemorrhagic E. coli (EHEC) most often contracted? |
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| Lack of good hygienic practices Ingestion of insufficiently cleaned or cooked foods Reservoir is usually adult cattle which are asymptomatic |
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| How is the progression of Enterohemorrhagic E. coli (EHEC) unique? |
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| Also involved in Type III secretion and pedestal formation May result in temporary or permanent systemic damage |
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| What are the signs and symptoms of Enterohemorrhagic E. coli (EHEC)? |
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| Watery diarrhea that progresses to *bloody diarrhea, abdominal cramps, +/- fever, may also develop hemolytic uremic syndrome (HUS) |
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| What causes hemolytic uremic syndrome (HUS)? |
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| o Toxin release into the bloodstream leads to lysis of erythrocytes, thrombocytes, and destruction of glomerular capillary endothelial cells Children and elderly are more susceptible, can be fatal |
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| Hemolytic uremic syndrome (HUS) is most commonly associated with what? |
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| O157:H7 |
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| What toxins are secreted by Enterohemorrhagic E. coli (EHEC)? |
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| Functionally and structurally related to the Shiga toxin AB type toxins The A subunit interacts with cellular ribosomes cleaving a single adenine residue from the 28S rRNA* leading to a shut-down of host protein synthesis |
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| What special consideration should be made in the treatment of Enterohemorrhagic E. coli (EHEC)? |
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| Monitoring for renal failure |
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| How is Enterohemorrhagic E. coli (EHEC) diagnosed? |
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| Cultures that fail to ferment sorbitol MacConkey agar using sorbitol instead of lactose ELISA for toxins MUG assay: EHEC typically do not produce b-glucoronidase while 92% of other strains do |
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| How is Enteroinvasive E. coli (EIEC) contracted? |
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| Fecal to oral contamination Reservoirs involve human sources |
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| What is unique about the progression of Enteroinvasive E. coli (EIEC) infections? |
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| Secretion of factors that induce uptake and transmission by M cells* Entry into the inferior or lateral sides of intestinal epithelial cells |
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| What are the signs and symptoms of an Enteroinvasive E. coli (EIEC) infection? |
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| Many are asymptomatic or with transient fever Early: Fever, severe cramps, Watery diarrhea Late: Reduced fever, increased diarrhea with blood*, urgency, tenesmus |
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| What additional treatment option can be used for Enteroinvasive E. coli (EIEC)? |
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| Antibiotics may be administered for more severe cases and will decrease the length of symptoms |
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| How is Enteroinvasive E. coli (EIEC) diagnosed? |
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| HE (Hektoen enteric) agar, MacConkey DNA probes are commercially available |
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| What is unique about the progression of Enteroaggregative E. coli (EAEC) infections? |
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| Bacteria replicate and aggregate in a unique “stacked brick” fashion (biofilm) |
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| What is a unique symptom of Enteroaggragative E. coli (EAEC) infection? |
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| May cause a protracted course of diarrhea (>14 days) in adults and children in all parts of the world |
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| What are the toxins secreted by Enteroaggragative E. coli (EAEC)? |
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| ShET1 (Shigella enterotoxin 1) similar to a toxin common in Shigella EAST1 shows similarity to ETEC toxin ST Pet: A serine protease that alters the enterocyte cytoskeleton (not in all strains) |
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| Which E. coli strains cause watery diarrhea? |
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| EPEC, ETEC, most Viral, (EAEC) |
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| Which E. coli strains cause bloody diarrhea? |
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| EHEC, Shigella spp./EIEC, (EAEC) |
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| Which E. coli strains cause watery and mucoid diarrhea? |
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| EPEC |
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| Which E. coli strains are associated with recent travels? |
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| ETEC, EAEC, Rotavirus |
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| What is the appearance of Yersinia spp.? |
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| Gram negative bacillus motile at 25C but not 37C |
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| What does Yersinia culture on? |
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| Most enteric media except Salmonella-Shigella agar Produces urease |
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| Yersinia is very sensitive to levels of what mineral? |
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| Iron |
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| How is Yersinia contracted? |
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| Ingestion of contaminated food or water Handling infected animals or carcasses Very rarely blood transfusion Swine is the primary reservoir |
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| What is unique about the pathogenesis of Yersinia infections? |
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| Bacteria invade the M cells of the gut and start replicating Phagocytic cells ingest Yersinia spreading them to the reticuloendothelial system, and are then killed by the bacteria delaying the immune response |
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| What are the signs and symptoms of a Yersinia infection? |
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| Enterocolitis Mesenteric adenitis and terminal ileitis Exudative pharyngitis Tender red nodules on extensor surfaces of limbs |
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| What symptoms does enterocolitis refer to? |
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| Fever lasting 1-3 weeks, diarrhea containing mucous and blood, abdominal cramps, anorexia, nausea and vomiting, Rectal bleeding in severe cases Potentially severe dehydration |
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| What post-infectious syndrome is common in patients recovering from a Yersinia infection? |
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| Reactive arthritis |
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| What is the general function of toxins secreted by Yersinia? |
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| Most of the virulence factors are regulated in expression by the local environment and are aimed at suppressing the immune system |
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| How is Yersinia diagnosed? |
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| Stool culture on enteric media |
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| What media is used to culture Francisella tularensis? |
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| Requires special media for growth that is enriched in cysteine |
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| How is Francisella tularensis contracted? |
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| Insect bites (no human to human transmission) |
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| What are the signs and symptoms of Francisella tularensis? |
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| Fever (up to 104), chills, headache, myalgias, possible delirium Inflamed blister that fills with pus and opens to form an ulcer, swollen lymph nodes Severe sore throat Chest and abdominal pain, fatigue, weight loss, diarrhea |
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| How is Francisella tularensis diagnosed? |
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| Serology is negative the first week but still the best means for confirmation Diagnosis is usually based on clinical suspicion |
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| How is Francisella tularensis treated? |
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| Antibiotics (gentamicin or ciprofloxacin) |
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| How is Brucella melitensis contracted? |
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| Direct contact with infected animals or their secretions through skin breaks Ingestion of unpasteurized dairy products derived from infected animals |
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| Describe the pathogenesis of Brucella melitensis |
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| Transport to regional lymph nodes and growth in lymphoid cells Spread from the lymph nodes to the reticuloendothelial system Bursts of bacteremia |
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| What are the signs and symptoms of Brucella melitensis? |
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| Usually 1 of 3 categories: Febrile illness that resembles typhoid but is less severe Fever and acute monarthritis, typically of hip or knee, in a young child Long-lasting fever, misery, and low-back or hip pain in older men |
