Staphylococcal scalded skin syndrome
Staphylococcal scalded skin syndrome is caused by staphylococcus aureus. Staphylococcal aureus commonly present in anterior nares and vagina. Staphylococcus may produce heat stable enterotoxins, alpha, beta, delta, gamma, leukocidins cytolyctic toxins, exfoliate toxins, enzyme such as lipase, coagulase, catalase, fibrinolysin an hyaluronidase and toxic shock syndrome toxin. Staphylococcus aureus infection may lead to food poisoning mostly by intoxication. Besides that staphylococcus aureus may also lead to condition such as toxic shock syndrome, bullous impetigo, staphylococcal scalded skin syndrome, acute endocarditis, carbuncles, pneumonia, folliculitis, styes, furuncles, osteomyelitis, pneumonia and organ abscess. Staphylococcal aureus is transmitted via direct contact. Staphylococcal is gram positive cocci, catalase positive which produce coagulase and able to ferment mannitol. Staphylococcal has a beta hemolytic properties on the blood agar plate. The component of staphylococcal aureus may include protein A, peptidoglycan and capsules. Staphylococcal aureus should be prevented with hand washing, proper wound cleaning, and good surgical practice.Staphylococcal aureus can be treated with oxacillin, methicillin and nafcillin and vancomycin.
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Dengue Fever
Dengue fever is cause by dengue virus. Dengue virus will inoculated into the bloodstream by the mosquito. Dengue virus will be spreads to cells of the monocyte - macrophages lineage within the vasculature of the target organ. Dengue virus is a member of the flavivirus. Dengue fever is an acute febrile illness. Dengue fever may be mild, moderate to severe. There is a possibility of fatality. The common symptoms of dengue fever may include rash, myalgia, headache, retro ocular pain and pain in the bone. Dengue fever is also known as breakbone fever. The common complication of dengue fever may include dengue shock syndrome and dengue hemorrhagic fever. Dengue shock syndrome and dengue hemorrhagic fever may be caused by activation of the complement, release of cytokines, activation of the lymphocytes and damage to the tissue. Dengue shock syndrome and dengue hemorrhagic fever is characterized by skin hemorrhage, gastrointestinal hemorrhage, shock, coma and death. Dengue fever is an endemic in southeast asia. Dengue fever is detected via the present of virus specific IgM antibody. There is no treatment for dengue fever. The treatment is supportive treatment and prevention of dengue virus by controlling the mosquito vector( mosquito net, insect propellant). Shingles
Shingles is also known as herpes zoster. Shingles is caused by varicella zoster virus. Varicella zoster virus will infect the epithelial cells of the respiratory which later spread to the skin via the blood and lymphatic system that lead to eruption of the vesicular rash. Latent infection at the dorsal root ganglia may occur due to the spreading of the virus to the neurons and nerves. The latent infection can be triggered by immuno compromise state due to AIDS or malignancy, currently on immunosuppressive therapy in case of organ transplantation and increasing age. Varicella zoster virus infection primarily may lead to chicken pox. Chicken pox ( varicella ) is characterized by generalized vesicular rash, fever and malaise which later progress into scabs and pustules. The reactivation of varicella zoster virus may lead to shingles in adult. Shingles is characterized by painful vesicular lesion in the dermatome innervated by sensory ganglia. Shingles / herpes zoster may only occur in patient who previously suffer from chicken pox. Varicella zoster virus is highly contagious and transmitted via respiratory droplets. Varicella zoster virus is detected via varicella zoster virus specific antibody staining or through Tzanck smear of lesion’s cell which may reveal multinucleated giant cells. The common complication of herpes zoster / shingles is postherpetic neuralgia. Varicella zoster infection can be prevented with live attenuated vaccine or passive varicella zoster virus immune globulin in immunocompromised patient. The treatment may include anti viral such as famciclovir, valacyclovir and acyclovir. Mumps
