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The growth observed on the anaerobic blood agar plate after 48 hours incubation (see upper photograph), revealed a spreading colony. The spreading nature of the colony is better observed in the close-in photograph (lower). No growth was observed on subcultures incubated aerobically indicating that this isolate is truly an anaerobe (although aerotolerance studies would be needed for confirmation). The spreading nature of the colony and the lack of hemolysis are highly suggestive of Clostridium septicum. However, biochemical confirmation is necessary.

Ladhani S. Joannou CL. Lochrie DP. Evans RW. Poston SM.: Clinical, microbial, and biochemical aspects of the exfoliative toxins causing staphylococcal scalded-skin syndrome. Clinical Microbiology Reviews. 12:224-242, 1999The exfoliative (epidermolytic) toxins of Staphylococcus aureus are the causative agents of the staphylococcal scalded-skin syndrome (SSSS), a blistering skin disorder that predominantly affects children. Clinical features of SSSS vary along a spectrum, ranging from a few localized blisters to generalized exfoliation covering almost the entire body.The toxins act specifically at the zona granulosa of the epidermis to produce the characteristic exfoliation, although the mechanism by which this is achieved is still poorly understood.Despite the availability of antibiotics, SSSS carries a significant mortality rate, particularly among neonates with secondary complications of epidermal loss and among adults with underlying diseases.

Although not performed that often, the following tests are useful in separating E. corrodens from other closely related members of the HACEK group:KIA showing an alk/alk reaction; Glucose fermentation (-); Reduction of nitrates to nitrites (+); Production of indole (-); Ornithine decarboxylase (+) The positive nitrate reduction reaction eliminates Cardiobacterium hominis, Kingella kingae and other Kingella species.The positive ornithine decarboxylase reaction eliminates Kingella denitrificans (which also denitrifies nitrate to nitrogen gas, a reaction negative for E. corrodens).Eikenella corrodens is asaccharolytic, whereas most other closely related species produce acid from one or more carbohydrates.

Although lipoproteins of a particular class are generally within a given size range, there are many biochemical processes that interact with lipoproteins to alter their size, density, and lipid composition. When low-density lipoprotein (LDL) becomes smaller and denser, it is more likely to interact with the arterial wall, leading to deposition of cholesterol and initiating or worsening atherosclerosis. Research has shown that high numbers of smaller, denser LDL are more atherogenic than larger, lighter LDL particles. Small, dense LDL particles are associated with more than a three-fold increase in the risk of coronary heart disease.

Blood flow is arrested by way of a complex series of interrelated physiological and biochemical processes. There are a wide variety of factors that influence the effectiveness of hemostatic processes including the following: Type of, and degree of, vessel damage Ability of vasoconstriction to occur Availability of platelets & their functionality Availability of clotting factors & their functionality Absence of inhibitors & anticoagulants

Exposure to contact substances, such as collagen, can activate the intrinsic pathway. The exposed collagen is the location where a complex between High Molecular Weight Kininogen (HMWK), Prekallikrein (also known as Fletcher Factor, which activates to Kallikrein), and factor XII (Hageman Factor) forms. Together, this three biochemical complex, adhered to the collagen binding site, catalyzes the conversion of factor XII to its activated form, XIIa, thereby triggering the intrinsic pathway.

In addition to hereditary hemochromatosis (HH), there are other conditions of iron overload that must be considered in a differential diagnosis. Disorders such as sickle cell disease, thalassemia, sideroblastic anemia, congenital dyserythropoietic anemia, and liver disease may also cause iron overload. Transfusion-dependant patients and persons who abuse iron-containing vitamin supplements are also at risk. These conditions are usually described as secondary iron overload, in contrast to the primary iron overload of HH.Patient history, clinical signs and symptoms, biochemical and hematologic laboratory analyses, and possibly results of a liver biopsy may be needed to establish a diagnosis of a condition causing secondary iron overload. DNA tests for common HFE mutations are very likely the most important diagnostic tool for identifying HH as the cause of iron overload. In some patients, both secondary causes and HH may be contributing to iron overload. Differentiating the secondary causes of iron overload from HH is heavily dependent on the results of laboratory assays, but a complete discussion is beyond the scope of this course.

Round cells in semen are of two types: immature sperm and white blood cells. To determine the percentage of white blood cells (specifically granulocytes) a special leukocyte screening test must be done. This test involves staining for the peroxidase enzyme present in the granulocytes.The 1999 WHO manual contains a protocol for doing this test (Appendix III). There is also at least one test kit on the market for this assessment (Leukoscreen: Bioscreen, Inc.).Laboratories with particular expertise in doing CBC and assessing granulocytes in stained blood smears may be able to do a differential count by this method rather than using a biochemical test for leukocyte screening.