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Toxic Shock Syndrome or Rocky Mountain Spotted Fever?

Many illnesses manifest themselves in similar ways, making it hard for clinicians to diagnose and treat patients accurately; two of these infections are Toxic Shock Syndrome and Rocky Mountain Spotted Fever. It is important that clinicians, toxicologists, and expert witnesses are able to recognize the possibility of either of these infections and their overlapping symptoms. There is such an overlap that misdiagnosis of one infection for the other must be carefully guarded against and always regarded as a possibility.

In 1978, Todd, Fishaut, Kapral, and Welch first reported and named Toxic Shock Syndrome (TSS) after treating seven children aged 8–17, of which one died and one developed gangrene of the toes. There was an outbreak of Toxic Shock Syndrome in 1981 found to be associated with menstruating women and tampon use. Since then, much has been discovered about TSS, but there is much left unknown.

Many people associate Toxic Shock Syndrome exclusively with tampon use, however, “the incidence of nonmenstrual TSS now exceeds that of menstrual TSS” (Issa & Thompson, 2001). Non-menstrual TSS may come from multiple different “surgical procedures (e.g., rhinoplasty, nasal packing, postpartum procedures) and medical conditions (e.g., pneumonia, influenza, infection)” (Issa & Thompson). TSS may affect men, children, and non-menstruating women, contrary to popular belief. The disorder “is now recognized as a toxin-mediated, multisystem illness that strikes primarily in healthy people of any age” (Issa & Thompson). This infection may attack anywhere the bacterium Staphylococcus aureus enters the blood stream, from the smallest prick to a surgical site and, as it is a systemic illness, it affects the entire body (Nemours Foundation, 2007).

The bacterium S. aureus causes TSS “by release of superantigens into the blood stream” (Todar, 2005). S. aureus “secretes two types of toxin with superantigen activity, enterotoxins, of which there are six antigenic types (SE-A, B, C, D, E and G), and toxic shock syndrome toxin (TSST-1). . . . TSST-1 is expressed systemically and is the cause of toxic shock syndrome (TSS). When expressed systemically, enterotoxins can also cause toxic shock syndrome. In fact, enterotoxins B and C cause 50% of non-menstrual cases of TSS. . . . TSST-1 is responsible for 75% of TSS, including all menstrual cases. TSS can occur as a sequel to any staphylococcal infection if an enterotoxin or TSST-1 is released systemically and the host lacks appropriate neutralizing antibodies” (Todar). Ninety percent of the population has these neutralizing antibodies preventing them from being infected because S. aureus may be a part of the body’s normal bacteria, existing in the nose or vagina (University of Utah Health Sciences Center, 2003). “S. aureus can be transmitted by direct contact with infected persons. Individuals who develop TSS usually have not developed antibodies against S. aureus. Therefore, it is not usually considered a contagious infection” (University of Utah Health Sciences Center).

Although the proportion of menstrual-related TSS cases has declined in recent years, “the proportion of postsurgical TSS cases has been increasing” (Salandy & Brenner, 2005). S. aureus may enter a person’s body during a surgical procedure, causing the person to suddenly experience TSS, although “the wound appears relatively benign” and “is usually not grossly suppurative and not initially identified as the site of infection” (Kreiswirth, Kravitz, Schlievert, & Novick, 1986). Making a clinical diagnosis in this instance is challenging because the surgical site may not present the classical signs of infection (Issa & Thompson, 2001). At that stage, “reopening the surgical wound may be the only way to confirm the diagnosis and may also provide therapeutic benefit by minimizing systemic absorption of toxin” (Kreiswirth et al., 1986).

Symptoms of TSS include a fever greater than 102 degrees Fahrenheit; a flat rash, called a TSS Rash, similar in appearance to a sunburn that covers most of the body; strawberry tongue, in which red bumps rise above a yellow/white coating covering the tongue; headache; muscle aches; sore throat; cough; nausea and vomiting; profuse diarrhea; abdominal pain; fainting; confusion and disorientation; low blood pressure (systolic less than 90 mm Hg); and in women with menstrual related TSS, vaginal inflammation and discharge (HCG, 2007).

TSS can mirror other diseases or infections, making it difficult for clinicians to diagnose. It is extremely important for clinicians to rule out other infections with similar symptoms, such as Rocky Mountain Spotted Fever, when diagnosing and treating a patient (University of Utah Health Sciences Center, 2003). To be diagnosed with TSS, a patient must present with the fever, low blood pressure, and rash described above. The infection must involve 3 or more organ systems, and there must be an absence of evidence of other infections or diseases (Salandy & Brenner, 2005).

