PATHOLOGY: Implications for the Physical Therapist

MEDICAL MANAGEMENT

DIAGNOSIS, TREATMENT, AND PROGNOSIS.

Prevention is the key to avoiding gas gangrene before treatment is required. To prevent gangrene in an open wound, the wound should be kept as clean as possible. Special wound care is particularly important in people with diabetes mellitus, malnutrition, and immunodeficiency.

Early, immediate intervention is necessary with surgical debridement and excision of necrotic tissue. Diagnosis can be established by frozen section of muscle. Gram stain and culture also verify the diagnosis but not as rapidly. Radiographs may show evidence of gas formation, although gas may not be seen in early stages. Antibiotics are administered, but if significant gangrene develops amputation may be necessary. Hyperbaric oxygen therapy is controversial.¹⁶⁴

With prompt treatment, 80% of people with gas gangrene of the extremities survive; prognosis is poorer for gas gangrene in other sites such as the abdominal wall, uterus, or bowel.

8-4 SPECIAL IMPLICATIONS FOR THE THERAPIST

Gas Gangrene

PREFERRED PRACTICE PATTERNS

7A:

Prevention/Risk Reduction for Integumentary Disorders

7B:

Impaired Integumentary Integrity Associated with Superficial Skin Involvement

7E:

Impaired Integumentary Integrity Associated with Skin Involvement Extending into Fascia, Muscle, or Bone and Scar Formation

Careful observation may result in early diagnosis. With any postoperative or posttraumatic injury, look for signs of ischemia such as cool skin; pallor or cyanosis; sudden, severe pain; sudden edema; and loss of pulses in the involved limb. Record carefully and immediately report these findings to the medical staff. Throughout this illness adequate fluid replacement is essential; assess pulmonary and cardiac functions often.

Special care to prevent skin breakdown is important, and meticulous wound care following surgery is imperative. To prevent gas gangrene, routinely take precautions to render all wound sites unsuitable for growth of Clostridia by attempting to keep granulation tissue viable; adequate debridement is imperative to reduce anaerobic growth conditions. Notify the physician immediately of any devitalized tissue. Position the client to facilitate drainage.

Psychologic support is critical, as these clients can remain alert until death, knowing that death is imminent and unavoidable. The therapist must be prepared for the foul odor from the wound and prepare the client emotionally for the large wound after surgical excision. Wound care requires sterile procedures to prevent spread of bacteria; dispose of drainage material and dressings in double plastic bags for incineration. No special cleaning measures are required after the client is discharged.

Pseudomonas

Overview.: Pseudomonas aeruginosa is a major opportunistic pathogen and one of the most common hospital-(particularly ICU) and nursing home–acquired (nosocomial) pathogens. Pseudomonas is uncommon in community-acquired infections and healthy individuals. The organism infrequently colonizes human beings, but it can cause disease, particularly in the hospital environment, where it is associated with pneumonia, wound infections,¹⁴³ urinary tract disease, and sepsis in debilitated people.

Burns, urinary catheterization, cystic fibrosis, chronic lung diseases, neutropenia associated with chemotherapy, and diabetes all predispose to infections with P. aeruginosa. It thrives on moist environmental surfaces, making swimming pools, whirlpool tubs, respiratory therapy equipment, flowers, endoscopes, and cleaning solutions prime targets for growth.

This organism produces several virulence factors and is inherently antibiotic resistant. Spread of the organism in a health care setting is by contact, typically from a reservoir as described above. HCWs have been known to pass the organism on their hands or under fingernails.¹² Colonization usually precedes infection, although colonization is not indicative of future infection. It is unclear which factors lead from colonization to invasive disease.¹²²

Pathogenesis.: P. aeruginosa produces of an array of proteins, which allow it to attach to, invade, and destroy host tissues while avoiding host inflammatory and immune defenses. Injury to epithelial cells uncovers surface molecules that serve as binding sites for P. aeruginosa.

Many strains of this pathogen produce a proteoglycan that surrounds the bacteria, protecting them from mucociliary action, complement, and phagocytes. The organism releases extracellular enzymes, which facilitate tissue invasion and are partially responsible for the necrotizing lesions associated with Pseudomonas infections. This pathogen can also invade blood vessel walls and produce systemic pathologic effects through endotoxin and several systemically active exotoxins.

Clinical Manifestations.: Signs and symptoms of Pseudomonas infection vary with the site of infection and the state of host defenses.¹²² If the host has the capacity to respond to the invading bacteria with neutrophils, an acute inflammatory response results.

The Pseudomonas organism often invades small arteries and veins, producing vascular thrombosis and hemorrhagic necrosis, particularly in the lungs and skin. Blood vessel invasion predisposes to bacteremia, dissemination, and sepsis. This bacterium causes infections of the respiratory tract (pneumonia), bloodstream, CNS, skin (see Fig. 8-4) and soft tissues, bone and joints, and other parts of the body.

Figure 8-4 Pseudomonas. Blue-green color in a burn wound indicates infection by Pseudomonas aeruginosa. (Reprinted from Gould BE: Pathophysiology for the health professions, ed 3, Philadelphia, 2006, W.B. Saunders, courtesy Judy Knighton, Ross Tilley Burn Center, Sunnybrook and Women’s College Health Center, Toronto, Ontario, Canada.)

Respiratory Tract Infections.: Pneumonia caused by P. aeruginosa is one of the most common causes of nosocomial pneumonia.¹²⁸ The infection may be primary (contained to the lungs) or cause a bacteremia with metastasis of infection. Primary pneumonia is most often seen in clients with a predisposing history of chronic lung disease, congestive heart failure, or AIDS who are in a hospital setting. These individuals are often intubated and in the intensive care unit.

Signs and symptoms are typical of pneumonias seen with other organisms, such as dyspnea, fever, productive cough, low oxygenation, elevated white cell count, and delirium. Cavitary lesions may be seen on chest radiograph (particularly if the client has AIDS), and pleural effusions are common.

Pneumonia secondary to P. aeruginosa can be severe and life threatening. Bacteremic pneumonia begins as a respiratory tract infection but spreads to the bloodstream and metastasizes to other viscera, causing hemorrhaging and necrosis. This bacteremia is often associated with clients who are neutropenic and unable to control the infection. Symptoms include those of pneumonia with sepsis, which is rapid and severe. The chest radiograph may demonstrate necrotizing pneumonia with cavitary lesions.

Chronic infections with Pseudomonas are noted in children or young adults with cystic fibrosis. Over time there is chronic progression of symptoms with acute exacerbations of disease. Clients typically experience mucous plugging and airway inflammation, which predispose to P. aeruginosa infection. The bacteria then contribute to further mucous plugging and cause a supportive reaction leading to bronchiectasis and atelectasis. Episodes of pneumonia are seen more frequently as more lung is damaged and becomes fibrotic.

Bacteremia.: Bacteremia may occur without prior pneumonia and is an important cause of serious, life-threatening bloodstream infections in clients with neutropenia. P. aeruginosa bacteremia is typically acquired in the hospital and may be primary (no identifiable source) or secondary to a focal infected site (e.g., skin, lungs, intravascular source, indwelling catheters, GI or urinary tracts).

As with other Pseudomonas infections, bacteremia is rapidly progressive without treatment, with high morbidity and mortality rates. Clients experience fever, tachypnea, tachycardia, hypotension, and delirium, which can lead to renal failure, acute respiratory distress syndrome, and death. Rarely characteristic lesions of Pseudomonas bacteremia, ecthyma gangrenosum, develop on the skin. These vesicles are initially hemorrhagic with progressive necrosis and ulceration. They occur as single lesions or in small groups.

Central Nervous System Infections.: Pseudomonas infections of the CNS result from extension from a contiguous structure such as the ear, mastoid, or paranasal sinus; direct inoculation into the subarachnoid space or brain by means of head trauma, surgery, or invasive diagnostic procedures (e.g., lumbar punctures, spinal anesthesia, intraventricular shunts); and bacteremic spread from a distant site of infection such as the urinary tract, lung, or endocardium.

The clinical manifestations of Pseudomonas meningitis are like those of other forms of bacterial meningitis (see Chapter 29) and include fever, headache, stiff neck, nausea, and confusion. The onset of disease may be acute and occur suddenly or may be more gradual and insidious. Rapidly progressive and toxic disease is seen more frequently in clients who are bacteremic, while those without associated bacteremia may have few systemic signs and symptoms (e.g., those whose meningitis is related to neurosurgery or extension from a contiguous site of chronic infection).

Skin and Soft Tissue Infections.: Pseudomonas disease of the skin and mucous membranes can result from primary or metastatic foci of infections. Common predisposing factors for primary skin and soft tissue infections are a breakdown in the integument, especially resulting from surgery, burns, trauma, and pressure ulcers; whirlpool use; and chemotherapy-induced neutropenia.

The wound is hemorrhagic and necrotic and rarely may have a characteristic fruity odor (sweet, grapelike odor) with a blue-green exudate that forms a crust on wounds (Fig. 8-4). Pseudomonas bacteria may produce distinctive skin lesions known as ecthyma gangrenosum, as described above, associated with Pseudomonas bacteremia.

Pseudomonas burn wound sepsis is a dreaded complication of extensive third-degree burns and is characterized by multifocal black or dark-brown discoloration of the burn eschar; degeneration of the underlying granulation tissue with rapid eschar separation and hemorrhage into subcutaneous tissue; edema, hemorrhage, and necrosis of adjacent healthy tissue; and erythematous nodular lesions on unburned skin.

Systemic manifestations may include fever, hypothermia, disorientation, hypotension, oliguria, ileus, or leukopenia. The diagnosis is based on clinical signs and symptoms; biopsy of the burn site, which demonstrates evidence of invading bacteria; and culture positive for Pseudomonas.

Bone and Joint Infections.: Pseudomonas infections of the bones and joints result from hematogenous spread from other sites or extension from contiguous sites of infection. Contiguous infections are usually related to penetrating trauma, surgery, or overlying soft tissue infections. Injection drug users may contaminate drugs or water with Pseudomonas, which often seeds the sternoclavicular or other joints.¹³¹

P. aeruginosa is the most common cause of osteochondritis of the foot following a puncture wound.⁸ Infection involves the cartilage of the small joints and the bones of the foot. Typically, the person experiences early improvement in pain and swelling following a puncture wound only to have the symptoms recur or worsen several days later. The average duration of symptoms before diagnosis is several weeks; fever and other systemic signs are usually absent. An area of superficial cellulitis is evident on the plantar surface of the foot, or there may merely be tenderness to deep palpation.

Bloodborne Pseudomonas, from injection drug use or pelvic surgery, appears to have a predilection for fibrocartilaginous joints such as the symphysis pubis.¹³⁰ Vertebral osteomyelitis caused by P. aeruginosa is occasionally associated with complicated urinary tract infections and genitourinary surgery or instrumentation.

This disease occurs most often in older adults and involves the lumbosacral spine. Physical signs include local tenderness and decreased range of motion in the spine; fever and other systemic symptoms are relatively uncommon. Mild neurologic deficits may be present (see further discussion in Chapter 27).

Other Pseudomonas Infections.: Pseudomonas is noted to cause disease of the external ear, which may be benign (“swimmer’s ear”) or malignant (invasion of bone, soft tissue, and cartilage). P. aeruginosa infection of the cornea causes bacterial keratitis or corneal ulcers.

Corneal ulcers can progress rapidly with complications such as corneal perforation, anterior chamber involvement, and endophthalmitis. Native heart valves or prosthetic valves can become infected with P. aeruginosa, causing endocarditis. Infection of native valves is seen in injection drug users, and multiple valves may be involved.

Right-sided endocarditis may be complicated by septic pulmonary emboli causing pulmonary disease, while left-sided endocarditis may cause heart failure, brain abscess, or mycotic aneurysms. P. aeruginosa is the most common cause of nosocomial urinary tract infections often arising from urinary catheters, instrumentation, or surgery. The prostate or kidney stones may harbor the bacteria, resulting in recurrent infections.