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| How is Brucella melitensis diagnosed? |
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| Culture from blood, bone marrow, or other tissues Grows very slowly so allow extra time in cases of suspicion Serum agglutination test may also be used |
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| Describe the appearance of Brucella melitensis |
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| Small gram-negative rod |
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| Describe the appearance of Bacteroides fragilis |
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| Gram-negative rod |
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| What media is used to culture Bacteroides fragilis? |
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| Forms colonies overnight on blood agar |
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| What are the virulence factors and toxins of Bacteroides fragilis? |
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| Capsule resists phagocytosis and can independently lead to abscess formation Secretes a heparinase that promotes clotting Some strains secrete a 20 kDa metalloprotease toxin (BFT) that causes disease without the need for epithelial breaks |
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| How is Bacteroides fragilis contracted? |
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| Can be part of the normal flora and these strains require a break in the anatomic mucosal barriers (unless metalloprotease toxin is present) |
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| How is Bacteroides fragilis treated? |
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| If causing acute diarrhea due to ingestion, is self limiting If due to epithelial break: Abscess drainage and antibiotics |
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| What is the physical appearance of Helicobacter pylori? |
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| Gram negative curved rod with multiple sheathed flagella for motility |
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| How is H. pylori cultured? |
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| Grows on Skirrow media Requires a microaerophilic atmosphere and is slow (3-5 days) to grow |
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| How is H. pylori transmitted? |
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| Person to person by fecal-oral route |
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| What is the most common cause of gastritis, gastric ulcer, and duodenal ulcer? |
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| H. pylori Considered a class I carcinogen |
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| What mediates the virulence factor of H. pylori? |
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| VacA is toxic and directly influences inflammation CagA stimulates cytokine IL-8 and neutrophil-activating protein (NAP) Net effect is gastritis, thinning of gastric mucosa, ulcers |
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| How are T and B lymphocytes involved in the creation of gastric ulcers? |
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| H. pylori infection causes lymphocyte infiltration which causes epithelial tissue damage rather than removal of the pathogen |
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| What is the purpose of urease secreted by H. pylori? |
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| Converts urea to ammonia which tends to neutralize the gastric acid |
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| What are the symptoms of H. pylori induced gastritis? |
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| Often symptom free In symptomatic: belching, nausea, anorexia, vomiting, epigastric pain, bleeding Possible pyloric stenosis |
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| How is an H. pylori infection diagnosed? |
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| Endoscopic biopsy and culture Detection of urease activity via urease breath test with 13C- or 14C-labeled urea Serology for specific antibody |
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| How is H. pylori treated? |
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| Combo of antimicrobials and acid reducers Metronidazole, tetracyclin, clarithromycin*, and amoxycillin* Proton pump inhibitor |
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| What is the general pathogenic mechanism of bacterial intestinal diseases? |
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| Attachment by pili or other adhesion Some bacteria transfer substances into host cell that mediate bacterial attachment Toxin production Cell division Loss of microvilli |
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| What is the physical appearance of Vibrio cholera? |
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| Curved gram neg rod commonly found in salt water Highly motile with single polar flagellum Cells may be linked end to end forming S shapes and spirals |
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| How is Vibrio cholera cultured? |
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| Oxidase positive and can grow both in aerobic and anaerobic conditions Grown on Thiosulfate Citrate Bile Salt Sucrose (TCBS) medium which inhibits gram pos |
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| What is the major virulence factor for Vibrio cholera? |
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| Cholera toxin Colonizing factor known as the toxin-coregulated pilus (TCP) |
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| How is Virbrio cholera detected by serology? |
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| H and O antigens (especially enterobacteriae) |
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| What is the mechanism of action of cholera toxin? |
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| Catalyzes the ADP-ribosylation of the GS (stimulatory) regulatory protein, "locking" it in the active state Causes persistent activation of adenylate cyclase which causes cAMP accumulation for active secretion of Na+, K+, HCO3-, and water out of the cell |
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| How does Vibrio cholera cause fluid loss? |
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| Increased adenylate cyclase via cholera toxin |
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| What is the osmotic make up of diarrheal fluid? |
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| Can amount to many liters per day, with approximately the same sodium content as plasma but two to five times the potassium and bicarbonate concentrations |
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| What regulates the virulence factors of Vibrio cholera? |
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| Transmembrane protein (ToxR ) that "senses" environmental changes in pH, osmolarity, and temperature which convert it to an active form |
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| What are the symptoms of cholera? |
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| Rapid onset, abd pain, rushes of peristalsis, loose, watery stool containing mucus flecks- the “rice-water stool” Muscle cramp due to electrolyte imbalance In severe, hypotension, shock and death may occur within hours if untreated |
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| How is cholera diagnosed? |
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| Isolation of the organism from stool by culture on common bacteriological medium (e.g. blood agar and MacConkey agar) or on a selective medium (thiosulfate-citrate-bile salt-sucrose agar) Latex agglutination test |
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| How is cholera treated? |
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| Immediate fluid replacement Antimicrobials: tetracycline or TSX and erythromycin Usually self-limiting |
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| Less common vibrio species?? |
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| Describe the physical appearance of Campylobacter jejuni (dysentery) |
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| Curved motile gram neg rod Have polar flagella that are often attached to the ends giving an “S” or a “seagull” appearance |
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| How is Campylobacter jejuni cultured? |
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| Microaerohilic (requires low oxygen tension), oxidase positive Slow growing (2-4 days, sometimes as long as one week) in selective medium (Campy-blood agar or Skirrow agar) at higher temperature (42C) |
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| What is the leading bacterial diarrheal illness in the US? |
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| Campylobacteriosis |
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| How is campylobacter usually contracted? |
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| Domestic animals or consumption of contaminated meat (poultry) Ingestion of non-pesteurized cow and goat milk as well |
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| How is campylobacter associated with Guillain-Barre syndrome |
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| Antibody elicited by ganglioside-like structures in the C. jejuni LPS core oligosaccharide cross-reacts w/ molecules in the host nerve myelin These abs are found in the serum of pts w/Guillain-Barre syndrome Similar to molecular mimicry in rheumatic fever |
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| What are the symptoms of a campylobacter infection (dysentery)? |
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| Fever Lower abd pain (may be severe enough to mimic acute appendicitis) Dysenteric stool containing blood and pus Vomiting (often not present) Is invasive Usually self-limiting, recovers within 3-5days |
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| How is campylobacter diagnosed? |
