Background
Anemia, like a fever, is a symptom of disease that requires investigation to determine the underlying etiology. Often, practicing physicians overlook mild anemia. This is similar to failing to seek the etiology of a fever. The purpose of this article is to provide a method of determining the etiology of an anemia.
Anemia is strictly defined as a decrease in red blood cell (RBC) mass. Methods for measuring RBC mass are time consuming, are expensive, and usually require transfusion of radiolabeled erythrocytes. Thus, in practice, anemia is usually discovered and quantified by measurement of the RBC count, hemoglobin (Hb) concentration, and hematocrit (Hct). These values should be interpreted cautiously because they are concentrations affected by changes in plasma volume. For example, dehydration elevates these values, and increased plasma volume in pregnancy can diminish them without affecting the RBC mass.
Pathophysiology
Erythroid precursors develop in bone marrow at rates usually determined by the requirement for sufficient circulating Hb to oxygenate tissues adequately. Erythroid precursors differentiate sequentially from stem cells to progenitor cells to erythroblasts to normoblasts in a process requiring growth factors and cytokines. This process of differentiation requires several days. Normally, erythroid precursors are released into circulation as reticulocytes.
Reticulocytes remain in the circulation for approximately 1 day before reticulin is excised by reticuloendothelial cells with the delivery of the mature erythrocyte into circulation. The mature erythrocyte remains in circulation for about 120 days before being engulfed and destroyed by phagocytic cells of the reticuloendothelial system. Read more »
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Posted in medicalmatrix | February 13, 2010 | 
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Background
Malaria, which predominantly occurs in tropical areas, is a potentially life-threatening disease caused by infection with Plasmodium protozoa transmitted by an infective female Anopheles mosquito vector. Individuals with malaria may present with fever and a wide range of symptoms.
The 4 Plasmodium species known to cause malaria include Plasmodium falciparum, Plasmodium vivax, Plasmodium ovale, and Plasmodium malariae. A fifth species, Plasmodium knowlesi, has recently been identified as a clinically significant pathogen in humans. Timely identification of the infecting species is extremely important, as P falciparum infection can be fatal and is often resistant to standard chloroquine treatment. In some cases, individuals with malaria are infected with multiple Plasmodium species. P falciparum and P vivax are responsible for most new infections. Each Plasmodium species has a defined area of endemicity, although geographic overlap is common. Species can usually be distinguished by morphology on a blood smear. P falciparum is distinguished from the rest of plasmodia by its high level of parasitemia and the banana shape of its gametocytes.
Malaria in travelers typically manifests weeks after the individual leaves the endemic area. Presentation more than 4 weeks after returning from the endemic area is unusual. In some individuals, disease manifests months or years later, usually due to the presence of P vivax or P ovale hypnozoites, which can remain dormant in the liver and reactivate years after infection. Relapse with P vivax or P ovale infection is rare more than 5 years after initial infection. Because symptomatic delay is common, history of even a remote exposure to an endemic area should be elicited. Symptoms of malaria are nonspecific, and, because timely diagnosis and treatment are necessary, malaria should be considered in all patients from tropical areas who present with fever. Read more »
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Background
Rabies is a viral disease that affects the CNS. The genus Lyssavirus contains more than 80 viruses. Classic rabies, the focus of this article, is the prototypical human Lyssavirus pathogen. Ten viruses are in the rabies serogroup, most of which only rarely cause human disease. The genus Lyssavirus, rabies serogroup, includes the classic rabies virus, Mokola virus, Duvenhage virus, Obodhiang virus, Kotonkan virus, Rochambeau virus, European bat Lyssavirus types 1 and 2, and Australian bat Lyssavirus. In 1997, an unusual bat Lyssavirus caused a brief outbreak of a rabieslike illness in Australia.
The fatal madness of rabies has been described throughout recorded history, and its association with rabid canines is well known. For centuries, dog bites were treated prophylactically with cautery, unfortunately, with predictable results. In the 19th century, Pasteur developed a vaccine that successfully prevented rabies after inoculation and launched a new era of hope in the management of this uniformly fatal disease. Rabies is recognized as a zoonosis worldwide. Animal-control and vaccination strategies currently supersede postexposure prophylaxis in preventing the spread of rabies. Through such programs, rabies has been eliminated in several nations and some areas in the US territories.