VIRAL INFECTIONS

Bloodborne Viral Pathogens

The bloodborne viruses that most endanger HCWs are the bloodborne pathogens hepatitis B virus (HBV), hepatitis C virus (HCV), and HIV. In 1991 the U.S. Congress passed the Bloodborne Pathogens Standard, prepared by the Occupational Safety and Health Administration (OSHA) and written to help eliminate or minimize occupational exposure to HBV, HCV, HIV, and other bloodborne pathogens.¹⁶⁹

The guidelines are based on the use of standard precautions, including appropriate handwashing and barrier precautions, to reduce contact with body fluids potentially contaminated by these viruses. The use of safety devices and techniques to reduce the handling of sharp instruments can help in the reduction of significant contact with body fluids, particularly blood or blood-containing fluids.¹⁷⁹

8-6 SPECIAL IMPLICATIONS FOR THE THERAPIST

Bloodborne Viral Pathogens

PREFERRED PRACTICE PATTERNS

See individual disease discussion.

Hepatitis B

See discussion on HBV in Chapter 17. Nosocomial transmission of HBV is a serious risk for HCWs. The risk of acquiring HBV infection from occupational exposure is dependent on the degree of exposure to blood and the presence of HBV e antigen (HBeAg) from the source. An approximate 22% to 31% chance exists of acquiring HBV after percutaneous (needlestick) contact with a hepatitis surface antigen (HBsAg) and HBeAg seropositive source.¹⁶⁹ Yet the rate of development of hepatitis from a needlestick in a HBeAg-negative, HBsAg-positive source was only 1% to 6%.

HBV can be transmitted to HCWs via percutaneous injuries or by direct or indirect contact with blood from an infected client. Blood contains the highest amount of infected particles and is the most efficient means of transmission. HBV in blood is able to survive up to 1 week on environmental surfaces. The incubation period is 45 to 180 days (average 60 to 90 days).

Preexposure HBV vaccination of HCWs who are at risk (e.g., those who work in an area likely to have contact with blood and body fluids) is strongly recommended and can prevent acquisition of HBV (see Table 8-4).²⁴ Once a HCW has been exposed, the HBsAg status of the person and vaccination and vaccine-response status of the exposed HCW must be determined. Postexposure prophylaxis (PEP) should then be given if the HCW is unvaccinated or nonresponsive to previous vaccine and the source is HBsAg positive.

Studies done in perinatal situations have shown that the combination of HBV immunoglobulin (HGIB) and HBV vaccine is 85% to 95% effective in preventing HBV as compared to either agent alone. Data show that HGIB and the HBV vaccine are effective as single PEP for preventing clinical disease in occupational exposures (70% to 75%).

Although data are not available comparing the combination PEP in occupational exposures, the current recommendations have been extrapolated from other studies and the combination presumed to be as effective as either one alone.¹⁶⁹ HGIB and the vaccine are both tolerated well with only rare reports of anaphylaxis.

The OSHA bloodborne pathogen standard mandates that HBV vaccine and HGIB be made available, at the employer’s expense, to all HCWs with potential occupational exposure. In addition, strict adherence to handwashing and standard precautions (see Appendix A) is critical in prevention of the transmission of hepatitis-contaminated body fluids. Transmission is also prevented by use of barriers during sexual activity and by not sharing personal or other items that may have blood on them.

For the HCW who is positive for HIV, HBV, or HCV, the CDC guidelines are based on the assumption that the risk of transmission to others is greatest during invasive procedures that include (for the therapist) sharp debridement or digital palpation of a needle tip (or other sharp instrument) in a poorly visualized or highly confined anatomic site.

Any therapist performing such procedures should determine his or her own HIV, HBeAg, and HCV antigen status. Those who are infected should not perform the procedures unless they have obtained guidance from an expert panel about when and how they may safely do so. Although the CDC does not mandate restricted practice, the requirement that clients of an infected HCW be notified of the provider’s infection status before undergoing these procedures is a restriction on practice.⁵⁷

Some experts consider these practice guidelines and the idea of mandatory testing of all clinicians performing invasive procedures cost prohibitive and unnecessary given the fact that HCWs are far more likely than their clients to contract bloodborne pathogens from exposure to infected blood. Viewed in this context, extraordinary measures to protect clients undergoing these interventions may not be warranted, and the current CDC recommendations are considered overly conservative.^18,57

Hepatitis C

See the section on HCV in Chapter 17.

HCV is the most common etiologic agent in cases of non-A, non-B hepatitis in the United States. Seroprevalence studies among HCWs have shown a significant association between acquisition of disease and health care employment, specifically client care or laboratory work. Accidental percutaneous injuries (needlesticks or cuts with sharp instruments) are the highest risk vehicle for transmission to HCWs from people with acute or chronic HCV.

The incubation period for HCV is 6 to 7 weeks, and nearly all individuals with acute infection will have chronic (more than 3 to 6 months’ duration) HCV infection with persistent viremia and the potential for transmission to others over an extended period.

Serologic assays to detect HCV antibodies (not protective antibodies) are available and are used to determine source and HCW status after exposure. More than 75% of all people with HCV develop chronic hepatitis, and cirrhosis may develop in up to 25% of those with chronic HCV. A risk of developing hepatocellular carcinoma (approximately 3% to 5% per year) exists, and a small percentage of people with HCV may progress to fulminant liver failure.¹¹⁸

Currently no vaccine against HCV is available, and no PEP can be recommended. PEP with immune globulin or antiviral agents does not appear to be effective in preventing HCV infection.¹⁶⁹ Follow-up HCV testing should be performed to verify if seroconversion occurs.

Strict adherence to handwashing and standard precautions (see Appendix A) is critical in prevention of transmission of hepatitis-contaminated body fluids. Transmission is also prevented by use of barriers during sexual activity and by not sharing personal or other items that may have blood on them.

Human Immunodeficiency Virus

See the section on HIV in Chapter 7.

Nosocomial transmission of HIV from clients to HCWs may occur after percutaneous or, infrequently, mucocutaneous exposure to blood and body fluids containing blood. According to prospective studies, the risk of acquiring HIV infection following percutaneous exposure has been estimated to be about 0.3% and 0.09% after mucous membrane exposure for HCWs.¹¹⁸ Nonintact skin exposure risk is not precisely known but estimated to be less than mucous membrane exposure.

HIV seroconversion among HCWs after percutaneous exposure to blood containing HIV is associated with the following factors: (1) presence of visible blood on the device prior to injury, (2) a procedure that involved needle placement into a person’s vein or artery, or (3) deep injury with the contaminated device.

Transmission of HIV infection was also associated with injuries in which the source was terminally ill with AIDS, thus exposing the HCW to high titers of active virus. Assessing the viral load of the source of the exposure may be a surrogate for transmission risk, but studies are lacking and even very low viral titers do not negate the risk following exposure.¹¹⁸

In 2005 the CDC updated previously published provisional recommendations for postexposure chemoprophylaxis and use of antiretroviral therapies.¹¹⁸ HCWs who sustain needlestick or other high-risk exposures should be counseled and offered HIV baseline and follow-up blood testing as soon as possible and should then be treated with antiretroviral therapy per CDC protocol.

HCWs at high risk for acquiring HIV postexposure should be given at least three drugs; drug selection should also consider the source’s viral resistance. Data are lacking concerning the number of drugs offered HCWs who are at a low risk of acquiring HIV. Two-drug PEP therapy may be sufficient in these cases.

Postexposure, the involved area of contact should be immediately washed thoroughly (not scrubbed) with antiseptic soap and then rinsed with water. Therapy with antiretrovirals should be initiated immediately and should be continued for 4 weeks.¹¹⁸

Consultation with an infectious disease or HIV specialist should be quickly obtained for selection of an antiviral regimen. Since HCWs are not able to tolerate many of the antiviral medications because of side effects, careful monitoring should provided. Prevention of transmission includes the use of meticulous handwashing, standard precautions, and the same precautions described above for the bloodborne hepatitis viruses.

Herpesviruses

Overview and Definition

The term herpes is derived from the Greek word herpein, which means “to creep.” The word refers to the tendency for this type of viral infection to become chronic, latent, and recurrent. The known human herpesviruses (HHVs) are divided by genomic and biologic behavior into eight types (Box 8-9).

Box 8-9 TYPES OF HERPESVIRUSES

Herpes simplex virus (HSV)	Type 1
Herpes simplex virus (genital herpes)	Type 2
Varicella-zoster virus (VZV)	Type 3
Epstein-Barr infectious mononucleosis virus (EBV)	Type 4
Cytomegalovirus (CMV)	Type 5
Roseola (exanthema subitum) human herpes virus (HHV)	Type 6
Herpes virus serologically associated with roseola, human herpes virus (HHV)	Type 7
Human herpes virus associated with Kaposi’s sarcoma (HHV)	Type 8

All herpesviruses are morphologically similar, but the biologic and epidemiologic features of each are distinct. Subclinical primary infection with the herpesviruses is more common than clinically symptomatic illness, and each type then persists in a latent state for the rest of the life of the host.

With the herpes simplex virus (HSV) and varicella-zoster virus (VZV), the virus remains latent in sensory ganglia and, upon reactivation, lesions appear in the distal sensory nerve distribution. Virus reactivation in immunocompromised hosts may lead to widespread lesions in affected organs such as the viscera or the CNS. Severe or fatal illness may occur in infants and the immunocompromised. Association with malignancies includes EBV with Burkett’s lymphoma and nasopharyngeal carcinoma and HHV-8 with Kaposi’s sarcoma and body cavity lymphoma.^33,138

Herpes Simplex Viruses Types 1 and 2

See Table 8-7.

Table 8-7

Most Common STIs^*

PEP, Postexposure prophylaxis.

^*Listed in descending order by incidence.

^†All sexually transmitted diseases can be prevented by sexual abstinence and mutually monogamous sex between two uninfected partners. The CDC has come under criticism by the medical community for not stressing this point in their prevention programs for young people.

^‡Centers for Disease Control and Prevention: Control of communicable diseases manual, ed 17, Atlanta, GA, 2000, U.S. Department of Health and Human Services.

Modified from Centers for Disease Control and Prevention: Sexually transmitted disease surveillance, 2004, Atlanta, GA, 2005, U.S. Department of Health and Human Services.

Incidence, Etiologic Factors, and Risk Factors.: Approximately 70% of Americans older than 12 years harbor HSV-1, which is usually responsible for cold sores; 20% older than 12 years have HSV-2, the principal cause of genital herpes.¹³⁵ Since 1966, the incidence of genital herpes has continued to rise.

Both strains can infect any visceral organ or mucocutaneous site, and HSV-1 can be transmitted to the genital area during oral sex. HSV creates a significant health risk since infection with these viruses increases the risk of infection with HIV and increases production of the HIV virus once infected. Seroprevalence for both agents increases with age and with sexual activity for HSV-2.

Intermittent, asymptomatic shedding is common and is the typical time of transmission, usually during the period immediately preceding appearance of sores. Sexual contact during asymptomatic periods is less likely to result in transmission of the virus than when sores are present. However, since people with genital herpes are more likely to engage in sexual contact when they are free of sores, the rate of asymptomatic transmission is still significant.

Infants born to women with genital herpes can be infected with HSV when they pass through an infected birth canal. The virus can also be passed to other regions of the body by hand contact, particularly in people who are immunosuppressed (e.g., older adults, transplant recipients, people with cancer undergoing chemotherapy, and anyone with HIV or other conditions that weaken the immune system).

Pathogenesis.: Even though HSV-1 and-2 are the two most closely related herpesviruses and share antigenic cross-reactivity, these two agents are genetically and serologically distinct and produce different clinical symptoms. HSV-1 and-2 primarily affect the oral mucocutaneous (cold sores and mouth sores) and genital areas (genital herpes), respectively. Primary infection occurs through a break in the mucous membranes of the mouth, throat, eye, or genitals or via minor abrasions in the skin. Initial infection can be asymptomatic, although minor localized vesicular lesions may be evident.

Local multiplication occurs, followed by viremia and systemic infection with a subsequent lifelong latent infection and periodic reactivation of the virus. During primary infection, the virus enters peripheral sensory nerves and migrates along axons to sensory nerve ganglia in the CNS, allowing the virus to escape immune detection and response.

