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B. Dennis, M.S., Ph.D.

Professor, Frank H. Netter M.D. School of Medicine at Quinnipiac University

This chapter provides a very broad listing of the various parasitic agents commonly associated with infections at specific body sites and/or specific clinical manifestations (Table 70-1). This information is meant to be used in conjunction with Table 71-1 as an aid in establishing a differential diagnosis and selecting the most likely clinical specimens that will help establish a specific etiologic diagnosis. Other factors that may be important in determining the relative frequency with which specific parasites cause disease. Table 70-1 SummaryofParasitesAssociatedwithHumanDisease SystemAffectedandDisease Pathogens SystemAffectedandDisease Pathogens Blood Malaria Babesiosis Filariasis Plasmodium falciparum, P. The clinical manifestations of parasitic diseases are seldom specific enough to raise the possibility of these processes in the mind of the clinician, and routine laboratory tests are seldom helpful. Although peripheral eosinophilia is widely recognized as a useful indicator of parasitic disease, this phenomenon is characteristic only of helminthic infection and even in these cases is frequently absent. Thus the physician must maintain a heightened index of suspicion and must rely on detailed travel, food intake, transfusion, and socioeconomic history to raise the possibility of parasitic disease. Proper diagnosis requires that (1) the physician consider the possibility of parasitic infection, (2) appropriate specimens be obtained and transported to the laboratory in a timely fashion, (3) the laboratory competently performs the appropriate procedures for recovery and identification of the etiologic agent, (4) the laboratory results be effectively communicated to the physician, and (5) the results be correctly interpreted by the physician and applied to the care of the patient. In addition, for most parasitic diseases, appropriate test selection and interpretation is based on an understanding of the life cycle of the parasite as well as the pathogenesis of the disease process in humans. Numerous methods for diagnosing parasitic diseases have been described (Box 71-1). Some are useful in detecting a wide variety of parasites, and others are particularly useful for one or a few parasites. Although the mainstay of diagnostic clinical microbiology is isolation of the causative pathogen in culture, the diagnosis of parasitic diseases is accomplished almost entirely by morphologic (usually microscopic) demonstration of parasites in clinical material. Occasionally, demonstration of a specific antibody response (serodiagnosis) helps in establishing the diagnosis. The detection of parasite antigens in serum, urine, or stool now provides a rapid and sensitive means of diagnosing infection with certain organisms. In general, it is better for the laboratory to offer a limited number of competently performed procedures than to offer a wide variety of infrequently and poorly performed tests. This chapter provides a general description of the principles of specimen collection and processing necessary to diagnose most parasitic infections. Specific details of these and other procedures of general and limited usefulness may be found in several reference texts listed in the Bibliography. Understanding the life cycle of parasitic organisms is a key to understanding important features of geographic distribution, transmission, and pathogenesis of many parasitic diseases. For example, in the life cycle of filariae that infect humans, certain species. Sampling the blood of such patients during daytime hours may fail to detect the microfilariae, whereas blood specimens collected between 10 pm and 4 am may demonstrate many microfilariae. Likewise, intestinal nematodes such as Ascaris lumbricoides and hookworm, which reside in the lumen of the intestine, produce large numbers of eggs that can be detected easily in the stool of an infected patient. In contrast, another intestinal nematode, Strongyloides stercoralis, lays its eggs in the bowel wall rather than in the intestinal lumen. As a result, the eggs are rarely seen on stool examination; to make the diagnosis, the parasitologist must be alert for the presence of larvae. Finally, parasites may cause clinical symptoms at a time when diagnostic forms are not yet present in the usual site. For example, in certain intestinal nematode infections, migration of larvae through the tissues may cause intense symptomatology weeks before the characteristic eggs are present in feces. Because the majority of parasitologic examinations and identifications are based entirely on recognizing the characteristic morphology of the organisms, any condition that may obscure or distort the morphologic appearance of the parasite may result in an erroneous identification or missed diagnosis. As noted previously and in Box 71-1, there may be alternatives to microscopy for detection and identification of certain parasites. Sampling of perianal skin is a useful means of recovering the eggs of Enterobius vermicularis (pinworm) or Taenia species (tapeworm). Fecal Specimen Collection Patients, clinicians, and laboratory personnel must be properly instructed on collection and handling of specimens. Fecal specimens should be collected in clean wide-mouthed, waterproof containers with a tight-fitting lid to ensure and maintain adequate moisture.

