Pφ

Varicella zoster virus (VZV) is a medium-sized double-stranded DNA (dsDNA) virus that is a member of the herpesvirus group. Primary varicella infection (chickenpox) is acquired via the respiratory route. During the primary infection, the virus enters sensory nerve endings and establishes latent infection in dorsal root ganglia; infection is lifelong. Reactivation of viral infection may occur, and the virus travels centripetally from the dorsal root ganglion to the skin via the peripheral nerves to multiply in the skin, causing the formation of an eruption in a dermatomal distribution. Sensory symptoms (burning, paresthesias) may precede the development of the skin lesions by several days. Occasionally the host immune response will contain the viral reactivation before the skin lesions form, giving a syndrome of acute neuritis without the skin lesions (zoster sine herpete).

TP

Patients with zoster typically present with a skin rash in a dermatomal distribution; several contiguous dermatomes may be involved. When the first branch of the fifth cranial nerve is involved, zoster ophthalmicus must be considered. This is a sight-threatening condition requiring prompt ophthalmologic evaluation. The skin rash consists of vesicular lesions on an erythematous base that appear in groups (crops); lesions are generally in various stages of evolution (vesicles, pustules, and crusted lesions). Pain from the acute neuritis can be quite severe. Patients may develop persistent pain (postherpetic neuralgia [PHN]) that can be very debilitating. Age > 60 years is a risk factor for PHN.

Dx

The diagnosis of herpes zoster can usually be made based on the history and the typical clinical appearance of the rash. If the diagnosis is uncertain, a viral culture can be obtained; direct fluorescent antibody testing is also available for VZV. Older age may be the only factor that predisposes a patient to reactivation; however, the history and physical exam should be thorough to determine if there is any suggestion of underlying immunodeficiency that would require further evaluation.

Pφ

Lyme disease is caused by Borrelia burgdorferi, a spirochete. Infection is maintained in nature through the horizontal transmission of the organism from infected nymphal ticks to the white-footed mouse, and then from the mouse to the larval ticks. The nymphs are primarily responsible for the transmission of infection to humans. In the United States, Lyme disease is endemic in the northeast (Massachusetts to Maryland), upper Midwest (Wisconsin, Minnesota), and Pacific Northwest (northern California, southern Oregon). Lyme disease is transmitted to humans via the bite of the Ixodes tick. The organism multiplies at the site of inoculation, eliciting a local host inflammatory response. The organism may then disseminate via the bloodstream; involvement of the myocardium and the central nervous system (CNS) may occur during early disseminated disease, and involvement of the joints is characteristic of late disseminated disease.

TP

The skin lesion of early localized Lyme disease is referred to as erythema migrans (EM). The lesion begins as an erythematous macule or papule that expands to form a large annular lesion, often with a more intensely erythematous border and central clearing. EM lesions are generally not painful. Secondary skin lesions may develop in patients with early disseminated infection, who may present with neurologic (aseptic meningitis, peripheral seventh-nerve palsy) or cardiac (conduction abnormalities) involvement. Because the Ixodes tick is small, patients may not recall a history of tick bite.

Dx

The diagnosis of Lyme disease should be made based on clinical grounds with an appropriate epidemiologic history (outdoor exposure in an endemic area) and compatible clinical findings. Serologic tests are available, but they are neither sensitive nor specific in early infection and should be used only in selected cases.

Pφ

RMSF is caused by Rickettsia rickettsii, an obligate intracellular pathogen. The disease is endemic in the south Atlantic and east south central regions of the United States, but cases have been reported from almost every state. The organism is transmitted by a tick bite (several tick species are reservoirs for infection). After introduction into the skin, the pathogen disseminates hematogenously and infects vascular endothelial cells, inducing vascular injury that can affect almost any organ.

TP

The incubation period for RMSF is 2–14 days. The illness begins with nonspecific symptoms including fever, headache, and generalized malaise. Three to five days later the characteristic rash appears: an erythematous, petechial rash that begins in the periphery of the bite and then spreads centrally. Involvement of the palms and soles is characteristic, but may appear only later in the course of illness. Up to 10% to 15% of patients may not have a rash (so-called spotless RMSF); absence of rash is associated with delay in diagnosis, so it is important to consider this entity in the patient with febrile illness in the correct epidemiologic setting.

Dx

A presumptive diagnosis of RMSF is based on clinical and epidemiologic findings; the diagnosis can be confirmed serologically, but patients must be treated on an empirical basis. In patients with rash, the diagnosis may be made by immunohistochemistry in cutaneous biopsy specimens. The organism can be isolated from blood during acute illness; however, isolation requires substantial technical expertise and biohazard precautions, so it is not attempted except in research labs.

Pφ

DGI occurs as a result of hematogenous dissemination of Neisseria gonorrhoeae from the genital tract, the pharynx, or the rectum. The host immune response via immune complex formation is responsible for many of the symptoms of DGI. A number of pathogen-specific factors are associated with strains that cause DGI, including resistance to the bactericidal activity of human serum and marked susceptibility to penicillin. Host factors that predispose to DGI include terminal complement component deficiency (C5–C8), female sex, and menstruation.

TP

DGI most commonly presents as an arthritis–dermatitis syndrome. Patients experience polyarthalgia involving multiple distal joints; there may be objective evidence of tenosynovitis. The pattern of joint involvement is asymmetric. Fever and other signs of systemic toxicity are frequently mild. The characteristic skin lesions appear as necrotic vesiculopustular lesions on an erythematous base and occur most commonly on the extremities. Very careful examination of the skin is required, as the lesions may be few in number. If disease progresses without treatment, frank septic arthritis will occur, usually in a single joint.

Dx

Blood cultures should be obtained in patients with suspected DGI; however, bacteremia may be intermittent. In the arthritis–dermatitis stage, the organism may also be difficult to recover from joint fluid; however, joints with evidence of arthritis should always be aspirated for synovial fluid analysis. Specimens from the skin lesions should be submitted for Gram stain and culture but also have a low yield. The highest diagnostic yield can be obtained by demonstration of the organism from a mucosal site; specimens should be obtained from the cervix or urethra, the pharynx, and the rectum in all patients.