During latent infection of nerve cells, viral DNA is maintained and not integrated into surrounding cellular structures, thus maintaining true latency. Various disturbances such as physical or psychologic stress can disrupt the delicate balance of latency, and reactivation of the latent virus occurs. The virus travels back down sensory nerves to the surface of the body and replicates, forming new lesions. Although painful, most recurrent infections resolve spontaneously, recurring at a later time.

Clinical Manifestations.: Primary HSV-1 (first episode) typically affects the mouth and oral cavity, causing vesicles in the mouth, throat, and around the lips. Vesicles typically open to form moist ulcers after several days. Systemic symptoms can accompany the lesions such as fever, myalgias, and malaise. Symptoms and lesions resolve within 3 to 14 days.

Herpetic whitlows (herpetic infection of the fingers) can result from inoculation of the finger from a herpes lesion (Fig. 8-5). Prior to implementation of standard glove precautions HSV-1 was the most common cause of herpetic whitlow. Now, HSV-2 has been implicated more often than HSV-1. HSV-1 can also infect the genitourinary system, causing signs and symptoms similar to HSV-2.

Figure 8-5 Herpetic whitlow. Herpetic whitlow is an intense, painful infection of the hand involving one or more fingers and typically affecting the terminal phalanx. HSV-1 is the cause in approximately 60% of cases of herpetic whitlow, and HSV-2 is the cause in the remaining 40%. A, Herpes simplex infection of the finger in a child. B, Herpetic whitlow of the thumb in an adult. (Reprinted from Callen JP: Color atlas of dermatology, ed 2, Philadelphia, 2000, W.B. Saunders.)

Primary infection is often asymptomatic. Recurrences are usually milder, involve fewer lesions, are of shorter duration, and in immunocompetent hosts are confined to the lips (herpes labialis). Recurrent genital HSV-1 is milder and less frequent than HSV-2. Recurrences are most commonly induced by stress, fever, sunlight, infection, or other factors.

HSV-2 is most often acquired through sexual contact. Primary HSV-2 causes vesicles to form in the genitourinary tract. Lesions are usually painful, small, grouped, and vesicular, with possible burning and itching. The blisterlike lesions break and weep after a few days, leaving ulcerlike sores that usually crust over and heal in 1 to 3 weeks.

Genital ulcers may occur on the genital area, cervix, buttocks, rectum, urethra, or bladder, causing vaginal and urethral discharge, dysuria, cervicitis, proctitis, and tender inguinal adenopathy. Systemic symptoms occasionally noted include headache, malaise, myalgias, and fever. Primary infection can be asymptomatic. Genital HSV-2 reactivation may be associated with a prodrome such as tingling or pain.

First symptomatic episodes may not be the initial infection. Known as nonprimary infections, individuals may have been previously exposed to HSV-1 and produced antibodies but not developed symptoms until exposed to HSV-2 or vice versa. In these cases, the initial symptomatic nonprimary infection has fewer symptoms and complications as compared to a first episode without previous exposure.⁸⁰

HSV can be responsible for other infections. Viral meningitis from HSV is caused by inflammation of the meninges surrounding the brain. This occurs more commonly from HSV-2 than HSV-1. Aseptic meningitis may develop 3 to 12 days following the appearance of lesions. Typical symptoms are headache, nausea, stiff neck, and fever. The prognosis is good for immunocompetent hosts.³³ An association between HSV-1 and Bell’s palsy has also been established.

Herpes encephalitis (an infection of the brain tissue), although rare, is a more serious infection and accounts for 10% to 20% of all cases of acute, sporadic viral encephalitis in the United States. In children and young adults, primary infection is the main cause. Adults may have reactivation as the principal source. Presenting symptoms include fever, headache, behavioral and speech disturbances, and seizures. Abnormalities caused by HSV can be seen on MRI. Encephalitis carries high morbidity and mortality rates, and permanent neurologic sequelae often result even with treatment.

Herpetic keratitis (ulceration of the cornea due to infection) is the most common cause for corneal blindness in the United States. Onset is acute, accompanied by blurred vision, conjunctivitis, and pain. Despite treatment, recurrences are common and cause scarring, making this a chronic disease. Prophylactic acyclovir may reduce recurrences and long-term scarring.¹¹² Severe scarring is an indication for corneal grafting.

Recurrences of HSV-1 or-2 increase during pregnancy but do not appear to affect the fetus. Primary infection with HSV during pregnancy can occasionally cause visceral dissemination in the mother and possible transmission to the fetus. Neonatal herpes may also occur from unknown shedding in the mother’s genital tract at the time of delivery. If untreated, babies develop visceral dissemination or infection of the CNS, with an 80% mortality rate.¹⁷ Cesarean section reduces the risk of neonatal herpes in mothers known to be shedding the virus.

HSV can also disseminate to visceral organs, causing severe consequences such as hepatitis, thrombocytopenia, arthritis, and pneumonitis. Disseminated infection typically occurs in pregnant women (primary genital HSV) or immunocompromised persons (primary or recurrent HSV). HSV esophagitis is seen in immunocompromised hosts but rarely noted in immunocompetent persons.

MEDICAL MANAGEMENT

DIAGNOSIS, TREATMENT, AND PREVENTION.

Clinical diagnosis of herpes is often insensitive. Up to 30% of first-episode genital herpes are caused by HSV-1, which has a low recurrence rate compared to HSV-2,³⁴ making distinction between the two types important.

Viral cultures of vesicular fluid are the standard laboratory test. The sample must be collected during the first few days the lesion is present in order for the results to be accurate. Type-specific serologic tests, enzyme-linked immunosorbent assay (ELISA), or immunofluorescent assay (IFA) provide a more rapid diagnosis while culture results are pending. PCR tests are also available and are the test of choice for detection of HSV in spinal fluid. While PCR is very sensitive, it is expensive and only available in certain laboratories.

An HSV vaccine that showed promise in animals ultimately failed human testing. Although no immunization against HSV infection is available, antiviral drugs can be used to treat initial cases, reduce the frequency and degree of viral shedding, and suppress recurrences.

The CDC has released recommendations and guidelines for the treatment of HSV-2.¹⁸⁴ Acyclovir, famciclovir, and valacyclovir are approved for the treatment and suppression of HSV-2. Famciclovir can be used to treat recurrent mucocutaneous HSV in individuals infected with HIV; valacyclovir is approved for the treatment of cold sores. These medications do not eradicate the virus and, once discontinued, there is no change in frequency, duration, or severity of recurrences.

Counseling regarding transmission and education on how to recognize symptoms and defer sex are essential in preventing new cases. Daily suppressive use of valacyclovir along with safe sex can reduce transmission of HSV-2. Proper use of condoms can also reduce the risk of acquiring HSV-2.¹⁷³ This is particularly helpful for couples where one is seropositive and the other seronegative for HSV.

8-7 SPECIAL IMPLICATIONS FOR THE THERAPIST

Herpes Simplex Virus

PREFERRED PRACTICE PATTERNS

7B:

Impaired Integumentary Integrity Associated with Superficial Skin Involvement

5C, 5D:

Acquired Neuromuscular Involvement (meningitis)

Recurrent disease is best treated with acyclovir, and recurrent genital disease requires barrier precautions during sexual activity in addition to medication. Although herpes simplex is contagious, nosocomial transmission is rare. However, it has been reported in some high-risk areas such as nurseries, intensive care units, burn units, and other areas where immunocompromised individuals might be placed.

Nosocomial transmission of HSV occurs primarily through contact with lesions or with virus-containing secretions such as saliva, vaginal secretions, or amniotic fluid. Exposed areas of skin, particularly when minor cuts, abrasions, or other skin lesions are present, are the most likely sites of viral entry. The incubation period of HSV is 2 to 14 days.

HCWs may acquire a herpetic infection of the fingers (herpetic whitlow or paronychia) from exposure to contaminated oral secretions. Such exposures are a distinct risk for HCWs who have direct contact with either oral or respiratory secretions from clients.

HCWs can protect themselves from acquiring HSV by adhering to standard precautions and handwashing before all client contact and by the use of appropriate barriers such as a mask, gloves, or gauze dressing to prevent hand contact with the lesion. Some work restrictions may be appropriate for affected HCWs when active lesions are present (e.g., herpetic whitlow) (see Table 8-6). No reports are evident that HCWs with genital HSV infections have transmitted HSV to clients, so no work restriction for people with HSV-2 is indicated.¹⁶⁹

During the prodromal stage of herpes simplex, the levator scapulae becomes vulnerable to activation of its trigger points by mechanical stresses that are usually well within its tolerance. However, a stiff neck syndrome can develop a day or two before the fully developed symptoms of herpes simplex.¹⁴⁷

Careful questioning regarding previous history of herpes, presence of prodromal symptoms, and observation for the development of a new outbreak of sores during the episode of care will help the therapist in making an accurate assessment of the client’s presentation.

Varicella Zoster Virus (Herpesvirus Type 3)

Incidence.: VZV is HHV-3 and is known as chickenpox or shingles (see the section on Viral Infections: Herpes Zoster, in Chapter 10). Prior to the availability of the varicella vaccine, primary or first-infection VZV accounted for about 3 to 4 million cases of chickenpox per year in the United States.

Approximately 10% to 20% of the population develops the secondary, or reactivation, form of VZV, resulting in herpes zoster or shingles. Approximately 300,000 cases of shingles occur in the United States every year and cause significant pain and disability. Adults older than 50 years and anyone who is immunocompromised (e.g., HIV infection, chemotherapy, corticosteroid therapy, or cancer) are at greatest risk. Young adults such as college students living in dormitories are at increased risk for VZV as either chickenpox (first time) or shingles (recurrence).

Pathogenesis.: Like other herpesviruses, VZV has the capacity to persist in the body (in sensory nerve ganglia) as a latent infection after the primary infection. VZV is acquired from contact with infected airborne droplets (from coughing or sneezing) into the respiratory tract or by direct contact with vesicular fluid to the respiratory tract or eye.

The virus is believed to initially multiply at the site of entry, with subsequent viremia occurring 4 to 6 days after infection. The virus then disseminates to other organs such as the liver, spleen, and sensory ganglia and further replicates in the viscera, followed by a secondary viremia with viral infection of the skin and mucosa (mouth, respiratory tract, or eye). Viral infection of the skin and mucosa produces vesicles filled with high titers of infectious virus, which then shed more viruses. The incubation period is from 14 to 16 days from exposure with a range of 10 to 21 days. This may be prolonged in immunocompromised people. VZV is present in white blood cells up to 5 days before the rash is present, and individuals can be contagious a day or two prior to the appearance of the rash. Individuals remain contagious until the lesions have crusted.⁷

The exact mechanism for the reactivation of VZV remains unknown, although shingles occurs more often in immunocompromised adults such as older adults, those with hematologic malignancies, especially leukemia and lymphoma, and people with HIV.

Clinical Manifestations.: Disease manifestations are either chickenpox (varicella) or shingles (herpes zoster). (See Chapter 10 for discussion of clinical manifestations of herpes zoster.) Primary VZV is virtually always symptomatic. Second episodes of chickenpox are uncommon unless the child is younger than 1 year at the time of the first episode. A mild prodrome consisting of fever and malaise may precede the onset of the rash in adults, while in children the rash is often the first sign of disease.

The rash is classically described as a “dewdrop on a rose petal,” with a vesicle on an erythematous base. The lesions begin as macules that quickly progress to papules, vesicles, and then pustules before crusting. VZV usually appears first on the scalp and moves to the trunk and then the extremities. Successive crops appear over several days, with lesions present in several stages of evolution at any one time.⁷

The generalized pattern of eruption without specific dermatome distribution distinguishes varicella from herpes zoster (Fig. 8-6). Shingles in the adult present as blisterlike lesions that erupt along dermatomes, with the highest concentration of lesions on the trunk corresponding with dermatomes from T3 to L3 (Fig. 8-7). Pain and itching are common symptoms during the eruption of the vesicles.

