ROCKY MOUNTAIN SPOTTED FEVER

TRIVIAS
Major Marshall H. Wood, a US Army physician in Boise, Idaho, first recognized R rickettsii

infection and described RMSF in 1896. Originally described in Montana and Idaho in the 1870s, Rocky Mountain spotted fever was undoubtedly occurring in the eastern United States as early as 1901, but wasn't regularly appreciated and reported until the 1930s (Dumler 1991). The early investigative work of Dr. Howard Taylor Ricketts, published between 1906 and 1909, led to the isolation of the etiologic infective agent for Rocky Mountain spotted fever, Rickettsia rickettsii, and to an understanding of the vector role of ticks (Philip 1990). DEFINITION Rocky Mountain spotted fever is a disease brought on by a type of bacteria carried by ticks. CAUSES Rocky Mountain spotted fever is caused by Rickettsia rickettsii (R. Rickettsii), which is carried by ticks. The bacteria spread to humans through a tick bite. Risk factors include recent hiking or exposure to ticks in an area where the disease is known to occur. The bacteria are unlikely to be transmitted to a person by a tick that has been attached for less than 20 hours. Only about 1 in 1,000 wood and dog ticks carry the bacteria. Bacteria can also infect people who crush ticks they have removed from pets with their bare fingers. ASSESSMENT Symptoms usually develop about 2 to 14 days after the tick bite. They may include: Chills Confusion Fever Headache Muscle pain Rash -- usually starts a few days after the fever; first appears on wrists and ankles as spots that are 1 - 5 mm in diameter, then spreads to most of the body. About one-third of infected people do not get a rash. Other symptoms that may occur with this disease: Diarrhea Light sensitivity Hallucinations Loss of appetite Nausea Thirst Vomiting COMPLICATIONS Brain damage Clotting problems Heart failure Kidney failure

Lung failure Meningitis Pneumonitis (lung inflammation) Shock

LABORATORY AND DIAGNOSTIC TESTS Tests that may be done include: Antibody titer by complement fixation or immunofluorescence Complete blood count (CBC) Kidney function tests

Partial thromboplastin time (PTT) Prothrombin time (PT) Skin biopsy taken from the rash to check for R. rickettsii Urinalysis to check for blood or protein in the urine

MEDICAL MANAGEMENT Treatment involves careful removal of the tick from the skin and antibiotics to get rid of the infection. Doxycycline or tetracycline are the drugs of choice for both confirmed and suspected cases. Pregnant women may take chloramphenicol. Note: There is concern that tetracycline and doxycycline may stain the teeth of children whose permanent teeth have not yet formed. However, tooth discoloration is very unusual when a child takes these medicines for 14 days or less. These medicines are first-line treatment, even for children. NURSING MANAGEMENT Plan care to provide adequate rest. Ask patient about possible drug allergies before administering antibiotics. Administer analgesics and antipyretics as ordered. Monitor the patients vital signs, especially his temperature. Watch for signs and symptoms of complications, such as cardiovascular, renal or respiratory failure. Monitor the effectiveness of administered medication. Instruct the patient to take antibiotic medications as prescribed. Instruct patient to report reoccurrence of symptoms immediately; may be relapse. Stress prevention through avoidance of tick-infested areas, wearing protective clothing and tick repellent, inspecting body and clothes for ticks every 3-4 hours. Remove ticks with tweezers or forceps to avoid leaving mouth parts in skin. Health teaching o Avoid dogs with ticks and tick-infected areas o Use protective, light-colored clothing that covers arms and legs; tuck pants in socks to protect legs o Apply tick-repellent chemicals, such as diethyltoluamide (DEET, Autan) or permethrin, to pants and sleeves o Search the entire body every 3-4 hours when in an infested area; common areas of attachment are in scalp, pubic, or axillary hair