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| Stool isolation and culture via Campy-blood agar or Skirrow agar Plates are to be incubated in microaerophilic condition |
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| How is campylobacter contraction prevented? |
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| Pesteurization of milk and beverages and chlorination of water is helpful in preventing outbreaks Proper cooking and handling of poultry products |
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| How is campylobacter treated? |
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| Macrolides (erythromycin is the drug of choice) and fluoroquinolones Resistant to beta-lactams |
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| What are the relevant species of salmonella that causes diarrhea? |
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| S. enterica and S. typhi |
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| What is the physical appearance of salmonella? |
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| Gram-negative enterobacteria, motile |
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| How is salmonella cultured? |
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| Ferment glucoses with acid and sometimes gas; most of them produce hydrogen sulfide (H2S) not urease Grows on most common bacteriological media, resistant to chemicals such as bile and dyes |
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| Describe the pathogenesis of S. enterica |
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| Attaches to the enterocytes and M cells in the small and large intestine by pili Initiates a cytoskeletal change with formation of ruffles (extension of plasma membrane) Passes through the cells to the lamina propria to produce inflammation |
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| How does S. enterica avoid phagocytosis? |
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| Inducing macrophage apoptosis |
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| What are the symptoms of salmonella infection? |
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| Often described as “food poisoning” Nausea Vomiting Abdominal pain Loose motion Fever |
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| What is the classic contaminated food consumed in the contraction of salmonella poisoning? |
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| Potato salad |
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| What causes typhoid fever? |
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| Salmonella typhi Transmitted by contaminated drinking water, usually associated with travel Requires a large infecting dose |
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| Describe the pathogenesis of Salmonella typhii |
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| Similar to that of S. enterica Also kills macrophages by inhibiting phagosome fusion with lysosomes Capsular Vi antigen inhibits PMN phagocytosis |
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| How does the virulence of Salmonella typhii differ from other strains of salmonella? |
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| Prolonged survival within the macrophages due to its ability to inhibit oxidative burst Infected macrophages are carried in the lymphatic circulation to mesenteric nodes, spleen, liver and bone marrow |
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| What are the symptoms of typhoid fever? |
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| Involves multiple organs Incubation 13 days Fever, headache, faint rash on abd Diarrhea Relative bradycardia is characteristic |
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| What are the most important complications of typhoid fever? |
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| Intestinal (terminal ileum or proximal colon) perforation* and cholecsystitis* are the most important complications Chronic bacteremia and effects of endotoxins may lead to myocarditis, encephalopathy, or IVC |
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| How is Salmonella poisoning diagnosed? |
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| Hektoen enteric agar medium Bile salts and the indicator dyes inhibit the Gram-pos Fails to ferment lactose H2S forms black colonies |
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| How do common GI pathogens present on Hektoen enteric agar cultures? |
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| Fermenters produce yellow-pink colonies (e. g. E. coli) H2S producers (salmonella) form colonies with black precipitate Shigella colonies are green or transparent |
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| How is salmonella poisoning treated? |
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| Fluid and electrolyte replacement is the primary therapeutic approach Chemotherapy includes chloramphenicol (bone marrow depression is an important side effect, dangerous), STX, ampicillin, ceftriaxone, and quinolones |
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| Describe the physical appearance of Shigella |
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| Gram-negative straight rods, nonmotile and non-spore-forming |
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| How is shigella cultured? |
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| Selective Hektoen enteric agar Does not produce urease or H2S, most do not ferment |
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| How is shigella contracted? |
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| Strictly a human disease with no animal reservoirs Person to person transmission by fecal-oral route |
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| How does shigella differ in its pathogenesis from other intestinal bacteria? |
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| Invades the cells of the large intestine rather than the small intestine |
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| Describe the pathogenesis of Shigella |
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| Bacteria transcytose through the M cells in large intestine into the underlying phagocytic cells Infects the adjacent cells directly The cell by cell extension radially creates focal ulcers in the mucosa Intense acute inflammation in the lamina propria cause the characteristic dysenteric stool |
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| What is the significance of Shigella toxin? |
answer
| Not in all strain, increases severity Has a strong association with the hemolytic uremic syndrome characterized by break up of RBCs in the tiny blood vessels of the body resulting in anemia and kidney failure with occasional nervous system injury |
question
| What are the characteristics of dysentery syndrome? |
answer
| Cramps Painful straining to pass stools (tenesmus) A frequent, small-volume, bloody mucoid discharge |
question
| Most cases of shigella are due to S. sonnei, which presents with what symptoms? |
answer
| Fever Malaise, anorexia Myalgia (sometimes) Diarrhea (may become dysenteric) |
question
| How is shigella diagnosed? |
answer
| Culture on selective Hektoen enteric agar Slide agglutination tests using O group specific antisera (A, B, C, D) |
question
| How is shigella treated? |
answer
| Usually self limiting Antimicrobials help shortening the period of illness and excretion of the organisms Antispasmodics are contraindicated |
question
| What are the characteristics of Picornaviruses? |
answer
| Poliovirus (3 serotypes) Hepatitis A Virus Coxsackievirus groups A and B |
question
| Describe the pathogenesis of picornaviruses |
answer
| Initial infection is of intestinal epithelia or pharynx, persists throughout disease Spreads to submucosal lymphoid tissues (Peyer’s patches or tonsils) and regional lymph nodes Spreads to and replicates in organs of the reticuloendothelial system |
question
| What diseases processes/complications are seen with Group A Coxsackievirus infections? |
answer
| Asceptic Meningitis, Encephalitis, muscle weakness and paralysis (Poliomyelitis-like disease), cerebellar ataxia, exanthems and enanthems |
question
| What disease processes/complications are seen with Group B Coxsackievirus infections? |
answer
| Asceptic Meningitis, Encephalitis, Pericarditis, Myocarditis, Epidemic Mylagia, Orchitis |
question
| What disease processes/complications are seen with Echovirus and Enterovirus infections? |
answer
| Asceptic Meningitis, Encephalitis, muscle weakness and paralysis (Poliomyelitis-like disease), Exanthems and enanthems |
question
| What are the disease states of poliovirus? |
answer
| Abortive poliomyelitis, asceptic meningitis, paralytic poliomyelitis |
question
| How are picornavirus infections prevented? |
answer
| Both Inactivated virus (IPV) and Live-attenuated virus (OV) vaccines exist for poliovirus IPV is now the standard for use in the US |
question
| How are picornaviruses treated? |
answer
| Most picornavirus infections are mild and resolve on their own Injection of Ig to the infecting virus is used in severe cases of neonates or those with Ig deficiency Supportive care for cardiac or CNS |
question
| How are picornaviruses contracted? |
answer
| Fecal-oral route |
question
| Describe the pathogenesis of rotaviruses |
answer
| 24-48 hour incubation period Initial infection is of the mature villis tip cells of the small intestine Tip cell death leads to cell replacement by cells that cannot absorb nutrients as efficiently leading to osmotic diarrhea |
question
| What is the leading cause of severe dehydrating diarrhea in those under 3 years? |
answer
| Rotavirus |
question
| What are the general symptoms of rotavirus? |
answer
| Vomiting (typically the first symptom) Abdominal cramps Watery diarrhea May frequently occur along with a respiratory tract infection Lasts 2-8 days, a form of traveler's diarrhea |
question
| How is rotavirus immunity mediated? |
answer
| VP4 and VP7 (outer shell) are targets for neutralizing antibodies and humoral immunity plays a large role in viral clearance |
question
| How is rotavirus infection prevented? |
