Rabies

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 »

Bacterial Infections and Pregnancy

This article focuses on common bacterial infections in pregnancy and describes the manifestations of these infections and the therapies used to treat them.

Bacterial infections can affect pregnant women from implantation of the fertilized ovum through the time of delivery and peripartum period. They may also affect the fetus and newborn. Many women with these infections are asymptomatic, necessitating both a high degree of clinical awareness and adequate screening.

Grop B Streptococcus

Group B Streptococcus (GBS) is the most common cause of life-threatening infections in newborns; thus, GBS is the primary focus of any discussion about infections and pregnancy. Infections caused by GBS affect both mother and child. Since the emergence of this pathogen in the 1970s, the increased use of intrapartum prophylaxis has decreased the infection rate by 70%.

Etiology

Streptococcus agalactiae, or GBS, is a facultative, beta-hemolytic, fastidious, gram-positive coccus. GBS can be found as part of normal vaginal, rectal, and oral flora. The virulence of the organism depends largely on the polysaccharide capsule.

Transmission

Twenty to 25% of pregnant women are asymptomatic carriers of vaginal or rectal GBS. Intrapartum transmission occurs via ascending spread or at the time of delivery.

Clinical spectrum

Because only 0.5-1% of mothers who carry GBS develop signs and symptoms of disease, clinical diagnosis of GBS infection can be problematic.

In pregnant women, GBS is a cause of cystitis, amnionitis, endometritis, and stillbirth. Occasionally, GBS has caused endocarditis and meningitis in pregnant women, while, in postpartum women, GBS has been identified as a cause of urinary tract infections (UTIs) and pelvic abscesses. Read more »

Tetanus

Background

The word tetanus comes from the Greek tetanos, which is derived from the term teinein, meaning to stretch. Tetanus appears in military medical documents throughout the ages. Slapping infected dung on the umbilical cords of newborns (ie, as part of ritualistic ceremonies) caused rampant tetanus neonatorum or trismus nascentium in the West Indies and in Africa. Osler’s textbook describes the “eight days sickness” caused by umbilical sepsis, which killed 84 of 125 children within a fortnight of birth in St. Kilda, Scotland. During World War I, tetanus occurred in 1.47 per 1000 British wounded and in 12.5 per 1000 persons involved in the Peninsular campaign. Nicolaier discovered the anaerobic bacillus Clostridium tetani in 1885. In 1889, Koch’s pupil, Kitasato, obtained the bacillus of tetanus in pure culture and associated the disease to animals.

Although rare, the disease has not been eradicated, and early diagnosis and intervention are life saving. Prevention is the ultimate management strategy for tetanus. The 4 clinical types of tetanus are generalized, local, cephalic, and neonatal.

Neonatal tetanus is a major cause of infant mortality in underdeveloped countries, but this form is rare in the United States. Infection results from cord contamination during unsanitary delivery conditions, coupled with a lack of maternal immunization. At the end of the first week of life, infected infants become irritable, feed poorly, and develop rigidity with spasms. This form of tetanus has a very poor prognosis for survival.

Cephalic tetanus is uncommon and usually occurs following head trauma or otitis media. Patients with this form present with cranial nerve palsies. The infection may be localized or may become generalized.

Patients with local tetanus present with persistent rigidity in the muscle group close to the injury site. The muscular rigidity is caused by a dysfunction in the interneurons that inhibit the alpha motor neurons of the affected muscles. No further CNS involvement occurs, and this form has very low mortality rates. Read more »

Rheumatic Fever

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 »

Take Over Migraine

The light illness could be boomerang for the person itself. Sometime we do not realize that an a little pain could disturb our activity. So, we have to prevent it if we realize the symptoms. Have you ever got migraine headaches? A migraine headache is not a common headache. It has different symptoms than the common headaches.

What are the migraine symptoms? Actually, there are several symptoms that is common appear to the migraine victims. The aura is the warning sign of the migraine. What is aura? Aura is such kind a sign that the migraine will be happened. It can be blind spots, impaired vision, and a temporary loss vision. So, if you have ever experienced this way of the symptoms, now you can conclude it as a symptoms of migraine headache.

So, if you got a migraine, you can try to get the home remedy as well. Why? It is because the home remedy will affect more to your health. So, you can try to apply ice to your head. Then take a rest by sleeping within an hour. This will make you feel better. In addition, migraine treatment is also can be got by taking a tablet that you got from the doctor’s prescription.