| . |
| Yellow Fever Virus Member of the flavivirus family. Causes yellow fever in the tropical areas of Africa and South America. "Jungle" yellow fever is transmitted from monkeys to humans by mosquitoes. "Urban" yellow fever is transmitted from human to human by Aedes mosquitoes, i.e., humans are the reservoir in the urban form. Humans are not a "dead-end" host because viremia is high. There is no antiviral therapy. There is a live, attenuated vaccine for humans. |
| Dengue Virus Member of the flavivirus family. Causes dengue fever in the Caribbean region and other tropical areas. Transmitted by Aedes mosquitoes from one human to another. A monkey reservoir is suspected. Second episodes may result in dengue hemorrhagic fever, a life-threatening complication. There is no antiviral therapy and no vaccine for humans. |
| Human T-Cell Lymphotropic Virus (HTLV) Diseases Adult T-cell leukemia/lymphoma and HTLV-associated myelopathy (also known as tropical spastic paraparesis or chronic progressive myelopathy). Characteristics HTLV is a member of the retrovirus family. It causes malignant transformation of CD4-positive T cells (in contrast to HIV, which kills those cells). HTLV has three structural genes common to all retroviruses, namely, gag, pol, and env, plus two regulatory genes, tax and rex. The Tax protein is required for malignant transformation. It activates the synthesis of IL-2 (which is T-cell growth factor) and of the IL-2 receptor. IL-2 promotes rapid T-cell growth, which predisposes to malignant transformation. Transmission HTLV is transmitted primarily by intravenous drug use, sexually, and by breast feeding. Transmission by donated blood has greatly decreased in the United States because donated blood that has antibodies to HTLV is discarded. HTLV infection is endemic in certain geographic areas, namely, the Caribbean region including southern Florida; eastern South America; western Africa; and southern Japan. Pathogenesis HTLV induces malignant transformation of CD4-positive T lymphocytes by activating IL-2 synthesis as described above. It also causes HTLV-associated myelopathy (HAM), which is a demyelinating disease of the brain and spinal cord caused either by an autoimmune cross-reaction in which the immune response against HTLV damages the neurons or by cytotoxic T cells that kill HTLV-infected neurons. Laboratory Diagnosis Detect anti-HTLV antibodies in the patient's serum using the ELISA test. Western blot assay is used to confirm a positive ELISA result. PCR assay can detect the presence of HTLV RNA or DNA within infected cells. Treatment and Prevention No specific antiviral treatment for HTLV infection and no antiviral drug will cure latent infections by HTLV. No vaccine against HTLV. Preventive measures include discarding donated blood if anti-HTLV antibodies are present, using condoms to prevent sexual transmission, and encouraging women with HTLV antibodies to refrain from breast feeding. |
| Human Papillomavirus See summary in section on DNA Nonenveloped Viruses (Human Papillomavirus). |
| JC Virus Member of the papovavirus family. Causes progressive multifocal leukoencephalopathy (PML). Infection with JC virus is widespread, but PML occurs only in immunocompromised patients such as those with AIDS. Invariably fatal. No antiviral therapy and no vaccine. |
| Prions Diseases Creutzfeldt-Jakob disease (CJD), variant CJD, and kuru. These are transmissible spongiform encephalopathies. There is a hereditary form of CJD called Gerstmann-Sträussler-Scheinker (GSS) syndrome. Characteristics Prions are composed of protein only. They have no detectable nucleic acid and are highly resistant to UV light, formaldehyde, and heat. They are encoded by a cellular gene. The pathogenic form increases in amount by inducing conformational change in normal form. Normal conformation is alpha helix; abnormal is beta-pleated sheet. In GSS syndrome, a mutation occurs that enhances the probability of the conformational change to the beta-pleated sheet form. Transmission In most cases of CJD, mode of transmission is unknown. CJD has been transmitted by pituitary extracts, brain electrodes, and corneal transplants. Kuru was transmitted by ingestion or inoculation of human brain tissue. Variant CJD probably is transmitted by ingestion of cow brain tissue in undercooked food. Pathogenesis Aggregation of prion filaments within neurons occurs; vacuoles within neurons cause spongiform changes in brain; no inflammation or immune response occurs. Laboratory Diagnosis Brain biopsy shows spongiform changes. No serologic tests. Prions cannot be grown in culture. Treatment None. Prevention There is no drug or vaccine. |