This case emphasizes the importance of making an etiologic diagnosis of a pleuropulmonary process to differentiate paragonimiasis from tuberculosis in regions where both are endemic infectious diseases. Cercaria Penetrates intestinal wall in Eggs are coughed up crustacean Abdominal cavity and passed in sputum (crabs and crayfish) or Penetrates diaphragm swallowed and Redia passed in feces Pleural cavity In snail tissue Adult in cystic cavities in lungs and other sites (From ingestion to eggs-2-3 months) Unembryonated egg Diagnostic stage In feces and sputum Sporocyst Miracidium hatches and penetrates snail Embryonated egg in water fluke). Figure 76-7 shows a familiar fluke life cycle from egg to snail to infective metacercaria. The infective stage occurs in a second intermediate host: the muscles and gills of freshwater crabs and crayfish. In humans who ingest infected meat, the larval worm hatches in the stomach and follows an extensive migration through the intestinal wall to the abdominal cavity, then through the diaphragm, and finally to the pleural cavity. Adult worms reside in the lungs and produce eggs that are liberated from ruptured bronchioles and appear in sputum or, when swallowed, in feces. Epidemiology Paragonimiasis occurs in many countries in Asia, Africa, and Latin America. Its prevalence is directly related to consumption of uncooked freshwater crabs and crayfish. It is estimated that approximately 3 million people are infected with this lung fluke. As many as 1% of all Indochinese immigrants to the United States are infected with P. Human infections endemic to the United States are usually caused by a related species, P. As the destruction of lung tissue progresses, cavitation occurs around the worms, sputum becomes blood tinged and dark with eggs (so-called rusty sputum), and patients experience severe chest pain. Dyspnea, chronic bronchitis, bronchiectasis, and pleural effusion may be seen (Clinical Case 76-3). The location of larvae, adults, and eggs in ectopic sites may produce severe clinical symptoms depending on the site involved. Migration of larval worms may result in invasion of the spinal cord and brain, producing severe neurologic disease (visual problems, motor weakness, convulsive seizures) referred to as cerebral paragonimiasis. Migration and infection may also occur in subcutaneous sites, the abdominal cavity, and the liver. Laboratory Diagnosis Examination of sputum and feces reveals golden brown, operculated eggs (Figure 76-8). Serologic procedures are available through reference laboratories and can be helpful, particularly in cases with extrapulmonary. Clinical Syndromes the clinical manifestations of paragonimiasis may result from larvae migrating through tissues or from adults established in the lungs or other ectopic sites. The onset of disease coincides with larval migration and is associated with fever, chills, and high eosinophilia. The adult flukes in the lungs Treatment, Prevention, and Control the drug of choice is triclabendazole; praziquantel is an alternative. Education regarding consumption of uncooked freshwater crabs and crayfish found in endemic areas is critical. Pickling and wine soaking of crabs and crayfish do not kill the infective metacercarial stage. These large ovoid eggs and control of the disposal of human feces are essential to control efforts. The three schistosomes most frequently associated with human disease are Schistosoma mansoni, Schistosoma japonicum, and Schistosoma haematobium. They collectively produce the disease called schistosomiasis, also known as bilharziasis or snail fever. As discussed earlier, the schistosomes differ from other flukes: they are male and female rather than hermaphroditic, and their eggs do not have an operculum. They also are obligate intravascular parasites and are not found in cavities, ducts, and other tissues. The infective forms are skinpenetrating cercariae liberated from snails, and these differ from other flukes in that they are not eaten on vegetation, in fish, or in crustaceans. Infection is initiated by ciliated, free-swimming, freshwater cercariae that penetrate intact skin, enter the circulation, and develop in the intrahepatic portal circulation (S. The female has a long, slender, cylindrical body, whereas the shorter male, which appears cylindrical, is actually flat (Figure 76-10).