LYMES DISEASE TRIVIAS The original descriptions of the dermatologic manifestations of Lyme disease date back to 1883 in Europe, when a German physician, Alfred Buchwald, described what is now termed acrodermatitis chronica atrophicans (ACA). Several decades later in 1912, a Swedish dermatologist, Arvid Afzelius, described the rash, then called erythema chronicum migrans (ECM), which currently is referred to simply as erythema migrans (EM). DEFINITION A multisystemic disorder, Lyme disease is caused by the spirochete Borrelia burgdorferi, which is carried by the minute tick Ixodes dammini (also known as I. scapularis) or another tick in the Ixodidae family. It commonly begins in the summer months with a papule that becomes red and warm but isn't painful. This classic skin lesion is called erythema migrans. Weeks or months later, cardiac or neurologic abnormalities sometimes develop, possibly followed by arthritis of the large joints. CAUSES The primary risk factor for developing cutaneous manifestations of Lyme disease is exposure to Ixodes (deer) ticks (from areas likely to harbor ticks, such as woody, brushy, or grassy outdoor habitats), which transmit B burgdorferi from host to host. The life cycle of the Ixodes tick and B burgdorferi is important, as it relates to the epidemiology of Lyme disease. The complete genome of B burgdorferi, which has several distinct genetic groupings, was described in 1998; there is also evidence that additional strains or closely related Borrelia species also exist. The generic species is B burgdorferi (eg, sensu lato). Within this species exists several well-characterized groupings that account for the different clinical manifestations seen in North America and Europe. Three groups are well established, including B burgdorferi sensu stricto, B garinii, and B afzelii. Many other strains exist, but most are not pathogenic to humans. This is an area of active and constantly evolving research. Note the following:

B burgdorferisensu stricto is a broad category of closely related but genetically distinct genospecies that constitutes all North American isolates and is found in Europe as well. These subspecies are associated with different clinical presentations, probably due to genomic variation. Infection with this organism has a particular predilection to affect joints. In European erythema migrans, B afzelii can be isolated from about 80% of lesions and B garinii from 15%. B garinii, found exclusively in Europe, has some neurotropism and is the isolate that accounts for most cases of the neurologic syndrome lymphocytic meningoradiculitis (Bannwarth syndrome) and a white matter encephalitis, which is rare in North America. However, this organism can cause all the various cutaneous manifestations (see Clinical Presentation). Although B afzelii, found mainly in Europe, is the most common organism causing acrodermatitis chronica atrophicans, all 3 species groups have been isolated from these patients.

ASSESSMENT Prodromal signs and symptoms: Malaise Fatigue Headache Fever Lethargy Chills Arthralgia Myalgia Anorexia Sore throat Nausea Vomiting Abdominal pain Photophobia

Stage I: Initial red macule or papule that enlarges within days, forming an expanding annular lesion with a well-defined red border and central clearing (erythema migrans) with an average maximum diameter of 15 to 20 cm- center of lesion may become vesicular, indurated, or necrotic, or concentric rings may occur (when occurring on the face, neck, or scalp, only a linear streak may be noted) Multiple tick bites producing multiple erythema migrans lesions Erythema migrans lesions most commonly occurring in the proximal extremities, especially the axillae and groin As erythema migrans lesion evolves, possible development of postinflammatory erythema or hyperpigmentation, alopecia, or desquamation Additionally, a malar rash, diffuse urticaria, or subcutaneous nodules possible

Stage II: Low-grade fever in adults, high persistent fever in children- adenopathy Neurologic involvement occurs in up to 20% of untreated casesmeningitis, encephalitic signs (poor concentration, memory, and sleep, or irritability), cranial neuritis, radiculoneuropathy, and myelitis Cardiac involvement in up to 10% of untreated casesatrioventricular block, myopericarditis, left ventricular dysfunction Migratory pain in joints, bursae, tendons, bones, or muscles

Stage III: Fever and adenopathy Arthritis Chronic neurologic involvement

LABORATORY AND DIAGNOSTIC TESTS Assays for anti-B. burgdorferi show evidence of previous or current infection. Enzyme-linked immunosorbent technology or indirect immunofluorescence microscopy shows immunoglobulin (Ig) M levels that peak 3 to 6 weeks after infection- IgG antibodies detected several weeks after infection may continue to develop for several months and generally persist for years. Positive Western blot assay shows serologic evidence of past or current infection with B. burgdorferi. Lumbar puncture with analysis of cerebrospinal fluid reveals antibodies to B. burgdorferi.

MEDICAL MANAGEMENT Patients treated with appropriate antibiotics in the early stages of Lyme disease usually recover rapidly and completely. Antibiotics commonly used for oral treatment include doxycycline, amoxicillin, or cefuroxime axetil. Patients with certain neurological or cardiac forms of illness may require intravenous treatment with drugs such as ceftriaxone or penicillin. NURSING MANAGEMENT Plan care to provide adequate rest. Ask patient about possible drug allergies before administering antibiotics. Administer ananlgesics and antipyretics as ordered. If the patient has arthritis, help him with range of motion and strengthening exercises but avoid overexerting him. Protect the patient from sensory over load and reorient him if needed. Monitor the patients vital signs, especially his temperature. Watch for signs and symptoms of complications, such as cardiovascular or neurologic dysfunction and arthritis.