Figure 8-6 A, Early onset of varicella (chickenpox) in a young child. Painful itching can cause severe distress. Note the lesions on face and trunk. B, Varicella (chickenpox) with the more characteristic rash classically described as a “dewdrop on a rose petal,” with a vesicle on an erythematous base. (A, Courtesy Catherine Goodman. B, Reprinted from Callen JP: Color atlas of dermatology, ed 2, Philadelphia, 2000, W.B. Saunders.)

Figure 8-7 Herpes zoster (shingles). Small grouped vesicles occur along the cutaneous sensory nerve, forming pustules that crust over. Reactivation of VZV, the dormant chickenpox virus, is the underlying cause of this condition. A, Commonly seen on the trunk, these outbreaks can occur anywhere along the dermatome of the affected nerve. B, Lesions appear unilaterally and do not cross the midline. Usually external, these lesions can occur internally as well. Pain is often severe and can become chronic, a condition called postherpetic neuralgia. (A, Reprinted from Hurwitz S: Clinical pediatric dermatology: a textbook of skin disorders of childhood and adolescence, ed 2, Philadelphia, 1993, W.B. Saunders. B, Courtesy Mary Lou Galantino, Richard Stockton College of New Jersey, Pomona, NJ.)

Complications of varicella occur more often in adults, infants, and the immunocompromised. Adults are more likely to develop pneumonitis and CNS involvement (cerebellar ataxia and encephalitis) than are healthy children. The immunocompromised, especially those with leukemia or lymphoma who are receiving continuous chemotherapy, can develop disseminated disease with severe visceral involvement, including pneumonitis and encephalitis. The most common complication among persons affected with VZV is secondary bacterial skin infections.¹⁷⁶

Shingles also can lead to chronic, often debilitating nerve pain called postherpetic neuralgia (PHN), lasting years or even a lifetime and often resulting in significant morbidity and reduction in quality of life. Pain, hyperalgesia, and allodynia are typical of PHN.⁵⁰ Examples of allodynia include pain from the touch of clothing (touch allodynia) or pain that occurs from a draft of warm or cold air on the skin (thermal allodynia).

When contracted during the first or second trimesters of pregnancy, varicella carries a low risk of congenital malformations. Yet if a mother develops varicella within 5 days before delivery to 2 days after delivery, the newborn is at risk of serious disseminated disease.

MEDICAL MANAGEMENT

DIAGNOSIS AND TREATMENT.

Diagnosis is usually made based on clinical symptoms; however, with the advent of the varicella vaccine, the number of atypical cases has increased, making laboratory diagnosis more relevant. VZV may be cultured from vesicular fluid but requires time.

Real-time PCR for VZV is the test of choice for severe or atypical cases where results are needed quickly, although this is not readily available in most laboratories. The direct fluorescent antibody test is quick and found in most laboratories but requires careful specimen handling. Vesicular fluid from a new lesion on the skin is the best source of specimen. Stained smears from vesicular scrapings may reveal multinucleated giant cells consistent with VZV infection. Serologic testing is not routinely used but may be useful in adult vaccination programs.

Bed rest is important until the fever has gone down, and the person’s skin should be kept clean to avoid secondary bacterial contamination. Itching can be relieved with oral antihistamines, topical calamine lotion, and other skin-soothing lotions and baths.

The antiviral medications acyclovir, valacyclovir, and famciclovir can be used to treat individuals at high risk for complications but are not recommended for children with uncomplicated disease. Valacyclovir and famciclovir are only approved for treatment of adults with varicella. Oral acyclovir is recommended by some experts for pregnant women in their second or third trimesters while children who are immunocompromised should receive IV acyclovir. Persons with chronic lung or skin disease should also be considered for treatment.

Treatment should begin within 24 hours of the appearance of the rash. Antivirals may reduce the number of days new lesions appear and the severity of systemic symptoms, but they have not been shown to reduce transmission risk or reduce complications. Secondary bacterial infections of lesions are treated with antibacterial ointment or oral antibiotics if severe. Recovery from varicella infection usually results in lifetime immunity.

There is no cure for PHN. Treatment is often with nonopioid analgesics, tricyclic antidepressants, anticonvulsants, or topical local anesthetics based on the type of pain experienced (e.g., antidepressants for diffused pain, paroxysmal and local pain treated by anticonvulsants). Acyclovir has been shown to reduce the incidence of PHN; famciclovir reduces the duration of PHN. Evidence is lacking that oral corticosteroids given during the acute phase of the illness reduce the incidence or severity of PHN.⁷⁰

For individuals who are exposed but are without immunity to varicella, the varicella vaccine can be used up to 3 days postexposure (particularly in outbreaks) to aid in modifying symptoms or preventing the infection. For those individuals at high risk for severe complications and for whom the vaccine is contraindicated (such as immunocompromised persons, pregnant women, or in neonatal situations), there are other methods of PEP.

VZV immune globulin (VZIG) is a product that contains high amounts of the VZV antibody. It should be administered within 96 hours of exposure to the virus to modify or prevent complications. In December 2005 the manufacturer of VZIG discontinued production and availability is limited. If VZIG is not available, IV immune globulin can be used, although data supporting its efficacy are not available. Acyclovir has also been suggested as a postexposure treatment started between day 7 and 10 of exposure and given for a total of 10 days.

PREVENTION

The varicella vaccine is recommended for all adults who lack evidence of immunity, especially in those persons who have close contact with individuals at high risk for severe disease and complications.

Adults who are at high risk for exposure and transmission should also receive the vaccine (such as teachers of young children, child care employees, and residents and staff at medical facilities). Children between the ages of 12 and 18 months should routinely receive the vaccine. Currently, the varicella vaccine is available with the measles, mumps, and rubella (MMR) vaccine.

It is also recommended that all children who have not developed immunity by the age of 13 years should be vaccinated (see Table 8-4).⁷ Because the vaccine is a live attenuated vaccine, it is contraindicated in pregnant women, those who may become pregnant within 4 weeks of receiving the vaccine, and individuals with HIV or other immunosuppressed states.

Since the varicella vaccine became available in 1995, there has been a progressive decline in the incidence of chickenpox and hospitalizations from complications.^37,39,48 In 2004, there was an 80% to 90% decrease in acute varicella cases in active surveillance areas compared with 1995. The vaccine provides long-lasting (but not lifelong) immunity, with an 80% to 85% efficacy. Vaccine breakthrough cases are common but mild. Persons present with fewer lesions (usually less than 50) and lack systemic symptoms (such as fever).

The first shingles vaccine (Zostavax; zoster vaccine live) has been approved for adults aged 60 years and older. Zostavax has been shown to reduce the incidence of shingles by 51% and the incidence of PHN by 67% in adults aged 60 years and older. Among people who get shingles despite being vaccinated, it can reduce the disease’s severity. Approval of this drug for use in adults ages 50 to 59 years is pending more evidence to support its safety and effectiveness in this age group.¹¹⁵

8-8 SPECIAL IMPLICATIONS FOR THE THERAPIST

Varicella Zoster Virus

See Special Implications for the Therapist: Herpes Zoster in Chapters 10 and 39.

PREFERRED PRACTICE PATTERNS

7B:

Impaired Integumentary Integrity Associated with Superficial Skin Involvement

Varicella is highly contagious. The period of communicability extends from 1 to 2 days before the onset of the rash through the first 4 to 5 days or until all lesions have formed crusts. Immunocompromised individuals with progressive varicella are probably contagious during the entire period new lesions continue to appear.

Nosocomial transmission of VZV is well known. Sources for nosocomial exposures include clients or residents, HCWs, and visitors, including children or HCWs, with either varicella or zoster. It is generally advisable to allow only HCWs who are immune to varicella to take care of clients with VZV.

Because of the possibility of transmission to and development of severe illness in high-risk clients, HCWs with localized zoster should not take care of such clients until all lesions are dry and crusted. However, they may take care of others if they cover their lesions (see the section on Herpes Zoster in Chapter 10).

Because airborne transmission of VZV occurs, affected individuals in a hospital setting should be isolated in negative pressure rooms until crusts have dried. HCWs who do take care of VZV clients should use contact precautions, including careful use of barriers such as gloves, gowns, and masks whenever in contact with active lesions. If serologic immunity of the HCW cannot be verified, varicella vaccine is recommended (see Table 8-4).

When unvaccinated, susceptible HCWs are exposed to varicella, they are potentially infectious 10 to 21 days after exposure, and exclusion from duty is indicated from day 10 through day 21 after the last exposure or until all lesions are dry and crusted.

When vaccinated HCWs are exposed to varicella, serologic testing for antibodies may be done, and exclusion from duty can occur if they are seronegative or develop varicella symptoms. VZIG and acyclovir are not routinely recommended postexposure for healthy HCWs (exceptions may be made for pregnant or immunocompromised HCWs).⁷

Any patient or client suspected of having herpes zoster (shingles) requires immediate medical attention. Reports of prodromal pain, symptoms, or onset of rash are red flags to warrant immediate diagnosis and early treatment. Early intervention can reduce morbidity.

Infectious Mononucleosis (Herpesvirus Type 4)

Overview.: Infectious mononucleosis is an acute infectious disease caused by EBV, a member of the herpesvirus family. Although it may be seen at any age, it primarily affects young adults and children. In children, it is usually so mild that its presence often goes unnoticed.

Incidence, Etiologic Factors, and Risk Factors.: Infection with EBV is common in the United States, with 95% of people between the ages of 35 and 40 years having been infected. When an adolescent or young adult becomes infected with EBV, 35% to 50% of the time they will develop infectious mononucleosis. Both genders are affected equally. Incidence varies seasonally among college students but not among the general population. The reservoir of EBV is limited to human beings, and transmission is through contact with oral secretions, blood, or transplanted organs infected with the virus. Since about 80% of people carry EBV in the throat during the acute infection and for an indefinite period afterward, it is sometimes called the “kissing disease.”

Pathogenesis and Clinical Manifestations.: EBV causes lymphoid proliferation in the blood, lymph nodes, and spleen. Characteristically, the virus produces fever, sore throat, and tender cervical lymphadenopathy; headache, malaise, and abdominal pain (from splenic enlargement or hepatitis) may also be present. The incubation period is about 4 to 6 weeks.

Temperature fluctuations occur throughout the day, peaking in the evening. There is often an increase in the white blood cell count, with an elevation in atypical lymphocytes. Hepatomegaly (accompanied by elevated liver enzymes), palatal petechiae, and splenomegaly are manifested in more than 10% of cases. The spleen may enlarge to two to three times its normal size, causing left upper quadrant pain with possible referral to the left shoulder and left upper trapezius region. Affected individuals are at risk for splenic rupture, and care should be taken to avoid trauma. Both the peripheral nervous system and CNS can be involved.

Overall, major complications are rare but may include splenic rupture, aseptic meningitis, encephalitis, hemolytic anemia, aplastic anemia, idiopathic thrombocytopenia, myocarditis, and Guillain-Barré syndrome. Symptoms subside about 6 to 10 days after onset of the disease but may persist for weeks. Symptoms from EBV-related infectious mononucleosis rarely last longer than 4 months.

Studies support an association between infectious mononucleosis and the subsequent development of multiple sclerosis for both adults and children.^6,40,95 Young people who have had a strong immune response to the EBV are twice as likely to develop multiple sclerosis in adulthood. Scientists suspect this strong immune response could cross-react with brain substances, causing the brain to attack its own myelin in genetically susceptible individuals rather than the idea that the virus actually enters the brain.^35,40

MEDICAL MANAGEMENT

DIAGNOSIS, TREATMENT, AND PROGNOSIS.

Diagnosis is made either by culture (blood, sputum [from bronchoalveolar lavage], urine, throat swabs, or tissue samples) or by serologic identification of virus antigens. Positive results from urine or saliva samples do not necessarily indicate an acute infection since the virus may be shed for months to years. Traditional viral culture requires time; however, expedited results can be obtained with a tissue culture method (shell viral assay).