Treatment, Prevention, and Control Therapy for toxoplasmosis depends on the nature of the infectious process and the immunocompetence of the host. Most mononucleosis-like infections in normal hosts resolve spontaneously and do not require specific therapy. Such patients are currently treated with an initial high-dose regimen of pyrimethamine plus sulfadiazine and then continued on lower doses of both drugs indefinitely. Although this drug combination is the regimen of choice, toxicity (rash and bone marrow suppression) may necessitate changes to alternative agents. Most human infections with these amebae are acquired during the warm summer months by people exposed to the amebae while swimming in contaminated water. Inhalation of cysts present in dust may account for some infections, whereas ocular infections with Acanthamoeba spp. Clinical Syndromes Naegleria, Acanthamoeba, Balamuthia, Sappinia, and Para vahlkampfia organisms are opportunistic pathogens. Although colonization of the nasal passages is usually asymptomatic, these amebae can invade the nasal mucosa and extend into the brain (Clinical Case 74-3). Destruction of brain tissue is characterized by a fulminant, rapidly fatal meningoencephalitis. Symptoms include intense frontal headache, sore throat, fever, blocked nose with altered senses of taste and smell, stiff neck, and Kernig sign. Clinically, the course of the disease is rapid, with death usually occurring within 4 or 5 days. The patient had a history of diabetes and hypertension but denied any previous history of seizures. Approximately 2 weeks later, he was readmitted to the hospital because of a new left facial droop. Progressive generalized weakness developed, along with paralysis of the left upper extremity. His travel history was significant only for a trip to the Dominican Republic 2 years previously. Clinical examination was remarkable for dysarthria, a left facial droop, and left upper extremity paralysis. A magnetic resonance imaging scan of the head showed two large ring-enhancing lesions with possible central necrosis. A brain biopsy showed lymphocytic infiltration, predominantly in the perivascular areas. A closer examination revealed trophozoites and amebic cysts consistent with a diagnosis of amebic encephalitis. Balamuthia encephalitis has been described in both immunosuppressed and immunocompetent individuals. Many infected patients do not have a history of swimming or exposure to contaminated water. The portal of entry is believed to be the respiratory tract or skin ulceration, with dissemination to the brain. The majority of patients have died within weeks after the onset of neurologic symptoms, despite treatment with pentamidine. Although all cases were fatal before 1970, survival has now been reported in a few cases in which the disease was rapidly diagnosed and treated. Sappinia diploidea is a free-living ameba that is found in soil contaminated with the feces of elk and buffalo. In contrast to Naegleria, Acanthamoeba and Balamuthia organisms produce granulomatous amebic encephalitis and single or multiple brain abscesses, primarily in immunocompromised individuals. The course of the disease is slower, with an incubation period of at least 10 days. The resulting disease is chronic granulomatous encephalitis with edema of the brain tissue.

Treatment: Therapy will vary with the type and severity of the clinical presentation but may include sulfonamides, tetracyclines and chloramphenicol. Patients with localized disease may be managed with oral antibiotics for a duration of 60-150 days. Prophylaxis: Currently, no pre-exposure or post-exposure prophylaxis is available. Person-to-person airborne transmission is unlikely, although secondary cases may occur through improper handling of infected secretions. Contact precautions are indicated while caring for patients with skin involvement. Death results from respiratory failure, circulatory collapse, and a bleeding abnormality. Diagnosis: Suspect plague if large numbers of previously healthy individuals develop severe pneumonia, especially if coughing of blood is present. Treatment: Early administration of antibiotics is critical, as pneumonic plague is invariably fatal if antibiotic therapy is delayed more than 1 day after the onset of symptoms. Choose one of the following: streptomycin, gentamicin, ciprofloxacin, or doxycycline for 10-14 days. Prophylaxis: For asymptomatic persons exposed to a plague aerosol or to a patient with suspected pneumonic plague, give doxycycline 100 mg orally twice daily for seven days or the duration of risk of exposure plus one week. The previously available licensed, killed vaccine was effective against bubonic plague, but not against aerosol exposure. Isolation and Decontamination: Use Standard Precautions for bubonic plague, and Respiratory Droplet Precautions for suspected pneumonic plague. Take measures to prevent local disease cycles if vectors (fleas) and reservoirs (rodents) are present. Patients are not generally critically ill, and the illness lasts from 2 days to 2 weeks. Diagnosis: Q fever is not a clinically distinct illness and may resemble a viral illness or other types of atypical pneumonia. Treatment: Q fever is generally a self-limited illness even without treatment, but tetracycline or doxycycline should be given orally for 5 to 7 days to prevent complications of the disease. Prophylaxis: Antibiotic prophylaxis begun too early during the incubation period may delay but not prevent the onset of symptoms. Therefore, tetracycline or 8-8 doxycycline should be started 8-12 days post exposure and continued for 5 days. Isolation and Decontamination: Standard Precautions are recommended for healthcare workers. Patients exposed to Q fever by aerosol do not present a risk for secondary contamination or reaerosolization of the organism. Typhoidal tularemia presents with fever, headache, malaise, substernal discomfort, prostration, weight loss and a non-productive cough. Chest xray may reveal a pneumonic (lung) process, enlarged mediastinal lymph nodes or pleural effusion (fluid in the lung spaces). Treatment: Administration of antibiotics (streptomycin or gentamicin) with early treatment is very effective. Prophylaxis: A two-week course of tetracycline is effective as prophylaxis when given after exposure. This chapter covers three types of viruses that could potentially be employed as bio-terrorism agents: smallpox, alphaviruses. Prophylaxis: Immediate vaccination or revaccination should be undertaken for all personnel exposed. Isolation and Decontamination: Droplet and Airborne Precautions for a minimum of 17 days following exposure for all contacts. Patients should be considered infectious until all scabs separate and quarantined during this period. If quarantine is not possible, require contacts to check their temperatures daily.