| HIV Disease Acquired immunodeficiency syndrome (AIDS). Characteristics Enveloped virus with two copies (diploid) of a single-stranded, positive-polarity RNA genome. RNA-dependent DNA polymerase (reverse transcriptase) makes a DNA copy of the genome, which integrates into host cell DNA. Precursor polypeptides must be cleaved by virus–encoded protease to produce functional viral proteins. The tat gene encodes a protein that activates viral transcription. Antigenicity of the gp120 protein changes rapidly; therefore, there are many serotypes. Transmission Transfer of body fluids, e.g., blood and semen. Also transplacental and perinatal transmission. Pathogenesis Two receptors are required for HIV to enter cells. One receptor is CD4 protein found primarily on helper T cells. HIV infects and kills helper T cells, which predisposes to opportunistic infections. Other cells bearing CD4 proteins on the surface, e.g., astrocytes, are infected also. The other receptor for HIV is a chemokine receptor such as CCR5. The NEF protein is an important virulence factor. It reduces class I MHC protein synthesis, thereby reducing the ability of cytotoxic T cells to kill HIV-infected cells. Cytotoxic T cells are the main host defense against HIV. Laboratory Diagnosis HIV can be isolated from blood or semen, but this procedure is not routinely available. Diagnosis is usually made by detecting antibody with ELISA as screening test and Western blot as confirmatory test. Determine the "viral load," i.e., the amount of HIV RNA in the plasma, using PCR-based assays. A high viral load predicts a more rapid progression to AIDS than a low viral load. PCR-based assays can also detect viral RNA in infected cells, which is useful to detect early infections before antibody is detectable. Treatment Nucleoside analogues, such as zidovudine (AZT), lamivudine (3TC), stavudine (d4T), didanosine (ddI), and zalcitabine (ddC), inhibit HIV replication by inhibiting reverse transcriptase. Non-nucleoside inhibitors of reverse transcriptase, such as nevirapine and efavirenz, are used also. Protease inhibitors, e.g., indinavir, ritonavir, and saquinavir, prevent cleavage of precursor polypeptides. Highly active anti-retroviral therapy (HAART) consists of two nucleoside inhibitors and one protease inhibitor. Clinical improvement occurs, but the virus persists. Treatment of the opportunistic infection depends on the organism. Prevention Screening of blood prior to transfusion for the presence of antibody. "Safe sex," including the use of condoms. AZT with or without a protease inhibitor should be given to HIV-infected mothers and their newborns. Zidovudine (AZT), lamivudine (3TC), and a protease inhibitor should be given after a needle-stick injury. There is no vaccine. |
| Note Only the more important of the minor viral pathogens are summarized in this section. |
| Ebola Virus Member of the filovirus family. Causes Ebola hemorrhagic fever, which has a very high mortality rate. Animal reservoir and mode of transmission to humans are unknown. Human-to-human transmission, especially in hospital setting, is by blood and other body fluids. Diagnosis is usually a clinical one, but serologic tests are available. In electron microscope, see long "thread-like" viruses. Culturing the virus is very dangerous and should be done only in special laboratories. There is no antiviral therapy and no vaccine. |
| Hantavirus (Sin Nombe Virus) Member of the bunyavirus family. Causes hantavirus pulmonary syndrome. Sin Nombre virus (SNV) is a robovirus, i.e., it is rodent-borne. Deer mice are the reservoir, and the virus is acquired by inhalation of dried urine and feces. Diagnosis made by detecting viral RNA in lung tissue or by serologic tests. No antiviral therapy and no vaccine. |
| Japanese Encephalitis Virus Member of the flavivirus family. Causes outbreaks of encephalitis in Asian countries. Transmitted to humans by mosquitoes from the reservoir hosts, birds and pigs. No antiviral therapy. An inactivated vaccine is available. |