Fluid resuscitation and oxygen administration should begin before the patient arrives at the hospital if an ambulance has been called. Emergency room personnel should continue administration of fluid and oxygen at the hospital and begin cardiac and urine-output monitoring. All packing materials and tampons should be removed and the patient should begin antibiotic treatment as soon as TSS is confirmed. It is recommended that doctors closely follow-up with patients, as TSS reoccurs in 40%–50% of patients (Salandy & Brenner, 2005).

One of the most difficult aspects of treating TSS is accurately diagnosing the illness. There are no definitive tests that provide complete assurance the patient has TSS, and many of the symptoms mimic or are mimicked by other diseases. A primary focus of clinicians is to “rule out” other possible diseases that may cause the patient to present with similar symptoms. One of these diseases is Rocky Mountain Spotted Fever.

Like TSS, Rocky Mountain Spotted Fever (RMSF) is a potentially fatal disease caused by Rickettsia rickettsii and treated with antibiotics. It can be found in 47 of the 48 contiguous states, excluding Maine, and is carried by ticks infected with Rickettsia rickettsii, who transmit the infection to humans. Spread by the American dog tick, the lone-star tick, and the wood tick (Directors of Health Promotion and Education), RMSF is the “most common fatal tick-borne disease in the United States” (Amitai, Sinert, & Medlin, 2006).

Some sources report that an infected tick must feed for more than 6 hours before the Rickettsia rickettsii bacteria are introduced into the human, “enter[ing] the skin and spread[ing] via lymphatics to the bloodstream and attach[ing] to their target cells, vascular endothelial cells” (Amitai et al., 2006). Although not all sources agree on the number of hours, all agree that the longer the infected tick is attached, the greater the chance of infection. Conversely, if the fluid from an infected tick comes into contact with broken skin, possibly through squeezing or crushing, the person may become infected because Rickettsia circulates in tick bodily fluids (Mayo Clinic Staff, 2005). The patient will develop symptoms (clinical manifestations) of the infection typically 3–12 days after being bitten or infected, during which time the Rickettsia is replicating intracellularly (Amitai et al.). RMSF is not transmitted between people (Directors of Health Promotion and Education, n.d.).

Between 1998 and 2004, the number of reported cases of RMSF multiplied by more than four. Outbreaks are often seasonal, happening in warm weather with peaks in May and June (Amitai et al., 2006). Although a case of RMSF is “usually fairly mild” if treated promptly (Mayo Clinic Staff, 2005), RMSF has been reported to have a 4% mortality rate, and “patients treated 5 or more days after onset of symptoms experienced thee times the mortality rate of patients treated earlier” (Amitai et al.). It is believed that “a significant portion of this persistent mortality likely is due to delay in diagnosis and treatment” (Amitai et al.).

Symptoms of RMSF include a sudden fever typically greater than 102 degrees Fahrenheit that may last 2–3 weeks, a severe headache, tiredness, deep muscle pain or myalgias, and may include chills, nausea, anorexia, vomiting, diarrhea, abdominal pain, hypotension (abnormally low blood pressure), confusion, lethargy, stupor, delirium, and seizures. A rash that often begins on the legs and/or arms appears on the first day of symptoms for about 15% of patients, and appears by the third day for about 50% of patients. The rash may include the soles and palms and then rapidly spread to the trunk, and typically appears after the fever, headache, myalgias, and GI symptoms. A form of spotless fever, in which patients do not present with a rash, occurs in 10%–15% of patients. This is not a milder form, as the mortality rate is higher for spotless fever than for spotted fever. According to Freiman, Borsuk, and Sasseville, “multiorgan involvement may lead to a variety of symptoms, which makes the diagnosis challenging” (2005).