ELISA is the most common serologic test available and is able to distinguish between previous or active infection or, in the case of newborns, to detect passive maternal antibodies. Paired samples must be drawn at least 2 weeks apart to demonstrate increasing titers of antibodies and an active infection. PCR of viral DNA from blood or tissue is rapid but still undergoing refining. In seropositive transplant recipients, studies are underway to determine if prophylaxis or preemptive treatment is most beneficial posttransplant.¹⁶¹

In immunocompromised clients, pharmacologic treatment with ganciclovir and valganciclovir has proven effective. Foscarnet and cidofovir can be used in cases of resistance to ganciclovir but have more significant side effects. The prognosis for people with transplanted organs or who are immunocompromised is poor, as they may have fatal disseminated infections with multiple organ involvement.⁹⁶ Vaccines are currently in development.¹³⁷

8-10 SPECIAL IMPLICATIONS FOR THE THERAPIST

Cytomegalovirus

PRACTICE PATTERNS

6B:

Impaired Aerobic Capacity/Endurance Associated with Deconditioning

Other practice patterns depend on organ systems involved and clinical presentation.

The two principal reservoirs of CMV in health care institutions are (1) infants and young children and (2) immunocompromised individuals. However, HCWs who provide care to these high-risk populations have a rate of primary CMV that is no higher than among personnel without such client contact.

CMV transmission appears to occur directly, either through close, intimate contact with contaminated secretions or through excretions, especially saliva or urine.³⁶ Transmission by the hands of HCWs or individuals with the virus has also been suggested. The incubation period for person-to-person transmission is not known, and although CMV can survive on environmental surfaces or objects for a very short time, no evidence of fomite transmission exists.¹⁶⁹

Pregnant women and immunosuppressed people should avoid exposure to confirmed or suspected CMV infection. Pregnant women or women of childbearing age need to be counseled regarding the risks and prevention of transmission of CMV, but no data show that HCWs can be protected from infection by transfer to areas with less contact with individuals who have been diagnosed with CMV. Work restrictions for HCWs who contract CMV are not necessary since the risk of transmission of CMV can be reduced by careful adherence to handwashing and standard precautions.¹⁶⁹

Clients with CMV infection should be encouraged to wash their hands thoroughly and frequently to prevent spreading it. It is especially important to impress this on young children. As difficult as it may be, the child should not be allowed to kiss others, and parents and others should also avoid kissing the affected child.

Herpesviruses Types 6, 7, and 8

HHV-6 is a B-cell lymphotropic virus that is the principal cause of exanthema subitum (roseola infantum, or sixth disease).⁸⁶ Primary HHV-6 is common in children, with 90% infected by the age of 2 years. Although classically described as 3 to 5 days of high fever followed by a macular rash on the neck and trunk (roseola), children more commonly develop a fever, runny nose, and fussiness.⁸⁹ Its occurrence in adults is more complicated and associated with immunocompromised states such as AIDS and lymphoma. It has been associated with graft rejection and bone marrow suppression in transplant recipients and has been associated with multiple sclerosis.

HHV-7 is a T-cell lymphotropic virus that has also been serologically associated with roseola.⁸⁶ HHV-8 is associated with Kaposi’s sarcoma in AIDS and other immune-related diseases (e.g., body cavity lymphoma).^63,86 (See the section on Kaposi’s Sarcoma in Chapter 10.)

Viral Respiratory Infections

Viral respiratory infections (influenza, respiratory syncytial [RSV] virus) are common problems in health care settings. Many viral pathogens can cause respiratory infections, but influenza and RSV are associated with significant morbidity and mortality rates.

Influenza

Each year in the United States influenza viruses cause serious illness and even death, especially in young children with chronic diseases; immunocompromised adults; and the frail elderly. Influenza is caused by influenza viruses A or B and occurs in epidemics each winter between December and March. The mode of transmission is from person to person by inhalation of aerosolized virus or direct contact. Nosocomial transmission of influenza has been reported in acute and long-term health care facilities and has occurred from clients to HCWs, from HCWs to clients, and among HCWs. The incubation period is usually 1 to 4 days (average of 2 days).

Since 1997 influenza avian infections have been recognized. In 2005, an avian influenza A virus made the news for its ability to cause severe symptoms with fatal outcomes in humans. The subtype is H5N1 and was originally identified in Asia. Currently transmission is from infected birds to people in close contact with the birds, with rare person-to-person transmission.⁶⁶

Because of the severity of illness, with nearly 50% mortality, there is significant concern that the virus will undergo a mutation that will more readily allow person-to-person transmission.¹¹⁴ Zanamivir and oseltamivir may be beneficial in the treatment of this virus and studies are underway to develop and test an effective vaccine.

Influenza A and B resemble some other respiratory illnesses such as parainfluenza, RSV, and adenovirus. The onset is usually abrupt, with high fever, chills, malaise, muscular aching, headache, sore throat, nasal congestion, and nonproductive cough. The fever lasts about 1 to 7 days (usually 3 to 5). Children often manifest nausea, vomiting, and otitis media. The infection can progress rapidly in the first few days, causing pneumonia and respiratory failure, particularly in high-risk groups. Secondary bacterial pneumonia may also develop, usually 5 to 10 days after the onset of viral symptoms, particularly in the older adult.

MEDICAL MANAGEMENT

PREVENTION.

Vaccination is recommended before the beginning of each influenza season for people over age 50; people with chronic heart or lung disease, diabetes, renal dysfunction, or immunosuppression (including from HIV), pregnant women; nursing home residents; employees of medical or long-term care facilities; and HCWs (see Table 8-4).

In April 2000 the Advisory Committee on Immunization Practices (ACIP) lowered the age by 15 years from 65 and older to 50 and older. This policy changed because under the old guidelines, many people at risk for complications from influenza were being missed. About 25% of people between the ages of 50 and 64 have chronic medical conditions that place them at risk for influenza-related hospitalizations and possible death. The new plan recognizes that mass immunization programs based on age have been more successful than those targeting people with chronic diseases.

Vaccination against influenza is associated with reduced hospitalization rates and shorter hospital stays for pneumonia, diabetes, heart disease, and stroke in adults age 65 and older who are immunized. Mortality rates are also lower for all causes during influenza season in older adults who are immunized.^108,109 A live attenuated influenza vaccine is also available. It is given intranasally to healthy persons between the ages of 5 and 49 years, who are not in contact with immunosuppressed individuals and do not have chronic medical problems.¹²⁵

DIAGNOSIS

The virus may be isolated from nasal washes, nasopharyngeal swabs or aspirates, or throat swabs. These can be sent for a rapid detection of antigen (ELISA or IFA) and culture. With the advent of improved anti-influenza medications requiring initiation within 48 hours, the antigen detection method is a mainstay in many laboratories. Culture requires 3 to 10 days but should be performed if the rapid detection test is negative. Like other antigen detection methods, culture provides information regarding the subtype of Influenza virus yet provides a definitive diagnosis.

Genetic mutations in the influenza virus create hundreds of variations within the two main types; being immune to one variant does not ensure immunity to another. Trivalent influenza virus vaccine provides partial immunity (about 85% efficacy) for a few months to 1 year. The CDC updates the vaccine annually to include the most current influenza A and B virus strains.

TREATMENT.

Influenza antiviral agents can be given in conjunction with vaccine during institutional outbreaks of influenza. Amantadine and rimantadine are effective prophylaxis and treatment against influenza A, while oseltamivir can be effective prophylaxis and treatment of influenza A and B. Zanamivir is approved for treatment but not prophylaxis of influenza A and B.¹⁸¹

Antiviral agents used to treat influenza help decrease the duration and severity of signs and symptoms. Treatment must be initiated within the first 2 days of the illness and benefits those at high risk for complications. Resistance to these antivirals does occur and the Centers for Disease Control and Prevention monitors and recommends specific, effective treatment for each season.⁶⁸

Many people with influenza prefer to rest in bed; analgesics and a cough medicine mixture are often used. Droplet precautions (see Table 8-4) are imperative for all diagnosed and suspected cases of influenza. Antibacterial antibiotics are used only for treatment of bacterial complications.

PROGNOSIS.

The duration of the uncomplicated illness is 3 to 7 days, and the prognosis is usually very good in previously healthy people; Reye’s syndrome is a rare (almost eradicated) and severe complication of influenza and other viral diseases, especially in young children (to avoid Reye’s syndrome, acetaminophen should be used for fever instead of aspirin in children).

Most fatalities related to influenza are due to bacterial and viral pneumonia.⁶⁶ The mortality rate is low except in debilitated individuals. People at greatest risk for influenza-related complications are (1) individuals older than 65 years, (2) residents of chronic health care facilities such as nursing homes, (3) people with chronic pulmonary or cardiovascular disease, and (4) people with diabetes mellitus.¹⁶⁹

Respiratory Syncytial Virus

RSV causes annual outbreaks of pneumonia, bronchiolitis, and tracheobronchitis in infants and very young children and is the main cause of hospitalization for a respiratory illness in this group.⁶⁴

In adults and older children, reinfection is common and manifests itself as mild upper respiratory tract infection and tracheobronchitis. Serious pulmonary RSV infections have been described in older adults⁴⁷ and immunocompromised individuals, and there is a high mortality rate in bone marrow and solid organ transplant recipients.^53,90 In addition, infants with congenital heart disease, intensive care unit clients, those with cystic fibrosis, and older adults are at high risk for serious and complicated RSV.

Clients with HIV tend to have a less-severe course of the illness than transplant clients and although hospitalization for RSV is high, it rarely causes death. Annual epidemics occur in winter and spring. The incubation period is between 3 and 8 days. Inoculation occurs through the eyes or nose but rarely the mouth.

Nosocomial transmission of RSV occurs among clients, visitors, and HCWs. RSV is present in large numbers in the respiratory secretions of children with symptomatic RSV infections. It can be transmitted through large droplets (although not aerosolized) during close contact with such individuals or indirectly by hands or fomites that are contaminated with RSV. Hands can become contaminated through touching or handling of fomites or respiratory secretions and can transmit RSV by touching the nose or eyes.

Usually people shed the virus for 3 to 8 days, but young infants may shed the virus for as long as 3 to 4 weeks. Signs include low-grade fever, tachypnea, and wheezing. Hyperinflated lungs, decreased gas exchange, and increased work of breathing are also often present, and otitis media is a common complication.

Rapid diagnosis of RSV may be made by viral antigen identification of nasal washings using an ELISA or IFA. Culture of nasopharyngeal secretions is the standard for definitive diagnosis but requires 4 to 15 days. PCR for RNA of the virus is becoming more available but is not currently used in diagnosis except in research and large medical centers. These tests may have a decreased sensitivity in the older adult; therefore it is recommended that more than one be performed.

Treatment consists of hydration, humidification of inspired air, and ventilatory support as needed. Aerosolized ribavirin (an antiviral agent used in chronic HCV therapy) is FDA approved for the treatment of RSV in children, but close monitoring must be provided. Pregnant women should avoid ribavirin exposure since it is associated with fetal malformation or fetal death.

Palivizumab, a humanized monoclonal antibody (IgG), has been approved for prevention of serious lower respiratory tract illness in infants and young children who are at high risk of serious RSV, but it is expensive and must be administered intramuscularly. Growing amounts of data suggest a link with recurrent infections and the development of asthma later in life.

Avoidance of exposure to tobacco smoke, cold air, and air pollutants is also beneficial to long-term recovery from RSV bronchiolitis. A number of vaccines to prevent this infection are currently being studied, but because the immune response is neither durable nor complete it has been a difficult task.^64,81

8-11 SPECIAL IMPLICATIONS FOR THE THERAPIST

Viral Respiratory Infections

Influenza

HCWs must follow the guidelines in Tables 8-3 and 8-4 regarding prevention of transmission of influenza, both for themselves and their clients. Recommendations for immunization must be reviewed and acted on individually. Since the immunization for influenza does not provide immunity for the entire year or for all strains of influenza, common sense must prevail in the case of a HCW who suspects he or she has early signs and symptoms of influenza.

An early diagnosis can result in the use of antivirals to minimize intensity and duration of symptoms, especially in those at high risk for complications. HCWs must be aware of their responsibility to avoid transmission of infectious diseases such as influenza and either use personal protective equipment or practice self-isolation by staying home. This is especially important for the therapist in a setting with aged, immunocompromised, or chronically ill individuals.