answer
| A live-attenuated vaccine is available. The 3 shot course must be completed by 32 months of age due to concerns over a potentially fatal complication |
question
| How is rotavirus diagnosed? |
answer
| Shed in large amounts in the stool (only during an active infection), and a variety of molecular and enzymatic tests can confirm infection |
question
| How is rotavirus treated? |
answer
| Usually self limiting, can be treated with oral fluids |
question
| How are Norwalk agent and Noroviruses contracted? |
answer
| Fecal-oral route, associated with Foodborne outbreaks associated with unsanitary restaurant workers Waterborne outbreaks of viral gastroenteritis Uncooked shellfish |
question
| How do Norwalk agent and Norovirus infections progress? |
answer
| Intestinal villi and microvilli become blunted and shortened Malabsorption of carbohydrates and fats leads to osmotic diarrhea without involvement of adenylate cyclase Gastric motor function is delayed and may be the cause of nausea symptoms Lasts 12 to 60 hours |
question
| What are the symptoms of a Norwalk agent or Norovirus infection? |
answer
| Nausea, vomiting, cramps, and watery diarrhea Vomiting is more common in children, and diarrhea in adults Headache, fever, chills, and myalgias |
question
| How is immunity to Norwalk agents and Norovirus mediated? |
answer
| Short term immunity to infection by the same strain (2-3 months) Lasting immunity is not achieved to any strain |
question
| How are Norwalk agent and Norovirus infections treated? |
answer
| Treatment is usually not necessary as the disease is of short term, self-limiting, and is not severe |
question
| What symptoms appear in Picornavirus infections but no in Norovirus infections? |
answer
| Rashes, lesions, photophobia, tachycardia |
question
| Calicivirus infections are more common among what demographic? |
answer
| Older children and adults and have nausea as a primary symptom |
question
| What are the Helminths? |
answer
| Nematodes (roundworms) Cestodes (tapeworms) Trematodes (flukes) |
question
| How does the reproduction of helminths correlate with disease severity? |
answer
| Adult worms do not multiply in human hosts Symptoms are usually linked with “worm burden” (number of adults present) |
question
| What are the nematodes? |
answer
| Trichuris trichiura (Whipworm) Enterobius vermicularis (Pinworm) Ascaris lumbricoides (Roundworm) Necator americanus and Ancylostoma duodenale (Hookworm) Strongyloides stercoralis (Threadworm) |
question
| How is Trichuris trichiura (Whipworm) contracted? |
answer
| Ingestion of fecal contaminated soil or foods |
question
| What are the symptoms of Trichuris trichiura (Whipworm)? |
answer
| Light infections are asymptomatic Heavy infections can have Epigastric pain, vomiting, distention, flatulence, anorexia and weight loss may occur, severe cases have Trichuris dysentary syndrome, blood and mucous in stools |
question
| How is Trichuris trichiura (Whipworm) diagnosed? |
answer
| Eggs in stool |
question
| What kind of complications are seen with Trichuris trichiura (Whipworm)? |
answer
| Parasites typically induce an IgE response and hypereosinophilia Mast cell activation may lead to the increase in allergic responses and symptoms coincide with GI complaints Prolapse of rectum |
question
| How is Enterobius vermicularis (Pinworm) contracted/spread? |
answer
| Fecal-oral route of infection Person to person transmission is high, especially in children and institutionalized individuals Female lays eggs in perianal region causes intense itching, leading to scratching, leading to hand and nail contamination, etc. |
question
| How do Enterobius vermicularis (Pinworm) infections progress? |
answer
| Self-infection occurs by scratching perianal area without hand washing Larvae hatch in the small intestine after ingestion of infective eggs Adults grow in the colon Pregnant females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area |
question
| What are the symptoms of Enterobius vermicularis (Pinworm)? |
answer
| Intense nocturnal perianal itching Insomnia Can migrate to urogenital tract in females causing a vaginitis and lead to secondary bacterial UTI Scratching may lead to secondary bacterial skin infections |
question
| How is Enterobius vermicularis (Pinworm) diagnosed? |
answer
| Tape test from perianal region reveals eggs |
question
| How is Ascaris lumbricoides (Roundworm) contracted? |
answer
| Fecal-oral contamination |
question
| How does a Ascaris lumbricoides (Roundworm) infection progress? |
answer
| Adult worms live in the lumen of the small intestine, passes eggs in small intestines Larva penetrates the intestinal mucosa, carried via the portal vein, then systemic circulation to the lungs The larvae mature further in the lungs (10 to 14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed Egg ingestion to new egg passage takes approximately 9 weeks |
question
| What are the symptoms of Ascaris lumbricoides (Roundworm) infection? |
answer
| Usually asymptomatic Fever, jaundice, chachexia and mental retardation due to malnutrition, pulmonary symptoms, abdominal tenderness due to obstruction or bowel perforation, Loeffler's syndrome, Larva migrans |
question
| What is Loeffler's Syndrome? |
answer
| Originally reported as a benign, acute eosinophilic pneumonia of unknown cause characterized by migrating pulmonary infiltrates and minimal clinical manifestations |
question
| What is larva migrans |
answer
| Dog and cat ascarid larvae (Toxocara spp.) hatched from eggs that are accidentally swallowed Larvae migrate and encyst as second-stage larvae, terminating development Produces tracts with hemorrhagic necrosis and eosinophilic and lymphocytic infiltration Can migrate to the liver causing enlargement and studded nodules |
question
| How is Ascaris lumbricoides (Roundworm) diagnosed? |
answer
| Eggs in stool (negative in early infection) |
question
| How is Necator americanus and Ancylostoma duodenale (Hookworm) contracted? |
answer
| Direct contact (walking barefoot) or ingestion of soil contaminated with human fecal matter |
question
| How does a Necator americanus or Ancylostoma duodenale (Hookworm) infection progress? |
answer
| On contact with the human host, the larvae penetrate the skin and are carried through the veins to the heart and then to the lungs. They penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed Larvae reach the small intestine, where they reside and mature into adults. Adult worms live in the lumen of the small intestine, where they feed on erythrocytes of the host. |
question
| What are the symptoms of Necator americanus and Ancylostoma duodenale (Hookworm)? |
answer
| Infecting larvae induce pruritic maculopapular dermatitis at site of entry ("ground itch") Transient pneumonitis Epigastric pain, inflammatory diarrhea with eosinophilia Primary Syndrome: Iron deficiency anemia Occult blood in stool Larva migrans |
question
| How is Necator americanus and Ancylostoma duodenale (Hookworm) diagnosed? |
answer
| Eggs in fresh stool, larvae in old stool |
question
| How is Strongyloides stercoralis (Threadworm) contracted? |
answer
| Direct contact of contaminated soil (walking barefoot) or ingestion of contaminated soil |
question
| How does a Strongyloides stercoralis (Threadworm) infection progress? |
answer
| ? Colonization of bowel and maturation ? Can spread through lymphatics to blood stream and other organs leading to abscesses, granulomas, or sepsis Can cause reinfection by maturing in bowel and re-entering through skin in perianal region |
question
| What are the symptoms of a Strongyloides stercoralis (Threadworm) infection? |
answer
| "Ground itch", cough and Loeffler’s syndrome, chronic watery diarrhea with mucous, may contain blood, urticaria, Larva currens |
question
| What is Larva currens? |
answer
| • Occurs on the trunk or near the anus and is a linear eruption in which the larvae migrate under the skin causing an itchy, non-indurated wheal with a red flare that moves rapidly and disappears in a few hours |
question
| What are the cestodes (tapeworm)? What are their features? |
answer
| Taenia solium (pig tapeworm) Taenia saginata (beef tapeworm) Have proglottids and Cystercerci (tissue cysts) |
question
| How are Cestodes (tapeworms) and Taenias contracted? How does the infection progress? |
answer
| Ingestion of cystercerci in meat Ingestion of eggs Invasion of tissues and cystercerci formation, most commonly in brain |
question
| What are the symptoms of a Cestode (tapeworms) or Taenias infection? |
answer
| Likely to be asymptomatic Epigastric discomfort Nausea Sensation of hunger Diarrhea Cysticercosis if eggs are ingested |
question
| How are Cestode (tapeworms) or Taenias diagnosed? |
answer
| Detection of eggs or proglottids in stool Cystercerci: plain films reveal calcified “puffed rice” lesions |
question
| How are Trematodes (Fluke) contracted? |
answer
| Biliary infections: Ingestion of poorly cooked, pickled, or smoked fish Liver infections: Ingestion of metacercariae encysted on aquatic plants (watercress) |
question
| How does a trematode (fluke) infection progress in the biliary tract? |
answer
| Excyst in small intestines, migrate through ampulla of Vater into biliary ducts Worms lead to adenomatous hyperplasia, inflammation, and duct obstruction |
question
| How does a trematode (fluke) infection progress in the liver? |
answer
| Excyst in duodenum, pass through intestine into peritoneum, invade liver through Glisson’s capsule Granulomatous reactions, duct obstruction, etc. may occur |
question
| How does a biliary trematode (fluke) infection manifest? |
answer
| Acute infections noted by fever, eosinophilia, and hepatomegaly Heavy worm burden may lead to constitutional complaints and symptoms associated with cholelithiasis and pancreatitis |
question
| How does a liver trematode (fluke) infection manifest? |
answer
| Fever, hepatomegaly and/or abdominal pain Nausea, cough, diarrhea, and urticaria are also common Periods of jaundice |
question
| How is a biliary trematode (fluke) infection diagnosed? |
answer
| Ova can be identified in stools, dilation of ducts by imaging |
question
| How is a liver trematode (fluke) infection diagnosed? |
answer