As with TSS, there is not a specific test for RMSF, and “making an accurate clinical diagnosis of RMSF is not easy, even for experienced physicians who practice in areas where the disease is endemic” (Eloubeidi & Burton, 1997). This symptomatic disease mirrors other diseases, is easily confused because of the diversity of its symptoms, and “can occur simultaneously with other disease processes,” causing it to be easily “misdiagnosed as a hospital-acquired infection,” such as surgical TSS (Eloubeidi & Burton). “Because of its diverse clinical features, RMSF has been confused with community-acquired illnesses such as meningococcemia, numerous viral exanthems, hypersensitivity reactions to drugs, thrombotic thrombocytopenic purpura, S. aureus bacteremia, acute appendicits, and even acute cholocytitis,” according to Eloubeidi and Burton (emphasis added). Serology tests are usually done to confirm RMSF; however, those tests are “only useful after acute infection,” leaving patients at higher risk (Amitai et al., 2006). Eloubeidi and Burton state that “RMSF is a disease that can be a ‘wolf in sheep’s clothing,’ and it also can act as a ‘great imitator’ of other disease processes.” It has been stated that, “a high index of suspicion is the most important aspect of diagnosing RMSF” (Amitai et al.). Much RMSF treatment is treating of the symptoms, such as intravenous hydration and supplemental oxygen, along with antibiotics for the infection. If the tick is still present, it is removed. Of the confirmed cases of RMSF, 72% required hospitalization (Amitai et al.). Initial symptoms of RMSF are often nonspecific, and TSS and RMSF share many of the same symptoms, such as fever over 102 degrees, hypotension, headache, multiorgan involvement, and rash. It is imperative that clinicians discover quickly which disease the patient is manifesting, as different treatment modes are required. Both TSS and RMSF are potentially life-threatening diseases that should be taken seriously and understood to the best of the expert’s abilities and resources, as a misdiagnosis may result in loss of life.

Amitai, A., Sinert, R., & Medlin, R. Jr. (2006, January 3). Tick-borne diseases, rocky mountain spotted fever. emedicine. Retrieved August 27, 2007, from http://www.emedicine.com/EMERG/topic510.htm

Directors of Health Promotion and Education. (n.d.). Rocky mountain spotted fever. Retrieved August 27, 2007, from http://www.astdhpphe.org/infect/rms.html

Eloubeidi, M. A. S., & Burton, C. S. (1997, September). The great imitator: Rocky mountain spotted fever occurring after hospitalization for unrelated illnesses. Southern Medical Journal, 90(9), 943–946.

Freiman, A., Borsuk, D., & Sasseville, D. (2005, November 22). Dermatologic emergencies. Canadian Medical Association Journal, 173(11), 1317¬–1319.

HCG. (2007). Common bacterias can cause quite a toxic shock! Staphylococcus & Streptococcus. Associated Content. Retrieved August 28, 2007, from http://www.associatedcontent.com/pop_print.shtml?content_type=article&content_type_id=12459

Issa, N. C., & Thompson, R. L. (2001, October). Staphylococcal toxic shock syndrome: Suspicion and prevention are keys to control. Postgraduate Medicine, 110(4), 55–62. Retrieved August 28, 2007, from http://www.postgradmed.com/issues/2001/10_01/issa.htm

Kreiswirth, B. N., Kravitz, G. R., Schlievert, P. M., & Novick, R. P. (1986, November). Nosocomial transmission of a strain of Staphylococcus aureus causing toxic shock syndrome. Annals of Internal Medicine, 105(5), 704–707.

Mayo Clinic Staff. (2005, September 9). Rocky mountain spotted fever. Retrieved September 4, 2007, from http://www.mayoclinic.com/print/rocky-mountain-spotted-fever/DS00600/DSECTION=all&METHOD=print

Nemours Foundation. (2007, January). TeensHealth: Toxic shock syndrome. Retrieved August 27, 2007, from http://kidshealth.org/PageManager.jsp?dn=KidsHealth&lic=1&ps=207&cat_id=20015&article_set=20277

Salandy, D., & Brenner, B. E. (2005, December 5). Toxic shock syndrome. emedicine. Retrieved August 27, 2007, from http://www.emedicine.com/emerg/topic600.htm

Todar, K. (2005). Staphylococcus. Todar’s Online Textbook of Bacteriology. Retrieved August 28, 2007, from http://www.textbookofbacteriology.net/staph.html

University of Utah Health Services Center. (2003). Infectious diseases: Toxic shock syndrome. Retrieved August 27, 2007, from http://healthcare.utah.edu/healthinfo/adult/infectious/toxic.htm

Spider contents other than venom may trigger harmful effects in humans, as when contacting eyes after a squashing and causing conjunctival inflammation.”

THE FORENSIC EXAMINER Winter 2007 www.acfei.com

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