Mumps may present with symptoms such as malaise, headache, fever and parotitis. Parotitis is an enlargement / swelling of the parotid gland which is painful. The complication of mumps may include orchitis ( swelling and inflamed testis) aseptic meningitis, encephalitis and sterility. Enlargement of the parotid gland is due to inflammation which lead to infiltration of the lymphocytes and edematous lesion. Mumps is cause by paramyxovirus ( mumps virus). Mumps virus can be detected by serological analysis of mumps virus specific antibody. Mumps virus is a single serotype paramyxovirus. The mode of transmission may include respiratory droplets, urine or salivary droplets. Mumps is a very contagious disease. Mumps initially infect the epithelial cells of the respiratory system which later spread to the regional lymph nodes and later disseminated to the central nervous system and salivary gland. There are no treatments for mumps. The prevention of mumps may include administrating live attenuated mumps virus vaccine which is given in combination with rubella and measles vaccine. Pityriasis Versicolor
Pityriasis versicolor is presented with hyperpigmented/ hypopigmented dry scaly lesion which present on the abdomen, arms and torso. Pityriasis versicolor is caused by Malassezia furfur. Microscopic examination of scaly skin scraping with potassium hydroxide preparation may reveal the present of yeast and hyphae in a “spaghetti and meatballs” characteristic. Pityriasis versicolor is common in tropical region, in patient with AIDS or patient with renal transplant. Pityriasis versicolor may be worsen and lead to systemic infection if the patient also suffers from seborrheic dermatitis ( AIDS patient) or patient currently on intralipid therapy. Pityriasis versicolor is transmitted via direct contact.The prevention technique may include applying good hygiene and topical treatment with miconazole or selenium sulfide. Lyme disease
Lyme disease is characterized by stages. Stage 1 is presented with erythema migrans or bull eye rash / clear center rash. Patient may also present with fever, myalgia and chills. Stage 2 is presented with Bell’s palsy, myocarditis, numbness of the limb, encephalitis and meningitis. Stage 2 develop weeks or months. Stage 3 is presented with poly arthritis and neurological impairment. Stage 3 occurs in months and years. Lyme disease is caused by Borrelia burgdorferi. Borrelia burgdorferi is a gram negative spirochete. Serology assay is useful in detected the present of Borrelia burgdorferi. The common mode of transmission is from the tick bites. Prevention of lyme disease may include removal of ticks, using insect repellant and protective clothing.The treatment for lyme disease may include amoxicillin, doxycycline, penicillin G and ceftriaxone. Tinea Nigra
Tinea nigra is presented with non scaly , flat, brown to black macular lesions of the sole and palms. Tinea nigra is commonly present in tropical countries. Tinea nigra is causesd by a dimorphic fungus known as Exophilia werneckii ( dimorphic fungus). Exophilia werneckii may be detected by microscopic examination of the skin scarping in the potassium hydroxide preparation. The microscopic finding may reveals brown pigmented yeast cells and hyphae. Exophilia werneckii is most commonly present in the soil. The common mode of transmission is through injury. Black colonies may be found in the culture which confirmed the present of tinea nigra. Tinea nigra is prevented with good / proper hygiene. The treatment may include topical application of salicylic acid. Common Cold
Common cold is caused by rhinoviruses. There are 100 rhinovirus serotypes. Rhinoviruses will enter the nasopharynx by attaching to the intracellular adhesion of molecule - 1 receptor ( ICAM -1). Virus will be replicated in the epithelial cells of the nasal and finally the virus will be shed in the respiratory secretion. The common pathological and clinical condition ( nasal congestion, headache, mild pharyngitis, fever and sneezing ) are associated with chemical mediators ( prostaglandin and bradykinin) of the inflammation process. This chemical mediator may lead to stimulation of the cough reflexes , sneeze, vasodilation and secretion of mucus. Common cold will have the incubation period of 2- 3 days. Common cold is transmitted through hand to eye contact or hand to nose contact of the contaminated respiratory droplets or contaminated respiratory secretions. Hand washing is important to prevent developing common cold. There are no specific treatment for common cold. |
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