| Fever, hepatomegaly or liver pain, proper clinical setting Serology, as ova may not be detected in stool |
question
| What are the general characteristics of Staphylococcus aureus? |
answer
| Ferments mannitol, coagulase-positive, catalase-positive Gram-positive, cocci in clusters Non-motile, non-sporeformer Facultative anaerobe |
question
| What causes Staph aureus food poisoning? |
answer
| Results from bacterial toxin in food, not an infection by the bacteria itself |
question
| What foods are commonly contaminated by Staph aureus? |
answer
| Usually by improper handling of meats Ham, salted pork (can grow in high salt content Custard-filled pastries Potato salad Ice cream |
question
| What are the toxins secreted by Staph aureus? |
answer
| Enterotoxin A and B Can lead to severe metabolic alkalosis |
question
| What types of media are capable of culturing Staph aureus |
answer
| ?-hemolytic sheep’s blood agar Selective media: Mannitol salt agar Phenylethylalcohol agar (PEA |
question
| What are the general characteristics of Clostridium perfringens |
answer
| Gram-positive, spore-formers Can be found in the intestinal flora of humans and in the soil |
question
| How is Clostridium perfringens food poisoning contracted? |
answer
| Ingestion of contaminated food via dirt or feces Often occur in institutions or after large gatherings, can incubate at moderate temps Most commonly in meat cooked in bulk and then left in warming trays |
question
| What increases the likelihood of food poisoning by Clostridium perfringens? |
answer
| The longer the meat is allowed to sit, more likely of getting sick |
question
| What types of media are capable of culturing Clostridium perfringens? |
answer
| EYA (egg yolk agar) with anti-toxin A in ? of the plate: precipitation forms around colonies to indicate lecithinase activity Double-zone of hemolysis on blood agar |
question
| How does Clostridium perfringens cause food poisoning? |
answer
| Heat-labile enterotoxin |
question
| What are the effects of clostridium enterotoxin? |
answer
| Maximum effect in the ileum Minimum effect in the duodenum Inhibits glucose transport Damages intestinal epithelium Causes protein loss into the intestinal lumen |
question
| What causes Enteritis necroticans? |
answer
| Clostridium perfringens, type C |
question
| How is enteritis necroticans contracted? |
answer
| Occurs after large consumption of improperly cooked pork during native feasts |
question
| What are the symptoms of Enteritis necroticans? |
answer
| Severe necrotizing disease of the small intestine Intense abdominal pain, distension, bloody diarrhea, vomiting & shock High mortality due to intestinal perforation |
question
| How does Clostridium botulinum cause food poisoning? |
answer
| Ingestion of secreted botulin toxin |
question
| What are the effects of botulin toxin? |
answer
| Small amounts can produce paralysis and death Attaches to neuromuscular junction of affected nerves Prevents release of acetylcholine Approximately 1 microgram of toxin is lethal |
question
| What is the most common route of botulin toxin food poisoning? |
answer
| Home-canned vegetables |
question
| What is the progression of botulin intoxication? |
answer
| Cranial nerve paralysis Respiratory muscle weakness which can be fatal Preceding or following onset of paralysis |
question
| How is botulin toxin food poisoning diagnosed? |
answer
| Presence of organism and/or toxin in vomitus, gastric fluid, or stool |
question
| How is botulin toxin food poisoning treated? |
answer
| A-B-E antitoxin Can slow progression of disease but will not neutralize toxin already bound to neuromuscular junctions |
question
| What are the possible pathologies caused by Bacillus cereus food poisoning? |
answer
| Gastroenteritis Ocular infections Intravenous catheter-related sepsis Diarrhea syndrome Vomiting syndrome |
question
| What are the general characteristics of Bacillus cereus? |
answer
| Spore-former ?-hemolytic on sheep blood agar Facultative anaerobe Motile, gram-positive rod |
question
| How does Bacillus cereus food poisoning cause diarrhea syndrome? |
answer
| Enterotoxin produced, adenylate cyclase is activated in intestinal cells Similar to action of cholera toxin |
question
| What foods are associated with Bacillus cereus induced diarrhea syndrome? |
answer
| Spaghetti sauces Dried potatoes, dried milk Foods are maintained at temperatures between 30-50 degC |
question
| What foods are associated with Bacillus cereus induced vomiting syndrome? |
answer
| Fried rice via a heat stable toxin that does not activate adenylate cyclase Large amounts can lead to liver failure |
question
| What are the toxins secreted by Bacillus cereus? |
answer
| Heat-stable, proteolysis-resistant enterotoxin: Emetic form Heat-labile enterotoxin: Diarrheal form |
question
| How is Bacillus cereus food poisoning diagnosed? |
answer
| Samples of contaminated food must be cultured Identification in stool specimens of symptomatic patients is strong evidence Grows rapidly on sheep blood aga |
question
| Cryptosporidium spp. infections are associated with what mode of contraction? |
answer
| Contaminated water |
question
| What are the general characteristics of Cryptosporidium spp.? |
answer
| A coccidian, subphylum, Sporozoa (protozoan) Lives on or just below the epithelial cells of the small intestine |
question
| What is significant about the life cycle of Cryptosporidium spp.? |
answer
| Asexual reproduction allows for continued autoinfection, oocysts are infective when passed Patients may remain infective after diarrhea ceases |
question
| What are the symptoms of a Cryptosporidium infection? |
answer
| Frequent, watery diarrhea Nausea, vomiting Abdominal cramps Low-grade fever |
question
| How does Cryptosporidium cause diarrhea? |
answer
| Alters osmotic pressure in the gut resulting in in influx of fluid, much like cholera Epithelial cells are damaged by Invasion of parasite T-cell mediated inflammation causing villus atrophy |
question
| How is Cryptosporidium infections diagnosed? |
answer
| Modified Ziehl-Nielsen acid-fast stain Microscopic observations of small, acid-fast oocysts in smears of fecal specimens |
question
| How is Cryptosporidium treated? |
answer
| Self limiting in most If immunocompromised, give Paromomycin |
question
| What are the general characteristics of Giardia lamblia? |
answer
| Flagellate Most commonly identified intestinal parasitic pathogen Cysts are resistant forms, survive in cold water for several months |
question
| How is Giardia lamblia most commonly acquired? |
answer
| Contaminated water and person contact in institutions or daycare centers |
question
| Describe the lifecycle of Giardia lamblia |
answer
| Trophozoites reproduce by longitudinal, binary fission in the lumen of the proximal small bowel Encystation occurs as parasites travel to the colon Cysts are passed out through nondiarrheal feces |
question
| What are the symptoms of acute Giardiasis? |
answer
| Diarrhea, abdominal pain, bloating, nausea, vomiting |
question
| How is Giardia lamblia diagnosed? |
answer
| Microscopic identification of cysts or trophozoites in feces |
question
| How is Giardia lamblia treated? |
answer
| Metronidazole, tinidazole |
question
| How is Entamoeba histolytica (a pathogenic amoeba) infection most commonly contracted? |
answer
| Oral/fecal route, contaminated water, food Cysts are found in formed stools Can survive for day-weeks in external environment, trophozoites die in the acidic stomach |
question
| What are the characteristics of invasive, intestinal amebiasis via Entamoeba histolytica? |
answer
| Dysentery, colitis |
question
| What are the characteristics of extra-intestinal amebiasis via Entamoeba histolytica? |
answer
| Liver abscess Peritonitis Pleuropulmonary abscess Cutaneous and genital amebic lesions |
question
| What is the mechanism of GI infection by Entamoeba histolytica? |
answer
| Mediated by an adherence lectin in instestin Disruption of intestinal barrier by secretion of proteolytic enzymes and invasion of intestinal epithelial cells |
question
| What are the characteristic appearance of Entamoeba histolytica GI lesions? |
answer
| Flask-shaped ulcers |
question
| E. histolytica is resistant to what immune mechanisms? |
answer
| Phagocytosis Complement-mediated cell lysis |
question
| What are the consequences of a heavy infection of Entamoeba histolytica? |
answer
| Causes vacuoles to coalesce Sloughing off of the lining causes bloody, mucus-filled stools |
question
| How does Entamoeba histolytica cause liver abscesses? |
answer
| May completely erode the intestinal mucosa Enters the circulation Organ most commonly colonized is the liver, causes abscess formation |
question
| How does Entamoeba histolytica cause lung abscesses? |
answer
| Penetration of the diaphragm from hepatic abscesses or from hematogenous spread |
question
| How is Entamoeba histolytica diagnosed? |
answer
| Microscopic evidence of trophozoites in stool specimens via wet mounts or trichrome-stained smears Sigmoid biopsies ELISA provides evidence of current infection but is not diagnostic |
question
| What are the general characteristics of Cyclospora cayetanensis? |
answer
| Spore-forming coccidia Unicellular, coccidian parasite Oocysts are passed in stools, not infective, distinguishes this organism from Cryptosporidium Sporulation occurs in the environment at temp. between 22-32 degC |
question
| How is Cyclospora cayetanensis most often transmitted? |
answer
| Fresh produce and water via contamination with sporozoites released asexually into the stool |
question
| How is Cylcospora cayetanensis infection prevented? |
answer
| Can be killed by washing or cooking Occurs primarily in the tropics and subtropics |
question
| How is a Cylcospora cayetanensis infection diagnosed? |
answer
| Evidence of oocysts in stool specimens by microscopy Stool specimens should be refrigerated or preserved in 10% formalin Requires 3 or more specimens collected at 2-3 day intervals due to intermittent release of oocysts Modified acid-fast stain |
question
| What are the symptoms of a Cylcospora cayetanensis infection? |
answer
| Watery diarrhea which can be severe Anorexia, nausea, vomiting, abd pain Low-grade fever, fatigue Flu-like symptoms Can persist for several weeks |