Influenza can cause substantial morbidity and mortality among persons aged 65 years and older and among adults aged 50 years and older who have chronic illnesses. Anyone in these two groups is vulnerable to the serious complications of influenza. Routine influenza vaccination has been associated with reductions in influenza-associated and all-case mortality during influenza season.¹⁰⁸ Despite the benefits from vaccination, utilization remains below target rates. Physical therapists can be instrumental in reducing morbidity and mortality rates by encouraging clients in these two groups to get a flu shot each year and to get one themselves.

Respiratory Syncytial Virus

Nosocomial RSV infections disseminate quickly, requiring rapid diagnosis, droplet and contact precautions (see Table 8-3), handwashing, and sometimes passive immunization to achieve prevention in hospitals. Because viral respiratory infections are so common during the winter and spring months, it is difficult for health care facilities to restrict workers with the virus from all client care duties. However, restricting HCWs with acute viral respiratory infections from care of high-risk clients may be necessary during community outbreaks of RSV and influenza.

MISCELLANEOUS INFECTIOUS DISEASES

Prostheses and Implant Infections

Any device implanted into the body of any synthetic material (e.g., titanium, cobalt, silicone)¹⁴² can give rise to serious life-threatening infections. Bioprostheses, implanted in large numbers in the 1970s and early 1980s, have now gone into the second decade of life since implantation, a time when biodegradation becomes more common. Multiple reoperations carry a higher risk of infection.

Likewise, as the population ages, an increasing number of primary and revision arthroplasties are being done. Early detection of infection or other problems can reduce complications and morbidity associated with these devices. Anyone with implants of any kind with onset of increasing musculoskeletal symptoms (especially in the area of the surgery) must be screened for the possibility of infection.

Normal radiographs and negative needle aspirates can delay medical diagnosis of infection. Knowing the risk factors for developing an antibiotic-resistant infection (e.g., multiple surgical procedures, previous S. aureus infection, multiple antibiotics) and recognizing red flag symptoms of infection can help the therapist recognize the need for persistence in obtaining follow-up medical care.

See Chapter 25 for complete discussion of this topic.

Lyme Disease

Definition and Overview

Lyme disease is an infectious multisystemic disorder caused by the tick-borne spirochete Borrelia burgdorferi. It was first recognized in 1976 when a group of children in Lyme, CT, developed an unusual type of arthritis and a bull’s-eye rash.¹⁵⁸ Some of these children also had a history of tick bites. Not until 1983 was the organism recovered from affected individuals and tick vectors established the relationship between the spirochete and the infection.^19,157

In the United States, the disease is only transmitted to human beings by certain ticks of the Ixodes species: Ixodes scapularis (formerly called I. dammini), known as the deer or black-legged tick in the Northeast (from Massachusetts to Maryland) and North Central United States (Wisconsin and Minnesota), and I. pacificus, the Western black-legged tick found on the western coast of northern California and Oregon. The ticks are extremely small, measuring approximately 1 to 2 mm. Several more genospecies of Borrelia are known to cause the disease in Europe, Asia, and Australia.⁷⁶

Incidence

Lyme disease has become the most prevalent vectorborne infectious disease in the United States.^71,76 In 1982, when the CDC began national surveillance, only 491 cases were reported,¹¹³ while in 2002 a total of 23,763 cases were brought to medical attention.¹⁰⁴ This increased frequency is most likely multifactorial, a result of both a heightened awareness of the illness in endemic areas and an increase in the number of infected vectors.^104,156

Most cases (more than 90%) have been reported from the mid-Atlantic, Northeastern, and North Central regions of the country. It has been reported in 49 states and the District of Columbia. In the United States, Lyme disease is often seen in the late spring and summer months when the tick nymphs are most active and human outdoor activities are greatest.

Pathogenesis

I. scapularis exists in larval, nymphal, and adult stages. Larvae contract B. burgdorferi by feeding on infected rodents. The bacteria are then passed to nymphs and then to adults. The host of the adult is the white-tailed deer, which is required for survival of the ticks.

Human beings generally acquire the infection from nymphs when they attach to the skin to feed. The tick becomes engorged with blood and turns a grayish color. After approximately 36 hours, the bacteria from an infected tick are passed into the host when a tick injects spirochete-laden saliva into the host.¹²⁰ Most commonly, however, the tick falls off or is removed before the bacteria are injected into the host’s bloodstream.

After incubating for 3 to 32 days, the spirochetes cause an inflammatory response, resulting in characteristic skin lesions at the site of the tick bite (see Clinical Manifestations below). The bacteria then disseminate to other organs via the bloodstream or lymphatic system.¹⁵²

The human host activates an immune response, producing cytokines and antibodies against the bacteria. Despite the host’s response and if untreated, B. burgdorferi can survive for years in certain areas of the body by genetically adapting and inhibiting host immune responses.¹⁵⁴

Clinical Manifestations

Like syphilis, Lyme disease can be described as an imitator since its signs and symptoms mimic those of many other diseases. Symptoms vary widely and may not develop for as long as 1 month after a bite; in some cases, symptoms do not develop at all. Clinical manifestations of the infection occur in three stages.

Stage 1, the early, localized stage, usually occurs within days following a tick bite. About 80% of affected individuals will have a red, slowly expanding rash called erythema migrans (Fig. 8-8).¹⁵³ Not all people with the disease develop the telltale rash, and because early symptoms are often mild, some people may remain undiagnosed and untreated. Erythema migrans resolves spontaneously without treatment within an average of 4 weeks. Flulike symptoms suggestive of early dissemination such as fatigue, chills, fever, headache, lethargy, myalgias, or arthralgias may also develop early in the course of the infection and may be the presenting symptoms for anyone without a rash.

Figure 8-8 Examples of erythema migrans associated with Lyme disease. A, Many sources describe a characteristic bulls-eye rash with Lyme disease. B, However, there is a wide range of skin reactions labeled as erythema migrans possible with Lyme disease, as shown. Some skin rashes may be so minor as to be ignored or go unnoticed by the affected individual. (A, From Swartz MH: Textbook of physical diagnosis: history and examination, ed 4, Philadelphia, 2002, W.B. Saunders. B, Reprinted from Mandel GL: Principles and practice of infectious diseases, ed 6, Edinburgh, 2005, Churchill Livingstone.)

Stage 2, disseminated infection, occurs within days to weeks after the spirochete spreads, particularly to the nervous system, heart, and joints. Neurologic symptoms may be the first to arise and occur in 15% of all cases,¹⁵³ most commonly manifested as aseptic meningitis with mild headache, stiff neck, and difficulty with mentation; cranial neuropathies, particularly Bell’s palsy; and radiculopathies (Box 8-10). Even in anyone who remains untreated, neurologic symptoms may improve or resolve.¹⁵⁴

Box 8-10 NEUROLOGIC MANIFESTATIONS OF LYME DISEASE

• Facial nerve palsy (Bell’s palsy)

• Cognitive impairment (e.g., forgetfulness, decreased concentration, personality changes)

• Inflammation of the brain, spinal cord, or nerves

• Cranial neuritis

• Encephalitis

• Encephalomyelitis

• Encephalopathy

• Meningitis

• Radiculoneuropathy

About half of those diagnosed may go on to develop painful Lyme arthritis characterized by unilateral inflammation and swelling in the large joints, especially the knees.¹⁵³ Migratory musculoskeletal pain in joints, bursae, tendons, muscle, and bone may occur in one or a few locations at a time, often lasting only hours or days in a given location. Weeks to months later, after the development of a marked cellular and humoral response to the spirochete, untreated people often have intermittent or chronic monarticular (one joint) or oligoarticular (affecting only a few joints) arthritis.

Some people (4% to 10%) experience cardiac signs and symptoms, including myocarditis and various types of heart block and dysrhythmias, which can result in irregular, rapid, or slowed pulses; dizziness; fainting; and shortness of breath. Involvement of the eye is rare but can cause serious damage to the eye.

Stage 3, late persistent infection, may become apparent weeks to months after the initial infection. In the United States about 60% of individuals left untreated develop stage 3 symptoms characterized by intermittent arthritis associated with marked pain and swelling, especially in the large joints (Fig. 8-9). Rarely, affected individuals may go on to develop erosions or permanent joint abnormalities.¹⁵⁹ In approximately 5% of untreated individuals, chronic neurological symptoms occur, including spinal radicular pain, distal paresthesias, and a mild encephalopathy with subtle cognitive disturbances.¹⁵⁴

Figure 8-9 Swollen knee of a youth with Lyme arthritis. (Reprinted from National Institutes of Health: Lyme disease: the facts, the challenge, NIH publication no. 92-3193, Bethesda, MD, 1992, U.S. Department of Health and Human Services, p 12.) U.S. Department of Health and Human Services

Postinfection syndromes. Several syndromes have been reported describing persistent symptoms despite antibiotic treatment. One such syndrome, called the post-Lyme syndrome or chronic Lyme disease, resembles fibromyalgia or chronic fatigue syndrome. Affected individuals describe disabling fatigue, severe headache, diffuse muscle or joint pain, cognitive difficulties, and sleep abnormalities.¹⁵⁵ Symptoms may begin with the infection or emerge soon after treatment and persist for months to years. Debate continues as to whether these patients ever had an active infection with B. burgdorferi.^145,156 Of those with documented, treated disease it is hypothesized that the bacteria may trigger a neurohormonal or immunologic process that causes symptoms despite eradication of the spirochete.¹⁵⁶

About 10% of the people who have Lyme arthritis will continue to have joint symptoms for months to years following treatment. Although evidence of the spirochete exists in the synovial fluid prior to treatment, posttreatment joint fluid is often negative for infection. This again may be immune rather than infection related.¹⁵⁶

MEDICAL MANAGEMENT

PREVENTION.

Prevention is the key to avoiding Lyme disease.^65,172 Lyme disease is most common during the late spring and summer months in the United States when nymphal ticks are most active and human populations are frequently outdoors and most exposed. People who live or work in residential areas surrounded by woods or overgrown brush infested by ticks or favored by white-tailed deer and live in the endemic geographic areas are at risk. In addition, people who participate in outdoor recreational activities in tick habitat are also at risk for Lyme disease.

In December 1998 the FDA licensed the vaccine LYMErix to aid in the prevention of Lyme disease. However, in February 2002 the vaccine was withdrawn from the market reportedly for poor sales. Drawbacks surrounding the vaccine included cost and multiple, repeated doses for efficacy. Prophylactic treatment is controversial, but a single dose of doxycycline for ticks attached to the skin between 36 and 72 hours may be helpful.¹⁰⁵ Box 8-11 provides specific strategies available for Lyme disease prevention.

Box 8-11 PREVENTION OF LYME DISEASE

Precautions for people living in tick-infested areas:

• Avoid tick-infested areas, especially in May, June, and July (check with local health departments or park services for the seasonal and geographic distribution in your area).

• Walk along cleared or paved surfaces rather than through tall grass or wooded areas.

• Wear long-sleeved shirts, long pants tucked into socks, and closed shoes (no part of foot exposed).

• Wear light-colored clothing to make it easy to detect ticks.

• Always check for ticks after being outdoors. If ticks are removed within 36 hours of attachment, the risk of infection decreases significantly.

• Shower as soon as possible after being outdoors. Ticks take several hours to attach themselves to the skin and can be washed away first.

• Wash clothing worn outdoors immediately and use a dryer (heat kills the ticks). If no access to laundry facilities is available, the clothing should not be stored in the bedroom; if camping, the clothing should not be stored in the same area where people are sleeping.

• If bitten by a tick, remove the tick immediately by grasping it as close to the skin as possible with tweezers and tugging gently. Do not twist or turn the tweezers; pull straight away from the skin. Do not use petroleum jelly, fingernail polish, or a hot match to remove ticks.

• To lessen the chance of contact with the bacterium, do not crush the tick’s body or handle the tick with bare hands. Clean the bite area thoroughly with soap and water, then swab the area with an antiseptic to prevent bacterial infection.

• Whenever possible, save the tick in a glass jar for identification should symptoms develop.

• If living in an area in which deer ticks are common, keep the weeds and grass around the house mowed. Consider using wood chips where lawns meet forested areas. Ticks are less able to survive in a dry environment.