| Dermatophytes (e.g., Trichophyton, Microsporum, Epidermophyton Species) Diseases Dermatophytoses, e.g., tinea capitis, tinea cruris, and tinea pedis. Characteristics These fungi are molds that use keratin as a nutritional source. Not dimorphic. Habitat of most dermatophytes that cause human disease is human skin, with the exception of Microsporum canis, which infects dogs and cats also. Transmission Direct contact with skin scales. Pathogenesis These fungi grow only in the superficial keratinized layer of the skin. They do not invade underlying tissue. The lesions are due to the inflammatory response to the fungi. Frequency of infection is enhanced by moisture and warmth, e.g., inside shoes. An important host defense is provided by the fatty acids produced by sebaceous glands. The "id" reaction is a hypersensitivity response in one skin location, e.g., fingers, to the presence of the organism in another, e.g., feet. Laboratory Diagnosis Skin scales should be examined microscopically in a KOH preparation for the presence of hyphae. The organism is identified by the appearance of its mycelium and its asexual spores on Sabouraud's agar. Serologic tests are not useful. Skin Test Trichophytin antigen can be used to determine the competence of a patient's cell-mediated immunity. Not used for diagnosis of tinea. Treatment Topical agents, such as miconazole, clotrimazole, or tolnaftate, are used. Undecylenic acid is effective against tinea pedis. Griseofulvin is the treatment of choice for tinea unguium and tinea capitis. Prevention Skin should be kept dry and cool. |
| Sporothrix schenckii Disease Sporotrichosis. Characteristics Thermally dimorphic. Mold in the soil, yeast in the body at 37°C. Habitat is soil or vegetation. Transmission Mold spores enter skin in puncture wounds caused by rose thorns and other sharp objects in the garden. Pathogenesis Local abscess or ulcer with nodules in draining lymphatics. Laboratory Diagnosis Cigar-shaped budding yeasts visible in pus. Culture on Sabouraud's agar shows typical morphology. Skin Test None. Treatment Itraconazole. Prevention Skin should be protected when gardening. |
| Histoplasma capsulatum Disease Histoplasmosis. Characteristics Thermally dimorphic, i.e., a yeast at body temperature and a mold in the soil at ambient temperature. The mold grows preferentially in soil enriched with bird droppings. Endemic in Ohio and Mississippi River valley areas. Transmission Inhalation of airborne asexual spores (microconidia). Pathogenesis Microconidia enter the lung and differentiate into yeast cells. The yeast cells are ingested by alveolar macrophages and multiply within them. An immune response is mounted, and granulomas form. Most infections are contained at this level, but suppression of cell-mediated immunity can lead to disseminated disease. Laboratory Diagnosis Sputum or tissue can be examined microscopically and cultured on Sabouraud's agar. Yeasts visible within macrophages. The presence of tuberculate chlamydospores in culture at 25°C is diagnostic. A rise in antibody titer is useful for diagnosis, but cross-reaction with other fungi (e.g., Coccidioides) occurs. Skin Test Histoplasmin, a mycelial extract, is the antigen. Useful for epidemiologic purposes to determine the incidence of infection. A positive result indicates only that infection has occurred; it cannot be used to diagnose active disease. Because skin testing can induce antibodies, serologic tests must be done first. Treatment Amphotericin B for disseminated disease; itraconazole for pulmonary disease. Prevention No vaccine is available. Itraconazole can be used for chronic suppression in AIDS patients. |
| Coccidioides immitis Disease Coccidioidomycosis. Characteristics Thermally dimorphic. At 37°C in the body, it forms spherules containing endospores. At 25°C, either in the soil or on agar in the laboratory, it grows as a mold. The cells at the tip of the hyphae differentiate into asexual spores (arthrospores). Natural habitat is the soil of arid regions, e.g., San Joaquin valley in California and parts of Arizona and New Mexico. Transmission Inhalation of airborne arthrospores. Pathogenesis Arthrospores differentiate into spherules in the lungs. Spherules rupture, releasing endospores that form new spherules, thereby disseminating the infection within the body. A cell-mediated immune response contains the infection in most people, but those who are immunocompromised are at high risk for disseminated disease. Laboratory Diagnosis Sputum or tissue should be examined microscopically for spherules and cultured on Sabouraud's agar. A rise in IgM (using precipitin test) antibodies indicates recent infection. A rising titer of IgG antibodies (using complement-fixation test) indicates dissemination; a decreasing titer indicates a response to therapy. Skin Test Either coccidioidin, a mycelial extract, or spherulin, an extract of spherules, is the antigen. Useful in determining whether the patient has been infected. A positive test indicates prior infection but not necessarily active disease. Treatment Amphotericin B or itraconazole for disseminated disease; ketoconazole for limited pulmonary disease. Prevention No vaccine or prophylactic drug is available. |