question
| How are Cylcospora cayetanensis infections treated? |
answer
| Usually self-limiting in both immunocompetent and immunocompromised individuals, give fluids Trimethoprim-sulfamethoxazole can reduce symptoms |
question
| What is Blepharitis? |
answer
| Noncontagious inflammation of the lower portion of the eyelids and eyelashes caused by Poor eyelid hygiene Excess oil Staphylococcus aureus Allergic reaction |
question
| What is Dacryocystitis? |
answer
| Inflammation of the lacrimal sac caused by partial or complete obstruction within the sac or nasolacrimal duct Bacteria are trapped initiating acute or chronic infection Older patients are predisposed |
question
| What is Conjunctivitis? |
answer
| Inflammation of the conjunctiva, the outermost layer of the eye covering the sclera Progressive keratitis can lead to ulceration, scarring, and blindness |
question
| What are the three causes of conjunctivitis? |
answer
| Bacterial (most common) viral, or allergies |
question
| What are the characteristics of viral conjunctivitis? |
answer
| Usually due to an upper respiratory infection Watery discharge Red eye Irritation Can spread to other eye |
question
| What symptoms of bacterial conjunctivitis help differentiate it from viral conjunctivitis? |
answer
| Stringy discharge Other symptoms: Swelling of the conjunctiva Redness, tearing Irritation (gritty feeling) Can spread to other eye |
question
| What is the most common cause of bacterial conjunctivitis? |
answer
| Adults: Staphylococcus aureus, Streptococcus pneumoniae, Haemophilus influenzae Infants: Neisseria gonorrhoeae, Streptococcus pneumonia, Haemophilus influenzae |
question
| How do you treat bacterial conjunctivitis? |
answer
| Antibiotic ointments or eyedrops Neomycin, polymyxin, bacitracin Gentamicin, tobramycin against gram-neg microorganisms |
question
| What is Ophthalmia neonatorum? |
answer
| Severe conjunctivitis of newborns, can acquire the infection at birth, typically due to STD pathogens Neisseria gonorrhoeae, Chlamydia trachomatis, Herpes simplex virus |
question
| What is Endophthalmitis? What causes it? |
answer
| Rare, intraocular infection of the aqueous or vitreous humor caused by normal flora of the eyelids: Staphylococcus epidermidis Rarely by pseudomonas (poor prognosis) |
question
| What is Uveitis? |
answer
| Inflammation or swelling of the eye structures responsible for the eye’s blood supply |
question
| What are the symptoms of Iritis (anterior uveitis)? |
answer
| Redness, pain, photophobia due to painful movement of inflamed iris Blurred vision in severe inflammation |
question
| What are the symptoms of Intermediate uveitis (cyclitis)? |
answer
| Blurring, presence of floaters (black dots or wispy lines which move across the field of vision) |
question
| What are the symptoms of posterior uveitis |
answer
| Blurring, gradual or sudden reduction in vision Usually painless |
question
| What is periorbital cellulitis? what are potential complications? |
answer
| Acute infection of the tissues surrounding the eye Can lead to orbital cellulitis and protrusion of the eyeball, meningitis if severe |
question
| What causes periorbital cellulitis? |
answer
| Absence of an effective drainage system, predisposes the parasinuses to invasion Bacteria, fungi, or parasites can gain access via trauma, surrounding infection, or upper respiratory infection |
question
| Haemophilus influenza is grown on what type of media? |
answer
| Chocolate agar Requires the 2 erythrocyte growth factors X (hemin) and V (nicotinamide adenine dinucleotide) for growth |
question
| What is the appearance of Haemophilus influenza? |
answer
| Gram-negative, bacillus (rod) Non-motile, non-spore forming Fastidious, facultative anaerobe |
question
| What mediates pathogenesis for Haemophilus influenza? |
answer
| Attachment to respiratory epithelial cells is accomplished using pili Endotoxin in the cell wall is toxic to ciliated respiratory cells |
question
| What is the most virulent strain of H. influenza which is responsible for infections such as bacteremia, meningitis, cellulitis, septic arthritis, and pneumoniae? |
answer
| Haemophilus influenzae type b (HiB) |
question
| Which H. influenza strain causes mucosal infections such as otitis media, conjunctivitis, bronchitis, and pneumoniae? |
answer
| Nonencapsulated (or non-typeable) strains 80% of individuals are colonized with the non-typeable strains COPD and cystic fibrosis pts particularly susceptible |
question
| What are the general characteristics of Streptococcus pneumonia |
answer
| Gram-positive, cocci Usually seen in pairs**(diplo) but not always Non-spore formers, non-motile |
question
| Strep pneumonia is cultured on what media? |
answer
| Blood agar medium results in alpha-hemolysis (partial hemolysis) Can grow very quickly under optimal conditions |
question
| What determines the virulence of Strep pneumonia? |
answer
| Capsule interferes phagocytosis by blocking C3b opsonization |
question
| What is the Quellung reaction? |
answer
| Serotyping used to identify a particular capsule type of strep pneumo Antibody reacts with a particular capsule type, causes capsular swelling |
question
| What allows Staph aureus to avoid phagocytosis? |
answer
| Protein A, a cellular component in the cell wall |
question
| What are the virulence factors of Staph aureus? |
answer
| Cytolytic toxins (alpha and beta hemolysin, staphylococcal leukocidin) Enzymes (coagulase, hyaluronidase, lipase) Protein A |
question
| How do you differentiate Staph epidermidis from Staph aureus? |
answer
| Staph epidermidis is coagulase-negative whereas Staph aureus is positive |
question
| What type of infections are caused by Staph epidermidis? |
answer
| Hospital acquired UTIs Osteomyelitis at prosthetic joints Native valve endocarditis due to catheters Bacteremia Almost ALL cases of infection are hospital acquired |
question
| What mediates the antibiotic resistance of Staph epidermidis? |
answer
| Plasmid-mediated, can also transfer to Staph aureus |
question
| What are the general characteristics of Chlamydia trachomatis? |
answer
| Obligate intracellular parasites Most common STD in the world, causes blindness and infertility |
question
| What is trachoma? |
answer
| Chlamydia infection of the eye transmitted through eye secretions and eye-seeking flies Inflammatory reactions results in scarring on the conjunctiva Eyelid to turns inward where the eyelashes can rub the cornea |
question
| What is unique about the life cycle of Chlamydia trachomatis? |
answer
| Alternates between a non-replicating, infectious elementary body and a replicating, noninfectious reticulate body |
question
| How is Chlamydia trachomatis diagnosed? |
answer
| Immunofluorescence |
question
| What is MOTT? |
answer
| mycobacteria other than tubercle bacilli Associated with contact lenses, trauma, and wound contamination with soil Causes Keratitis and Corneal ulcers |
question
| What are the most common MOTT pathogens? |
answer
| Mycobacterium chelonae Mycobacterium fortuitum |
question
| What are the general characteristics of Eikenella corrodens? |
answer
| Microaerophilic, gram-negative rods Normal flora of human, mucosal surfaces Culture requires CO2 environment and hemin in the medium, lab must be notified in advance Usually a part of a mixed infection with Streptococcus sp. Gets its name from the fact that it forms pits on the surface of agar medium |
question
| How is Francisella tularensis contracted? |
answer
| Primarily a pathogen of squirrels and rabbits. Humans are infected by the bite of an infected deer fly or tick or eating undercooked infected meat or handling infected rabbit carcasses |
question
| What are the symptoms of tularemia (Francisella tularensis infection) |
answer
| Highly infectious Skin ulcers Swollen, painful lymph nodes Inflamed eyes, sore throat, mouth sores |
question
| How is Francisella tularensis cultured? |
answer
| Grown on chocolate agar |
question
| What causes "cat scratch fever"? |
answer
| Bartonella henselae: Gram-negative bacillus |
question
| What are the characteristics of cat scratch fever (Bartonella henselae infection)? |
answer
| Parinaud’s Oculoglandular Syndrome, manifests as conjunctivitis, neuroretinitis Vitritis, posterior uveitis Discrete foci of retinitis manifested as white retinal or choroidal lesions |
question
| What are the characteristics of HSV blepharitis? |
answer
| Vesicles appear on lid margins and around the eyes Vesicles can break open forming lesions which can become superinfected by skin flora |
question
| What is ocular herpes and what are its characteristics? |
answer
| HSV infection of the conjunctiva Swelling of the eyelids If cornea is involved (Herpes Simplex Keratitis) Destructive ulceration and perforation of the cornea possible |
question
| What is Herpes Simplex Keratitis? |
answer
| Dendritic keratitis Secondary herpetic infections Virus branches out in a dendritic pattern** Virus deadens the nerves – no pain |
question
| What are the characteristics of varicella-zoster blepharitis? |
answer
| Vesicles may appear on the lid margins Wartlike lesions can form (molluscum contagiosum) from the pox virus Can cause keratitis, scleritis, infections of the lacrimal apparatus, endophthalmitis |
question
| What ocular infections are caused by adenovirus? |
answer
| Conjunctivitis and epidemic keratoconjunctivitis |
question
| What are the characteristics of CMV retinitis? |
answer
| Floaters, flashes, and blind spots Pizza pie retinopathy (CMV infiltrates the vascular endothelium) More common among immunocompromised or neonates from infected mothers |
question
| What are the characteristics of Aspergillus sp? |
answer
| Most commonly encountered genus of fungi in the clinical laboratory Erects conidiophores from a “foot cell” with a vegetative hyphae |
question
| What are the characteristics of Acremonium sp.? |
answer
| Filamentous fungi isolated from plant debris and soil Rare cases of keratitis and endophthalmitis Known to cause opportunisitic infections in immunocompromised Possess fine, narrow, septate hyphae |
question
| What are the characteristics of Penicillium sp.? |
answer
| Filamentous fungi Found in soil, decaying vegetation, air May cause infections in immunocompromised hosts Has a bottle brush look Can cause Keratitis and Endophthalmitis |