• Use flea and tick collars on pets; brush and examine them carefully after they have been outdoors. People can use insecticides such as permethrin or insect repellents containing diethyltoluamide (DEET).^*

^*The use of such chemicals may be objectionable to some people because they may cause neurotoxicity in children. Alternative methods are available.

DIAGNOSIS.

The CDC suggests a two-step process in diagnosing Lyme disease. The first step is to test the blood for antibodies to the spirochete. This is done with a sensitive enzyme immunoassay (EIA) or IFA. If this test is positive or equivocal, a Western immunoblot should be performed to confirm the diagnosis.²² Since antibodies are not present for 1 to 2 weeks following infection, these tests may not be positive early in the infection.

If erythema migrans is present, treatment can begin without serologic tests for Lyme disease. For those who present in the summer months with symptoms of Lyme disease without erythema migrans, empiric treatment with doxycycline can be considered. Since EIA may become negative with treatment, acute and convalescent blood samples can be collected for antibody titers to confirm infection. These tests are very sensitive in diagnosing infection in later stages.

The PCR uses gene segment amplification techniques to detect the DNA of the bacterium itself. PCR has detected bacterium DNA in synovial fluid, CSF, skin, blood, and urine. Synovial fluid may be tested to distinguish Lyme arthritis from acute septic arthritis. PCR is not routinely used in the diagnosis of Lyme disease and often is only available at specialized centers or for research purposes.

TREATMENT.

Early Lyme disease is treated with oral antibiotics, typically doxycycline or amoxicillin for pregnant women or children. Antibiotics are given for 14 to 21 days. If third-degree heart block or neurologic symptoms are present, other than isolated facial palsy, IV antibiotics are required for 14 to 28 days, typically with ceftriaxone. Lyme arthritis can be treated with oral or IV antibiotics, although oral therapy is easier and equally effective.

For anyone with continued arthritis despite recommended treatment, another 4-week oral or 2-week IV treatment may be given. If symptoms persist despite the second treatment, data do not support the continued use of antibiotics. Nonsteroidal medications, disease-modifying antirheumatic drugs, and arthroscopic synovectomy are used for arthritis pain. Guidelines for fibromyalgia or chronic fatigue syndrome are followed in anyone with post-Lyme syndrome who has negative PCR results.¹⁵⁶

PROGNOSIS.

Early treatment is vital for the prevention of long-term complications, but even so, complications involving the heart, joints, and nervous system occur in about 15% of people who do undergo early treatment. For most people, Lyme disease is curable with standard antibiotic therapy, and the effects of Lyme disease resolve completely within a few weeks or months of treatment. Unfortunately, no natural immunity develops from exposure to Lyme disease, and anyone can be reinfected. Although Lyme disease is rarely fatal, heart complications may cause life-threatening cardiac arrhythmias.

Great concern came about in the past regarding potential fetal infection and teratogenicity from Lyme disease contracted during pregnancy. However, in recent prospective studies no cases of congenital infection have been documented.^93,150,183

8-12 SPECIAL IMPLICATIONS FOR THE THERAPIST

Lyme Disease

PREFERRED PRACTICE PATTERNS

Stage 1

7B:

Impaired Integumentary Integrity Associated with Superficial Skin Involvement

Stages 2 and 3

4D:

Musculoskeletal Impairment Associated with Connective Tissue Disorder (rheumatoid arthritis)

5C, 5D:

Impaired Neuromuscular Function with Acquired Nonprogressive Disorder of the CNS

6D:

Impaired Aerobic Capacity/Endurance Associated with Cardiovascular Pump Dysfunction (cardiac arrhythmias)

Chronic arthritis is the most widely recognized result of untreated Lyme disease in the United States. Unlike other forms of rheumatoid arthritis, Lyme arthritis does not affect the joints bilaterally, though both sides may be affected alternately.

The condition has been called chronic because episodes can last months, occurring intermittently over a period of 1 to 3 years. Permanent joint damage and cartilage destruction can occur if excessive use occurs during the inflammatory period. Range-of-motion and strengthening exercises are important but must be carried out carefully and without overexertion.

Nervous system abnormalities can develop weeks, months, or even years following an untreated infection. These symptoms often last for weeks or months and may recur. The therapist may treat such a client at any time during the course of symptomatic presentation.

For anyone with known Lyme disease, frequent assessment of the person’s neurologic function and level of consciousness is important. Any signs of cardiac abnormality or increased intracranial pressure and cranial nerve involvement (e.g., ptosis, strabismus, diplopia) must be reported to the physician immediately. Both upper-and lower-extremity peripheral nerve problems can occur and are managed as any neuropathy from other causes.

It has been hypothesized that people who present with symptoms of multiple sclerosis but respond to antibiotics may have been bitten by ticks years ago. Along the same lines, the question has been raised whether Lyme disease triggers fibromyalgia since symptoms consistent with fibromyalgia and chronic fatigue syndrome develop in individuals with clear-cut Lyme disease, even after adequate treatment. To date no biologic relationship has been proven between these conditions and Lyme disease.¹⁰²

Sexually Transmitted Infections

Overview and Incidence

Each year 19 million Americans contract a sexually transmitted disease (STD) or infection (STI), and it is estimated that at least one out of every four sexually active people (56 million Americans) is carrying an infection other than HIV. It is likely that the incidence of STDs and STIs is underreported for several reasons.

Physicians fail to report STD cases to local health departments despite being mandated to do so. Physicians also rely on patients to notify their sexual partners, who may or may not be tested and/or treated.¹¹ A lack of free screening or reimbursement for screening may be a contributing factor.⁸²

Syphilis, once thought to be trending toward elimination, has steadily increased since 2000, particularly in black men and men who have sex with men.^28,104,129 Although the incidence of gonorrhea has reached an all-time low in the United States, chlamydia and human papillomavirus (HPV) remain significant health problems. Chlamydia is the most common reportable STD in the United States, with almost 1 million cases reported to the CDC in 2004.²⁶

HPV, which causes genital warts and can lead to cervical cancer, most likely infects over 6 million men and women per year. Additionally, more than 45 million people have chronic genital herpes, with perhaps 1 million new cases diagnosed every year. There were 73,000 new cases of HBV reported in 2003, with 1.25 million people chronically infected despite the availability of a preventative vaccine. In 2004, an estimated 1 to 1.1 million Americans were living with the HIV/AIDS virus, with an additional 42,000 cases newly reported.

STDs and STIs are spread primarily through sexual contact, but some cases may also be spread by sharing infected needles or by transmission from mother to child during vaginal childbirth. Many STDs and STIs are easily treated and cured, but others remain chronic. More than 50 different STDs and STIs have been described; only the most common ones are included here (Table 8-7).

Etiologic and Risk Factors

All groups of people are potentially at risk for STDs and STIs, but women, teens, men who have sex with men, and minorities have been disproportionately affected. Young people under the age of 18 years are considered at greatest risk for getting a sexually transmitted disease but, in fact, the over-50 population is also at risk.

Although 25% of all STDs and STIs occur in people younger than 25 years, numerous surveys of healthy adults have verified that older people are sexually active and less likely to practice safe sex. Risk factors vary but most often include multiple sex partners, a partner with a known risk factor, a history of a blood transfusion between 1977 and 1984, failure to use a condom (or use it properly) during sexual intercourse, and sharing needles during illicit drug use. The presence of STDs and STIs is a risk factor itself for facilitating the transmission of HIV. In fact, persons with an STD are two to five times more likely than a person without an STD of sexually acquiring HIV.¹⁷⁴

Pathogenesis and Clinical Manifestations

STDs and STIs are caused by bacteria, viruses and, occasionally, parasites and may have a considerable latency period when the infectious organism lies dormant before triggering symptomatic presentation (Fig. 8-10).

Figure 8-10 Sexually transmitted infections. A, Syphilis mimics so many diseases it is called “the great imitator.” Dark-field microscopy showing several spirochetes in scrapings from the base of a syphilitic chancre. B, Gonorrhea, called the “preventer of life,” can cause sterility. Gram-stained smear of urethral discharge showing intracellular gram-negative diplococci characteristic of gonorrhea. C, HPV, also known as genital herpes, is the most common cause of cervical and other reproductive cancers. D, Chlamydia is the most common STD reported in the United States. (A, Reprinted from Kumar V: Robbins and Cotran: pathologic basis of disease, ed 7, Philadelphia, 2005, W.B. Saunders, courtesy Paul Southern, Department of Pathology, University of Texas Southwestern Medical School, Dallas. B, Reprinted from Mandell GL: Principles and practice of infectious diseases, ed 6, Philadelphia, 2005, Churchill Livingstone. C, Reprinted from Kumar V: Robbins and Cotran: pathologic basis of disease, ed 7, Philadelphia, 2005, W.B. Saunders, courtesy Ian Frazer, Princess Alexandra Hospital, University of Queensland, Australia. D, Reprinted from Mandell GL: Principles and practice of infectious diseases, ed 6, Philadelphia, 2005, Churchill Livingstone, courtesy Robert Suchland, Seattle, WA.)

Clinical manifestations vary according to the STD present (Figs. 8-11 and 8-12; see also Table 8-7). STDs and STIs may be completely asymptomatic and therefore are less likely to be diagnosed until serious problems develop. Complications of STDs and STIs are more severe and more frequent among women than men. Once infected, women are more susceptible to reproductive cancers, infertility, and contracting other STDs and STIs.

Figure 8-11 Clinical manifestations of syphilis. Many STIs present with lesions of the skin and/or genitals. Each one presents differently based on the stage of the disease. A, Chancre in primary syphilis on the penis. B, Palmar lesions of a coppery color in secondary syphilis. C, Mucous patch of the mouth in secondary syphilis. D, Genital lesions called condylomata lata in a female (secondary syphilis). (A, C, and D, Reprinted from Forbes CD, Jackson WF: Color atlas and text of clinical medicine, London, 2003, Mosby. B, Reprinted from Habif TP: Skin disease: diagnosis and treatment, St Louis, 2001, Mosby.)

Figure 8-12 Alopecia of the scalp (balding) associated with secondary syphilis. This is a temporary, irregular presentation of alopecia sometimes referred to as “moth-eaten” alopecia. (Reprinted from Habif TP: Clinical dermatology, ed 4, St Louis, Mosby, courtesy Subhash K. Hira.)

MEDICAL MANAGEMENT

PREVENTION.

Prevention is the most important key to managing STDs and STIs. The only prevention that is 100% effective is abstinence and/or a mutually monogamous sexual relationship (single partner) between two uninfected people. For those who are sexually active, condoms, properly used, are able to reduce the transmission of sexually transmitted diseases spread by mucosal fluid (e.g., gonorrhea, chlamydia, and HIV).

However, condoms do not cover all surfaces and only protect the skin they cover, and are therefore less likely to protect against diseases acquired from skin-to-skin contact such as syphilis, HPV, and HSV.¹⁸⁴ Genital warts are contagious; avoid touching them. Spermicides with nonoxynol-9 may not be effective against gonorrhea, chlamydia, or HIV infection; the CDC does not recommend the use of nonoxynol-9 with or without condoms for STD or HIV protection.¹⁸⁴

Pregnant women should have blood tests for syphilis and HBV. Early syphilis, if untreated in pregnant women, can cause fetal death in 40% of cases. Even if syphilis is acquired up to 4 years before pregnancy, infection of the fetus will occur in 70% of cases.²⁶ A vaccine is available to protect anyone, especially women of childbearing age, against HBV (see Table 8-4).

Pregnant women should also be tested for gonorrhea, chlamydia, HPV, and HIV. Those with recurrent genital herpes and open sores benefit from cesarean section delivery to protect the child. Anyone with a STD or known possibility of infection must inform a physician and all partners to obtain appropriate treatment and prevent spreading the disease to others.

Drug users, especially injection-drug users, can prevent transmission of disease best by discontinuance of drugs. However, in most cases this is not immediately realistic. Programs have been set up to help reduce needle sharing by providing needle exchange centers and street education programs aimed at teaching more sterile practices.

SCREENING, DIAGNOSIS, TREATMENT, AND PROGNOSIS.