| Blastomyces dermatitidis Disease Blastomycosis. Characteristics Thermally dimorphic. Mold in the soil, yeast in the body at 37°C. The yeast form has a single, broad-based bud and a thick, refractile wall. Natural habitat is rich soil (e.g., near beaver dams), especially in the upper midwestern region of the United States. Transmission Inhalation of airborne spores (conidia). Pathogenesis Inhaled conidia differentiate into yeasts, which initially cause abscesses followed by formation of granulomas. Dissemination is rare, but when it occurs, skin and bone are most commonly involved. Laboratory Diagnosis Sputum or skin lesions examined microscopically for yeasts with a broad-based bud. Culture on Sabouraud's agar also. Serologic tests are not useful. Skin Test Little value. Treatment Itraconazole is the drug of choice. Prevention No vaccine or prophylactic drug is available. |
| Paracoccidioides brasiliensis Disease Paracoccidioidomycosis. Characteristics Thermally dimorphic. Mold in the soil, yeast in the body at 37°C. The yeast form has multiple buds (resembles the steering wheel of a ship). Transmission Inhalation of airborne conidia. Pathogenesis Inhaled conidia differentiate to the yeast form in lungs. Can disseminate to many organs. Laboratory Diagnosis Yeasts with multiple buds visible in pus or tissues. Culture on Sabouraud's agar shows typical morphology. Skin Test Not useful. Treatment Itraconazole. Prevention No vaccine or prophylactic drug is available. |
| Candida albicans Diseases Thrush, disseminated candidiasis, and chronic mucocutaneous candidiasis. Characteristics Candida albicans is a yeast when part of the normal flora of mucous membranes but forms pseudohyphae and hyphae when it invades tissue. The yeast form produces germ tubes when incubated in serum at 37°C. Not thermally dimorphic. Transmission Part of the normal flora of skin, mucous membranes, and GI tract. No person-to-person transmission. Pathogenesis Opportunistic pathogen. Predisposing factors include reduced cell-mediated immunity, altered skin and mucous membrane, suppression of normal flora, and presence of foreign bodies. Thrush is most common in infants, immunosuppressed patients, and persons receiving antibiotic therapy. Skin lesions occur frequently on moisture-damaged skin. Disseminated infections, such as endocarditis and endophthalmitis, occur in immunosuppressed patients and intravenous drug users. Chronic mucocutaneous candidiasis occurs in children with a T-cell defect in immunity to Candida. Laboratory Diagnosis Microscopic examination of tissue reveals yeasts and pseudohyphae. If only yeasts are found, colonization is suggested. The yeast is gram-positive. Forms colonies of yeasts on Sabouraud's agar. Germ tube formation and production of chlamydospores distinguish C. albicans from virtually all other species of Candida. Serologic tests not useful. Skin Test Used to determine competency of cell-mediated immunity rather than to diagnose candidal disease. Treatment Skin and mucous membrane disease can be treated with oral or topical antifungal agents such as nystatin or miconazole. Disseminated disease requires amphotericin B. Chronic mucocutaneous candidiasis is treatable with ketoconazole. Prevention Predisposing factors should be reduced or eliminated. Oral thrush can be prevented by using clotrimazole troches or nystatin "swish and swallow." There is no vaccine. |
| Cryptococcus neoformans Disease Cryptococcosis, especially cryptococcal meningitis. Characteristics Heavily encapsulated yeast. Not dimorphic. Habitat is soil, especially where enriched by pigeon droppings. Transmission Inhalation of airborne yeast cells. Pathogenesis Organisms cause influenzalike syndrome or pneumonia. They spread via the bloodstream to the meninges. Reduced cell-mediated immunity predisposes to severe disease, but some cases of cryptococcal meningitis occur in immunocompetent people. Laboratory Diagnosis Visualization of the encapsulated yeast in India ink preparations of spinal fluid. Culture of sputum or spinal fluid on Sabouraud's agar produces colonies of yeasts. Latex agglutination test detects polysaccharide capsular antigen in spinal fluid. Skin Test Not available. Treatment Amphotericin B plus flucytosine for meningitis. Prevention Cryptococcal meningitis can be prevented in AIDS patients by using oral fluconazole. There is no vaccine. |