question
| What are the characteristics of Rhizopus sp? |
answer
| Causative agent for a group of fungal infections classified as zygomycosis, frequently fatal Causes rhinocerebral infections Also known as the black bread mold |
question
| What predisposes someone to a rhinocerebral infection? |
answer
| Diabetic ketoacidosis Immunosuppression |
question
| Nosocomial rhinocerebral infections are usually contracted through what means |
answer
| Contaminated adhesive tape Contaminated, wooden tongue depressors |
question
| What is responsible for approximately 90% of rhinocerebral infections classified as zygomyosis? |
answer
| Mucormycosis |
question
| What causes endophthalmitis due to candida infections? |
answer
| Exogenously following surgery or trauma (rare) Endogenoushly due to embolic seeding in the retina (most common cause) |
question
| What pathogens can cause corneal ulcers due to improper contact lens use? |
answer
| Pseudomonas, Bacillus cereus, Acanthamoeba |
question
| Keratitis due to Acanthamoeba is associated with what kind of behavior? |
answer
| Wearing of nondisposable lenses Use of homemade sodium chloride solutions Wearing of contacts while swimming |
question
| Toxoplasma gondii is most often contracted via what vectors? |
answer
| Exposure to contaminated water containing tissue cysts Exposure to oocysts shed by infected cats Eating meat contaminated with oocysts Congenital transmission |
question
| Congenital infections by Toxoplasma gondii targets what organs? |
answer
| Retina (chorioretinitis) Brain |
question
| What are the different morphological forms of Toxoplasma gondii? |
answer
| Oocysts in intestines of members of the cat family (primary host) Tachyzoite – the invasive form responsible for acute disease Sporulated and unsporulated oocysts |
question
| How is Toxoplasma gondii diagnosed? |
answer
| Indirect immunofluorescent assay (IFA) Ring enhancing lesions on imaging is indicative |
question
| How is Loa loa (eyeworm) transmitted? |
answer
| Chrysops fly Confined to the rain forest and swamp forest areas of West Africa |
question
| How is Onchocerca volvulus transmitted? |
answer
| Spread by the vector, Simulium (the black fly) |
question
| What is caused by infection by Onchocerca volvulus? |
answer
| River Blindness Microfilaria can migrate into peripheral blood and the eyes during heavy infections, infects the cornea, optic nerve, choroid Dead microfilaria induce an inflammatory response in the eyes |
question
| What causes Myiasis? |
answer
| Infection of tissues or organs of animals or man by fly larvae Oestrus ovis (sheep botfly) Can cause severe conjunctivitis |
question
| What are the most common manifestations of a hematological infection? |
answer
| Anemia Pancytopenia Lymphocytosis Neutrophilia Eosinophilia |
question
| What is Pancytopenia? |
answer
| A decrease in all blood cell lineages due to toxic effects causing bone marrow necrosis, inflammatory mediators, and hemophagocytic syndrome |
question
| What causes Pancytopenia? |
answer
| Congestive splenomegaly due to infections such as: Salmonellosis, infectious mono Tularemia, hepatitis Syphilis Toxoplasmosis Schistosomiasis, malaria |
question
| What is Tularemia? |
answer
| AKA glandular fever, rabbit fever, tick fever, and deer fly fever Caused by infection by Francisela tularensis acquired from the bite of an infected tick (Ixodes, Dermacentor) |
question
| What are the general characteristics of Francisela tularensis? |
answer
| Gram-negative, non-motile rod Strict aerobe, fastidious Intracellular parasite Acquired from the bite of an infected tick (Ixodes, Dermacentor) |
question
| What is the most common clinical manifestation of Tularemia? |
answer
| Ulceroglandular tularemia Skin lesion (from a tick bite) is a painful papule which ulcerates having a necrotic center Leads to lymphadenopathy and bacteremia |
question
| How is Tularemia diagnosed? |
answer
| Direct immunofluorescent staining |
question
| What causes Toxoplasmosis? |
answer
| Toxoplasma gondii, an intracellular blood and tissue parasite Definitive host is the cat Infective oocysts are shed in cat feces Human infection is due to ingestion of improperly cooked meat or oocysts from cat feces |
question
| What is the infective form of Toxoplasma gondii? |
answer
| Trophozoites Responsible for initial infection and tissue damage |
question
| What are some of the more rare causes of Toxoplasmosis? |
answer
| Transplacental infections Transfusion infection via contaminated blood |
question
| T. gondii has a predilection for infecting which organs? |
answer
| Heart and lymphoid organs especially Lung, CNS, and eyes as well |
question
| An infant suffering from a congenital case of Toxoplasmosis experiences what symptoms? |
answer
| Anemia Jaundice, epilepsy, encephalitis, other neurological disorders |
question
| What are the symptoms of Hemophagocytic Syndrome (aka hemophagocytic lymphohistiocytosis (HLH)) |
answer
| Fever, splenomegaly* Jaundice Presence of activated macrophages phagocytizing erythrocytes, leukocytes, platelets, and other blood cell precursors Phagocytosis is detectable in the bone marrow |
question
| What is reactive hemophagocytic syndrome? |
answer
| Hemophagocytic syndromes secondary to an underlying infection |
question
| Sporadic and familial cases of HLH are caused by what? |
answer
| Acute infections |
question
| Hemophagocytic Syndrome can interfere with the diagnosis of what treatable infectious disease? |
answer
| Visceral leishmaniasis |
question
| What initial diagnostic tests should be performed if Hemophagocytic syndrome is suspected? |
answer
| Blood and urine cultures Chest radiography to screen for tuberculous infections Serological assays for viral infections Throat and rectal swabs for viral culture Fungal antigen testing Determine if an underlying T-cell lymphoma is present |
question
| Hemophagocytic syndrome is associated with HIV patients with what kind of underlying infections? |
answer
| Pneumococcal disease Pneumocystosis Histoplasmosis |
question
| What kind of infections associated with animal infections or travel need to be considered in cases of hemophagocytic syndrome? |
answer
| Leshmaniasis Brucellosis Rickettsioses Malaria |
question
| What are the most common symptoms of hemophagocytic syndrome? |
answer
| Fever*, splenomegaly* |
question
| What are the most common lab abnormalities associated with hemophagocytic syndrome? |
answer
| **Anemia, thrombocytopenia, neutropenia, hypertriglyceridemia, hypofriboginemia |
question
| How can the overactivation of macrophages cause hemophagocytic syndrome (HLH)? |
answer
| High levels of activating cytokines due to viral or nonviral causes Associated with EBV infection and the presence of episomal EBV genome in T cell lymphocytes |
question
| What is Brucellosis? |
answer
| Infection caused by Brucella sp. |
question
| What are the general characteristics of Brucella sp.? |
answer
| Small, nonmotile, gram-negative rods Requires complex growth media Strict aerobe Slow growth (at least 1 week) An intracellular parasite of the reticuloendothelial system |
question
| What are the two types of colony morphology of Brucella? What is it based off of? |
answer
| Based on the O antigen of LPS Smooth (translucent, homogeneous, more virulent) Rough (opaque, granular, or sticky) O chain of the smooth strain LPS is a marker for virulence |
question
| Describe the pathogenesis of Brucella |
answer
| An intracellular parasite of the reticuloendothelial system Microorganisms are phagocytosed by macrophages and monocytes Acidic environment of the phagolysosome induces virulence genes Phagocytosed bacteria are carried to the spleen, liver, bone marrow, lymph nodes, and kidneys, forms granulomas |
question
| How is Brucellosis contracted? |
answer
| Consuming contaminated, unpasteurized milk and other dairy products |
question
| What is Leishmaniasis? What causes Leishmaniasis? |
answer
| Infection by Leishmania sp. Vector-borne disease transmitted by sandflies |
question
| What causes the symptoms of a Leishmania infection? |
answer
| Amastigote forms found in reticulo-endothelial cells of the viscera Spleen, lymph nodes, liver, intestines |
question
| What is distinctive about the incubation period of Leishmaniasis? |
answer
| Incubation can be as short as 10 days or as long as a year |
question
| What are the symptoms of Leishmaniasis? |
answer
| Anemia, protrusion of abdomen due to splenomegally, and bleeding mucus membranes are most important* Low grade fever, malaise, wasting, facial edema, diarrhea, breathing difficulties |
question
| What causes Rickettsioses? |
answer
| Rickettsia sp. Transmitted by tick vectors |
question
| What are the general characteristics of Rickettsia? |
answer
| Obligate intracellular, aerobic, gram-negative rods |
question
| How is Rickettsia diagnosed? |
answer
| Giemsa stain is preferred |
question
| Describe the pathogenesis of Rickettsia? |
answer
| Enters eukaryotic cells by stimulating phagocytosis Degrades the phagosome membrane using a phospholipase to enter the cytoplasm, necessary for survival |
question
| What is the characteristic site of pathologic lesions of Rocky Mountain Spotted Fever? |
answer
| Small blood vessels Vessels may be blocked by thrombi causing vasculitis in the heart*, spleen*, skin, liver, kidneys, lungs, or CNS |
question
| Severe cases of Rocky Mountain Spotted Fever are in danger of what complication? |
answer
| Disseminated Intravascular Coagulopathy (DIC) |
question
| What is Rocky Mountain Spotted Fever |
answer
| Rickettsioses due to Rickettsia rickettsii transmitted through the tick |
question
| What is Epidemic typhus? |
answer
| Rickettsioses caused by Rickettsia prowazekii transmitted by exposure to human body louse feces (Pediculus humanus) |
question
| What are the symptoms of epidemic typhus? |
answer
| Splenomegaly*, hypotension*, vascular collapse* if severe High fever, headache, maculopapular rash |
question
| What is Scrub typhus? |
answer
| Rickettsioses caused by Rickettsia tsutsugamushi Transmitted to humans by chigger (mite larva) bites Occurs in Asiatic-Pacific areas |
question
| What are the clinical symptoms of scrub typhus? |
answer