Human rabies reflects the prevalence of animal infection and the extent of contact this population has with humans. Less than 5% of cases in developed nations occur in domesticated dogs; however, unvaccinated dogs serve as the main reservoir worldwide. Undomesticated canines, such as coyotes, wolves, jackals, and foxes, are most prone to rabies and serve as reservoirs. These reservoirs allow rabies to remain an indefinite public health concern, and ongoing public health measures are critical to its control. Raccoons, skunks, and insect-eating bats remain the prime vectors in the United States, followed by cats and cattle. Increasingly in the United States, the source of exposures cannot be identified, but the risk of death from rabies is exceedingly low, with fewer than 5 cases documented per year. Opossums are rarely infected and are not considered a likely risk for exposure. Read more »
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Background
Intracranial abscesses are uncommon, serious, life-threatening infections. They include brain abscess and subdural or extradural empyema and are classified according to the anatomical location or the etiologic agent. The term brain abscess is used in this article to represent all types of intracranial abscesses.
Intracranial abscesses can originate from infection of contiguous structures (eg, otitis media, dental infection, mastoiditis, sinusitis) secondary to hematogenous spread from a remote site (especially in patients with cyanotic congenital heart disease), after skull trauma or surgery, and, rarely, following meningitis. In at least 15% of cases, no source can be identified.
In recent years, the complex array of etiologic agents that cause brain abscess has become better understood.
Pathophysiology
Brain abscess is caused by intracranial inflammation with subsequent abscess formation. In at least 15% of cases, the source of the infection is unknown (cryptogenic). Infection may enter the intracranial compartment directly or indirectly via 3 routes.
Contiguous suppurative focus (45-50% of cases)
Direct extension may occur through necrotic areas of osteomyelitis in the posterior wall of the frontal sinus, as well as through the sphenoid and ethmoid sinuses.This direct route of intracranial extension is more commonly associated with chronic otitic infection and mastoiditis than with sinusitis. Odontogenic infections can spread to the intracranial space via direct extension or a hematogenous route. Contiguous spread could extend to various sites in the central nervous system, causing cavernous sinus thrombosis; retrograde meningitis; and epidural, subdural, and brain abscess. Read more »
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Background
Acute rheumatic fever (ARF) is an autoimmune inflammatory process that develops as a sequela of streptococcal infection. ARF has extremely variable manifestations and remains a clinical syndrome for which no specific diagnostic test exists. Persons who have experienced an episode of ARF are predisposed to recurrence following subsequent (rheumatogenic) group A streptococcal infections. The most significant complication of ARF is rheumatic heart disease, which usually occurs after repeated bouts of acute illness.
Pathophysiology
ARF is characterized by nonsuppurative inflammatory lesions of the joints, heart, subcutaneous tissue, and central nervous system. An extensive literature search has shown that, at least in developed countries, rheumatic fever follows pharyngeal infection with rheumatogenic group A streptococci. The risk of developing rheumatic fever after an episode of streptococcal pharyngitis has been estimated at 0.3-3%. More recent investigations of rheumatic fever occurring in the aboriginal populations of Australia suggest that streptococcal skin infections might also be associated with the development of rheumatic fever. In Oceania and Hawaii, streptococcal strains that are not typically associated with rheumatic fever have been found to cause the disease.
Molecular mimicry accounts for the tissue injury that occurs in rheumatic fever. Both the humoral and cellular host defenses of a genetically vulnerable host are involved. In this process, the patient’s immune responses (both B- and T-cell mediated) are unable to distinguish between the invading microbe and certain host tissues.The resultant inflammation may persist well beyond the acute infection and produces the protean manifestations of rheumatic fever.
Frequency
United States
The incidence of ARF has declined markedly in the past 50 years in both the United States and Western Europe. Most Western physicians see only the late sequelae of rheumatic heart disease; the diagnosis of an acute case is usually reason enough for a ground rounds presentation. This remarkable decline of rheumatic fever likely reflects improved socioeconomic conditions, as well the decline in prevalence of the classically described rheumatogenic strains of group A streptococci.
Following two decades of almost total absence, a resurgence of ARF occurred in the 1980s among middle-class white children in Salt Lake City, Utah. Clusters were also reported in US Army and Navy training camps during the same period. These limited outbreaks were associated with mucoid rheumatogenic strains that were rarely seen in the preceding 20 years. Today, ARF remains a rarity in most of the United States, although Hawaii and American Samoa continue to see a significant number of cases, many of which are caused by streptococcal strains not usually associated with rheumatic fever in persons of Polynesian descent. Read more »
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