STDs and STIs can often be identified by the clinical manifestations, but various screening tests are also available. Experts recommend that sexually active adolescents and women aged 25 years and younger, pregnant women aged 25 years and younger, and older women at high risk be screened for chlamydia. The interval of screening should take into account changes in partners, but women at high risk with a history of previous infection may benefit from screening every 6 to 12 months.¹⁰⁷ With the advent of urine-based testing, more frequent screening has been successful in both women and men.

HPV infection is another prevalent STD that has been found to cause cervical cancer in women. Since HPV slowly creates cellular changes prior to the development of cancer, recommendations for screening have been published (see Table 20-2). Liquid-based cytology is a newer technique that allows the sampled cells to be concentrated and better preserved for visual evaluation. The liquid-based samples can also be used for HPV DNA testing.

Evidence supporting the specific use of liquid-based cytology and HPV DNA testing is not currently available because of their relative newness; however, recommendations by multiple medical societies have been issued as guidelines. Although HPV is most often acquired in younger clients, older women continue to be at risk, so testing should take into consideration risk factors.⁶² Various immunoassays, serologic techniques, and culture methods are used to diagnose HIV, syphilis, gonorrhea, herpes, hepatitis, and other STDs and STIs.

Antibiotics can cure some STDs and STIs (see Table 8-7), although some may be drug resistant (e.g., gonorrhea resistance to quinolones). Limiting the number of sexual partners, practicing abstinence, and safe sex (proper use of condoms) are recommended to prevent the transmission of disease. Intercourse during an active infection dramatically increases the risk of transmitting STDs and STIs.

When working with clients with active disease, following contact precautions, frequent handwashing, and avoiding touching the affected areas are essential practices. A vaccine is now available for HBV, and vaccines against HPV, HIV, and herpes are under investigation. A new vaccine for HPV may soon be available, and questions are being raised as to the receptiveness of the public (especially adolescents and young adults) and how it may change sexual habits.¹⁶⁰

The prognosis varies with each STD, but with treatment symptoms can be minimized and complications prevented. Without treatment, serious complications can occur such as infertility, chronic pelvic pain, ectopic pregnancy and miscarriage, cardiovascular disease, CNS impairment, blindness, cervical cancer, and even death.

8-13 SPECIAL IMPLICATIONS FOR THE THERAPIST

Sexually Transmitted Diseases and Infections

PREFERRED PRACTICE PATTERNS

These are variable depending on specific disease entity and clinical presentation.

Any therapist treating men or women with clinical presentation of pelvic, buttock, hip, or groin pain of apparent unknown cause must be prepared to ask the client about past history of STDs and STIs, sexual activity, changes in sexual function, and presence of urogenital signs or symptoms (e.g., discharge from penis or vagina, painful urination, difficulty initiating or continuing a stream of urine). Any suspicion that the clinical manifestations may be correlated to an STD must be further evaluated by a physician.

Infections in Drug Users

Drug use in the United States continues to be a significant health problem, with over 19.5 million people, or 8.2% of the population, found to be using drugs in 2003.¹⁶⁸ Serious illnesses such as HIV and hepatitis are transmitted with injection drug use. Drug users as a whole also have a higher incidence of bacterial infections because of the various drugs used, the route and sites of administration, and preparation of the drug. Each of these factors determines risk for infection and the likelihood of specific bacterial infections.⁶¹

Drugs themselves may be contaminated or become contaminated when “cut” (diluted) with adulterants (dextrose or dyed paper). Black-tar heroin, produced in Mexico, has been associated with outbreaks of wound botulism. Since clean needles and skin are not protective, the black-tar heroin is most likely the cause of the infection. Contamination with Clostridium tetani or other clostridial spores may occur when adulterants are cut with the heroin.

IV use of black-tar heroin causes sclerosis of the veins and leads to “skin popping,” or injecting the drug subcutaneously. Continued injection into the same site creates a necrotic environment suitable for clostridial germination and toxin production. Necrotizing fasciitis with toxic shock syndrome can result from the spread of a clostridial infection.¹⁰³

Drug users, particularly IV drug users, vary the site of administration. Local abscess formation or infections from hematogenous seeding are seen in unusual places because of the site of injection (the femoral vein, or “groin hit,” and the neck, or “pocket shot”). Osteomyelitis may develop in the sternoclavicular, sacroiliac, or vertebral spine. Septic arthritis is often seen in the knees.

Environmental factors frequently contribute to infections. Some users may lick the skin or needle prior to injecting, leading to polymicrobial infections. Others crush tablets between their teeth or blow clots out of needles before reusing. Sharing of needles and paraphernalia is also common.⁶¹ Because of these habits, drug users are more likely to develop certain types of bacterial infections with specific organisms.

The four types of infections most often seen are of the skin or soft tissue, endovascular infections, respiratory infections, and musculoskeletal infections.⁶¹ S. aureus and streptococcal species (flora from the user’s skin) are the most common pathogens in drug-related infections. Drug users are more likely to be colonized with MRSA in the nares and skin than non–drug users; this most likely occurs because of tissue damage from inhaling or injecting drugs.

Abscess formation is common. More serious infections such as endocarditis, septic thrombophlebitis, mycotic aneurysms, and sepsis occur from hematogenous spread of organisms. In injection drug users S. aureus is the most common organism causing endocarditis. Although polymicrobial endocarditis is rare, it is most often seen in injection drug users. Complications of endocarditis include brain, lung, and splenic abscesses.

Drug users are more likely to develop a respiratory tract infection compared with nonusers, and respiratory infections, particularly pneumonia, are the most common infection in drug users. Damage to cells from inhaling drugs and chronic cigarette use (many drug users also smoke) may lead to inability to clear secretions. Aspiration may occur because of decreased mental alertness.

Clients with HIV may present with atypical features and radiographs, so a good history and physical examination are important. Pulmonary tuberculosis (and drug-resistant tuberculosis) is encountered more frequently in drug users who practice “shotgunning” (inhaling cocaine and blowing smoke into the mouth of another person), live in crowded spaces, delay diagnosis, or have HIV.

Musculoskeletal infections may occur in unusual places, as discussed above. Flora from the skin is the most common pathogen, although polymicrobial infections are seen, especially if saliva contaminates the skin, drugs, or needles. The infection may be subtle, with mild fever and pain.⁶¹

8-14 SPECIAL IMPLICATIONS FOR THE THERAPIST

Infections in Drug Addicts

See Special Implications for the Therapist: Substance Abuse in Chapter 3.

Being aware of the signs of substance abuse or drug addiction and the patterns of infection associated with drug addiction may assist the therapist in recognizing early signs of infection requiring medical evaluation and treatment. Any therapist involved in wound care management, needle electromyography, or other high-risk practice techniques who has not already been immunized against HBV should be vaccinated.

References

1. Advisory Committee on Immunization Practices (APIC): APIC brochure, 2000. Available at http://www.apic.org Accessed April 25, 2007.

2. Advisory Committee on Immunization Practices. Prevention and control of influenza. MMWR. 1996;45(5):1–24.

3. Advisory Committee on Immunization Practices. Update, vaccine side effects, adverse reactions, contraindications and precautions. MMWR. 1996;45(12):1–35.

4. Agha, R. Complications of immunizations. Pediatr Rev. 1997;18(2):66–67.

5. al Saif, N, Brazier, JS. The distribution of Clostridium difficile in the environment of South Wales. J Med Microbiol. 1996;45:133–137.

6. Alotaibi, S, Kennedy, J, Tellier, R, et al. Epstein-Barr virus in pediatric multiple sclerosis. JAMA. 2004;291(15):1877–1879.

7. Atkinson W, et al, eds. Epidemiology and prevention of vaccine preventable diseases, ed 9, Washington, DC: Centers for Disease Control and Prevention, 2006.

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11. Beltrami, JF, Weinstock, HS, Berman, SM, et al. Primary and secondary syphilis-United States, 2003-2004. MMWR. 2006;55(10):269–273.

12. Boyce, JM, Pittet, D. Guideline for hand hygiene in health-care settings. Recommendations of the Healthcare Infection Control Practices Advisory Committee and the HICPAC/SHEA/APIC/IDSA Hand Hygiene Task Force. MMWR. 2002;51(RR16):1–44.

13. Boyce, JM, Pittet, D. Guideline for hand hygiene in health-care settings: recommendations of the Healthcare Infection Control Practices Advisory Committee and the HICPAC/SHEA/APIC/IDSA Hand Hygiene Task Force. Infect Control Hosp Epidemiol. 2002;23(12 Suppl):S3–40.

14. Bouckenooghe, A, Shandera, W. Infectious diseases: viral and rickettsial. In Tierney L, McPhee S, Papadakis M, eds.: Current medical diagnosis and treatment, ed 39, New York: Lange Medical Books/McGraw-Hill, 2000.

15. Brause, B. Infections with prostheses in bones and joints. In Mandell G, Bennett J, Dolin R, eds.: Principles and practice of infectious diseases, ed 5, Philadelphia: Churchill Livingstone, 2000.

16. Brouqui, P. Chronic Bartonella quintana bacteremia in homeless patients. N Engl J Med. 1999;340:21–32.

17. Brown, Z, Preventing herpes simplex virus transmission to the neonate. Herpes. 2004(Suppl 3):175A–186A.

18. Brueggmann, A, Doern, G, Wingert, E. Antimicrobial resistance with Streptococcus pneumoniae in the United States, 1997/1998. Emerg Infect Dis. 1999;5(6):757–765.

19. Burgdorfer, W, Barbour, AG, Hayes, SF, et al. Lyme disease-a tick-borne spirochetosis? Science. 1982;216:1317–1319.

20. Cantrell, M, Norman, D. Infections. In Duthrie E, Katz P, eds.: Practice of geriatrics, ed 3, Philadelphia: W.B. Saunders, 1998.

21. Castle, SC, Uyemura, K, Rafi, A, et al. Comorbidity is a better predictor of impaired immunity than chronological age in older adults. J Am Geriatr Soc. 2005;53(9):1565–1569.

22. Centers for Disease Control and Prevention. Notice to readers recommendations for test performance and interpretation from the Second National Conference on Serologic Diagnosis of Lyme Disease. MMWR. 1995;44(31):590–591.

23. Centers for Disease Control and Prevention. Staphylococcus aureus with reduced susceptibility to vancomycin-United States, 1997. MMWR. 1997;46:813–815.

24. Centers for Disease Control and Prevention. Immunization of healthcare workers recommendations of the Advisory Committee on Immunization Practices (ACIP) and the Hospital Infection Control Practices Advisory Committee (HICPAC). MMWR. 1997;46(RR-18):1–41.

25. Centers for Disease Control and Prevention. Recommended adult immunization schedule-United States, 2003-2004. MMWR Morb Mortal Wkly Rep. 52, 2003. [965-918].

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Streptococcus pneumoniae

Gas Gangrene (Clostridial Myonecrosis)

MEDICAL MANAGEMENT

Pseudomonas

MEDICAL MANAGEMENT

VIRAL INFECTIONS

Herpesviruses

Herpes Simplex Viruses Types 1 and 2

MEDICAL MANAGEMENT

Varicella Zoster Virus (Herpesvirus Type 3)

MEDICAL MANAGEMENT

PREVENTION

Infectious Mononucleosis (Herpesvirus Type 4)

MEDICAL MANAGEMENT

Cytomegalovirus (Herpesvirus Type 5)

MEDICAL MANAGEMENT

Herpesviruses Types 6, 7, and 8

Viral Respiratory Infections

Influenza

MEDICAL MANAGEMENT

DIAGNOSIS

TREATMENT.

PROGNOSIS.

Respiratory Syncytial Virus

MISCELLANEOUS INFECTIOUS DISEASES

Lyme Disease

Incidence

Pathogenesis

Clinical Manifestations

MEDICAL MANAGEMENT

DIAGNOSIS.

TREATMENT.

PROGNOSIS.

Sexually Transmitted Infections

Etiologic and Risk Factors

Pathogenesis and Clinical Manifestations

MEDICAL MANAGEMENT

SCREENING, DIAGNOSIS, TREATMENT, AND PROGNOSIS.

Infections in Drug Users

References