Monitor the effectiveness of administered medication. Instruct the patient to take antibiotic medications as prescribed. Urge the patient to return for follow up check up care and to report recurrent or new symptoms to the physician. Inform the patient and his family about ways to prevent lyme disease.

ACUTE GLOMERULONEPHRITIS DEFINITION Acute glomerulonephritis refers to a group of kidney diseases in which there is an inflammatory reaction in the glomeruli. It is not an infection of the kidney, but rather the result of the immune mechanisms of the body. CAUSES

Occurs after an infection elsewhere in the body or may develop secondary to systemic disorders. An antigen-antibody reaction produces immune complexes that lodge in the glomeruli, producing thickening of glomerular basement membrane; the renal vasculature, interstitium, and tubular epithelium may also be affected. Immune complexes activate a variety of secondary mediators such as the complement pathways, neutrophils, macrophages, prostaglandins, and leukotrienes. These affect vascular tone and permeability, resulting in tissue injury. Eventual scarring and loss of filtering surface may lead to renal failure.

ASSESSMENT Mild disease is frequently discovered accidentally through a routine urinalysis. History of infection: pharyngitis or impetigo from group A streptococcus, such viral infections as Epstein Barr and hepatitis B Tea-colored urine, oliguria Puffiness of face, edema of extremities Fatigue and anorexia, possible headache Hypertension (mild, moderate, or severe), headache Anemia from loss of RBCs into the urine The clinical course of acute glomerulonephritis proceeds as follows from onset of symptoms to recovery, more than 90% of patients regain normal renal function within 60 days: o Diuresis usually starts 1 to 2 weeks after onset of symptoms. o Renal clearances and blood urea concentration return to normal. o Edema decreases, and hypertension lessens. o Microscopic proteinuria or hematuria may persist many months. COMPLICATIONS Hypertension, heart failure, endocarditis Fluid and electrolyte imbalances in the acute phase, hyperkalemia, hyperphosphatemia, hypervolemia Malnutrition Hypertensive encephalopathy, seizures ESRD LABORATORY AND DIAGNOSTIC TESTS Urinalysis for hematuria (microscopic or gross), proteinuria, cellular elements, and various casts. 24-hour urine for protein (increased) and creatinine clearance (reduced) outline the degree of renal function. Elevated BUN and serum creatinine levels, low albumin level, increased antistreptolysin titer (from reaction to streptococcal organism), and decreased serum complement. Needle biopsy of the kidney reveals obstruction of glomerular capillaries from proliferation of endothelial cells. MEDICAL MANAGEMENT Management is symptomatic and includes antihypertensives, diuretics, drugs for management of hyperkalemia (due to renal insufficiency), H2 blockers (to prevent stress ulcers), and phosphate-binding agents (to reduce phosphate and elevate calcium). Antibiotic therapy is initiated to eliminate infection (if still present). Fluid intake is restricted. Dietary protein is restricted moderately if there is oliguria and the BUN is elevated. It is restricted more drastically if acute renal failure develops.

Carbohydrates are increased liberally to provide energy and reduce catabolism of protein. Potassium and sodium intake is restricted in presence of hyperkalemia, edema, or signs of heart failure.

NURSING MANAGEMENT Monitor vital signs, intake and output, and maintain dietary restrictions during acute phase. Encourage rest during the acute phase as directed until the urine clears and BUN, creatinine, and blood pressure normalize. (Rest also facilitates diuresis.) Administer medications as ordered, and evaluate patient's response to antihypertensives, diuretics, H2 blockers, phosphate-binding agents, and antibiotics (if indicated). Carefully monitor fluid balance; replace fluids according to the patient's fluid losses (urine, respiration, feces) and daily body weight as prescribed. Monitor pulmonary artery pressure and CVP, if indicated. Monitor for signs and symptoms of heart failure: distended neck veins, tachycardia, gallop rhythm, enlarged and tender liver, crackles at bases of lungs. Observe for hypertensive encephalopathy, any evidence of seizure activity. Explain that the patient must have follow-up evaluations of blood pressure, urinary protein, and BUN concentrations to determine if there is exacerbation of disease activity. Encourage patient to treat any infection promptly. Tell patient to report any signs of decreasing renal function and to obtain treatment immediately.