| *Splenomegaly, *interstitial myocarditis Fever, headache, macular rash Delirium, stupor, muscle twitching |
question
| What causes increased levels of hepcidin with release of cytokines in cases of anemia due to chronic infection? |
answer
| Iron is trapped in the reticuloendothelial system Erythropoietin levels decrease Cytokines suppress hematopoiesis in the bone marrow |
question
| What is the function of Hepcidin? |
answer
| Key regulator in iron metabolism Regulates absorption of iron from foods and iron transport across the placenta Regulates the release of iron from macrophages and the recycling of aged RBCs |
question
| How does inflammation affect the actions of Hepcidin and cause anemia? |
answer
| Production is 100x higher than normal Results in increased sequestration of iron in macrophages |
question
| What are the best known parasitic infections that cause hemolytic anemia? |
answer
| Malaria (Plasmodium falciparum) Bartonellosis (Bartonella bacilliformis) Babesiosis (Babesia microti) |
question
| What causes malaria? |
answer
| Sporozoites of Plasmodium falciparum in the salivary glands of mosquitoes that have ingested blood infected with malarial gametocytes |
question
| Describe the pathogenesis of Plasmodium falciparum (malaria) |
answer
| Sporozoites travel to the liver where they invade and replicate Merozoites leave the liver through the circulatory system and invade red blood cells Merozoites continue to replicate, lyse RBCs, and invade other RBCs |
question
| Plasmodium falciparum (most severe form of Malaria) feeds on what? |
answer
| Hemoglobin and other proteins Ultimately causes destruction of the spleen Merozoites adhere to glycophorin molecules on the red blood cell surface |
question
| Which organisms cause relapsing malaria? |
answer
| Plasmodium vivax and Plasmodium ovale After treatment, treatment-resistant parasites reside dormant in the liver Eventually they invade RBCs and begin a typical erythrocytic cycle |
question
| Which organism causes long-lasting malarial infections that are most often asymptomatic? |
answer
| Plasmodium malariae |
question
| RBCs parasitized by Plasmodium vivax display small purplish red granules (with Wright’s stain) called what? |
answer
| Schuffner’s dots |
question
| How is malaria diagnosed? |
answer
| Giemsa or Wright stains are gold standard |
question
| What are other forms of malarial diagnosis? |
answer
| Malarial RDTs (rapid diagnostic test) |
question
| What is Babesiosis? |
answer
| Zoonosis caused by animal-specific protozoan parasites Parasites invade RBCs and induce a febrile disease Hemolytic anemia, hemoglobinuria, shock, death |
question
| What Babesia species are responsible for majority of human infections? |
answer
| Babesia microti Babesia divergens |
question
| What are the most common hosts for Babesia? |
answer
| White-footed mouse Deer tick Humans are accidental hosts, no human to human transfer |
question
| How is Babesiosis diagnosed? |
answer
| Direct blood smears show tetrad formation in RBCs Indirect fluorescent antibody test |
question
| What is Oroya fever (acute)? |
answer
| Infection by Bartonella bacilliformis (Bartonellosis) Motile by polar flagellum Adheres to and invades RBCs |
question
| What causes Bartonellosis (Oroya fever)? |
answer
| Transmitted by the nocturnal sandfly Limited to a small area in the Andes Mountains |
question
| How does intraerythrocytic Bartonella bacilliformis avoid the immune response? |
answer
| Lacks MHC molecules on the surface of mature erythrocytes Presentation of Bartonella antigens to the immune system is not possible |
question
| How is Bartonellosis diagnosed? |
answer
| Serologic testing Microscopic examination of Giemsa-stained blood smears |
question
| What alpha toxin is secreted by Clostridium perfringens? |
answer
| Lecithinase |
question
| *What are the actions of the alpha-toxin lecithinase secreted by Clostridium perfringens? |
answer
| Reacts with red blood cell membrane lipoproteins to produce lysolecithin Disrupts cell membranes of host cells including Erythrocytes and Leukocytes Mediates massive hemolysis, increased vascular permeability, and bleeding Causes myocardial dysfunction |
question
| What is the action of Theta-toxin (?-toxin) secreted by Clostridium perfringens? |
answer
| Is a heat-labile & oxygen-labile hemolysin Alters capillary permeability Toxic to heart muscle Pore-forming (cytolytic) |
question
| What is responsible for initial cell destruction in respiratory tract by Clostridium perfringens? |
answer
| Hydrogen peroxide Damages erythrocyte membranes* |
question
| How does Mycoplasma pneumoniae cause cold autoimmune hemolytic anemia? |
answer
| Auto-IgM antibodies are directed against the I antigen on red blood cells Cause agglutination of RBCs* transiently in the fingers, ears, nose |
question
| Mycoplasma pneumoniae is inherently immune to what types of antibiotics? |
answer
| Beta-lactams due to lacking a cell wall |
question
| What are the general characteristics of Mycoplasma pneumoniae? |
answer
| Slow rate of growth Obligate aerobe Receptor on Mycoplasma pneumoniae is integral in attachment to eukaryotic host cell membranes in the respiratory tract and RBCs |
question
| What are the possible complications of measles vaccination? |
answer
| Thrombocytopenia* |
question
| What are the characteristics of a Rubella infection? |
answer
| Respiratory transmission Viruses replicates in the nasopharynx & lymph nodes Viremia* with spread to other tissues |
question
| What are the hemorrhagic manifestations* of a Rubella infection? |
answer
| Rare, primarily children Low platelet count, vascular damage Thromobocytopenic purpura GI, cerebral, intrarenal hemorrhaging can occur |
question
| What are the IgG antibodies that react with RBCs in the cold (below body temperature) |
answer
| Donath-Landsteiner antibodies cause a rare form of cold-autoimmune hemolytic anemia referred to as Paroxysmal cold hemoglobinuria Can be idiopathic or associated with Syphilis, Varicella, Mumps, Measles, etc. |
question
| What kind of infection can cause Ag/Ab complexes bind to RBC surface and induce hemolysis? |
answer
| Hemophilus influenzae type b meningitis |
question
| What is Polyagglutination? |
answer
| A rare form of hemolysis caused by metabolites from infectious agents forcing RBCs to exposed normally hidden surface antigens Example: enteric bacteria can produce neuraminidase |
question
| What kinds of infections can cause a disruption of the gastrointestinal or genitourinary mucosa leading to anemia by blood loss? |
answer
| Helicobacter pylori Helminthic infections such as nematodes and trematodes |
question
| What is the most cause for blood loss anemia in developed countries? |
answer
| H. pylori |
question
| How do Ancylostoma duodenale & Necator americanus (hookworms) cause blood loss? |
answer
| Due to feeding worms Microcytic, hypochromic anemia develops |
question
| Describe the pathogenesis of Schistosomiasis? |
answer
| Cercaria penetrate the skin and enter the venous system Travel to heart, lungs, and portal circulation |
question
| What are the symptoms of Acute schistosomiasis (Katayama’s fever) |
answer
| *Diarrhea (bloody), *Hepatosplenomegaly, *eosinophilia, Cystitis, ureteritis with hematuria* (can lead to bladder cancer) Fever, cough, abd pain, occasional CNS lesions, pulmonary hypertension |
question
| How is Fasciolopsis buski (intestinal fluke) contracted? |
answer
| Ingestion of encysted larva in aquatic vegetation like water chestnuts Found only in China, Vietnam, Thailand, parts of Indonesia, Malaysia, India |
question
| Attachment of the flukes (Fasciolopsis buski) to the small intestines causes what? |
answer
| Hemorrhage* Marked eosinophilia* Inflammation and ulceration |
question
| What parasite causes Megaloblastic Anemia? |
answer
| Diphyllobothrium latum (Cestode) (Fish tapeworm) Common in areas where raw or pickled fish are eaten |
question
| What is characteristic of carriers of Cestodes (fish tapeworm) suffering from megaloblastic anemia? |
answer
| Low serum levels of vitamin B12 |
question
| What are the characteristics of Trypanosoma? |
answer
| Flagellated, insect-transmitted protozoa that infects RBCs and tissues |
question
| What causes Chagas’ Disease? |
answer
| Trypanosoma cruzi transmitted by feces of Triatomine (reduviid) bugs, the "kissing bug" |
question
| What are the acute symptoms of Chaga's disease? |
answer
| Romana’s sign: Eye on one side swells (at location where triatomine bug fecal matter gets rubbed in) Occur in about 1% of cases |
question
| What are prolonged symptoms of Chaga's disease? |
answer
| Enlarged liver or spleen* Fever, fatigue, swollen lymph glands Brain damage and death in younger |
question
| What causes African Sleeping Sickness? |
answer
| Trypanosoma brucei gambiense (slow progressing) Trypanosoma brucei rhodesiense (rapidly progressing) Kinetoplastids (mitochondrial DNA) |
question
| What is characteristic of the acute blood stage of infection for African Sleeping Sickness? |
answer
| Fever, headaches |
question
| What causes relapses of African Sleeping Sickness? |
answer
| Antigenic variation of trypanosomal surface Life cycle exhibits different morphologies |
question
| What are the symptoms of African Sleeping Sickness? |
answer
| Apathy, fatigue, confusion, motor changes (tics, slurred speech) Changes in sleep patterns Extreme fatigue during day, extreme agitation during night |
question
| What are potential complications of African Sleeping Sickness? |
answer
| Trypanosomes cross the blood-brain barrier resulting in meningoencephalitis Untreated can progress to coma or death |
question
| What is Filariasis? |
answer
| Caused by infections with nematodes (roundworms) Infective larvae are transmitted by arthropods |
question
| How do nematodes (roundworms) cause filariasis? |
answer
| Female worms produce microfilariae Microfilariae enter and circulate in the bloodstream |
question
| What are the clinical manifestations of lymphatic filariasis? |
answer
| Eosinophilia is prominent* Many are asymptomatic though some develop lymphatic dysfunction |
question
| How is filariasis diagnosed? |
answer
| Identify presence of microfilariae in blood Blood collection must be timed with periodicity of organism |