| Aspergillus fumigatus Diseases Invasive aspergillosis is the major disease. Allergic bronchopulmonary aspergillosis and aspergilloma (fungus ball) are important also. Characteristics Mold with septate hyphae that branch at a V-shaped angle (low-angle branching). Not dimorphic. Habitat is the soil. Transmission Inhalation of airborne spores (conidia). Pathogenesis Opportunistic pathogen. In immunocompromised patients, invasive disease occurs. The organism invades blood vessels, causing thrombosis and infarction. A person with a lung cavity, e.g., from tuberculosis, may develop a "fungal ball" (aspergilloma). An allergic person, e.g., one with asthma, can develop allergic bronchopulmonary aspergillosis mediated by IgE antibody. Laboratory Diagnosis Septate hyphae invading tissue are visible microscopically. Invasion distinguishes disease from colonization. Forms characteristic mycelium when cultured on Sabouraud's agar. See chains of conidia radiating from a central stalk. Serologic tests detect IgG precipitins in patients with aspergillomas and IgE antibodies in patients with allergic bronchopulmonary aspergillosis. Skin Test None available. Treatment Amphotericin B for invasive aspergillosis. Some lesions (e.g., fungus balls) can be surgically removed. Steroid therapy is recommended for allergic bronchopulmonary aspergillosis. Prevention No vaccine or prophylactic drug is available. |
| Mucor & Rhizopus Species Disease Mucormycosis. Characteristics Molds with nonseptate hyphae that typically branch at a 90-degree angle (wide-angle branching). Not dimorphic. Habitat is the soil. Transmission Inhalation of airborne spores. Pathogenesis Opportunistic pathogens. They cause disease primarily in ketoacidotic diabetic and leukemic patients. The sinuses and surrounding tissue are typically involved. Hyphae invade the mucosa and progress into underlying tissue and vessels, leading to necrosis and infarction. Laboratory Diagnosis Microscopic examination of tissue for the presence of non-septate hyphae that branch at wide angles. Forms characteristic mycelium when cultured on Sabouraud's agar. See spores contained within a sac called a sporangium. Serologic tests are not available. Skin Test None. Treatment Amphotericin B and surgical debridement. Prevention No vaccine or prophylactic drug is available. Control of underlying disease, e.g., diabetes, tends to prevent mucormycosis. |
| Pneumocystis carinii Although there is molecular evidence that Pneumocystis carinii is a fungus, it is described in this book in the section on protozoa that cause blood and tissue infections (see Pneumocystis). |
| Entamoeba histolytica Diseases Amebic dysentery and liver abscess. Characteristics Intestinal protozoan. Motile ameba (trophozoite); forms cysts with four nuclei. Life cycle: Humans ingest cysts, which form trophozoites in small intestine. Trophozoites pass to the colon and multiply. Cysts form in the colon, which then pass in the feces. Transmission and Epidemiology fecal–oral transmission of cysts. Human reservoir. Occurs worldwide, especially in tropics. Pathogenesis Trophozoites invade colon epithelium and produce flask-shaped ulcer. Can spread to liver and cause amebic abscess. Laboratory Diagnosis Trophozoites or cysts visible in stool. Serologic testing (indirect hemagglutination test) positive with invasive (e.g., liver) disease. Treatment Metronidazole or tinidazole for symptomatic disease. Iodoquinol or paromomycin for asymptomatic cyst carriers. Prevention Proper disposal of human waste. Water purification. Hand washing. |
| Giardia lamblia Disease Giardiasis, especially diarrhea. Characteristics Intestinal protozoan. Pear-shaped, flagellated trophozoite, forms cyst with four nuclei. Life cycle: Humans ingest cysts, which form trophozoites in duodenum. Trophozoites encyst and are passed in feces. Transmission and Epidemiology Fecal–oral transmission of cysts. Human and animal reservoir. Occurs worldwide. Pathogenesis Trophozoites attach to wall but do not invade. They interfere with absorption of fat and protein. Laboratory Diagnosis Trophozoites or cysts visible in stool. String test used if necessary. Treatment Metronidazole. Prevention Water purification. Hand washing. |
| Cryptosporidium parvum Disease Cryptosporidiosis, especially diarrhea. Characteristics Intestinal protozoan. Life cycle: Oocysts release sporozoites; they form trophozoites. After schizonts and merozoites form, microgametes and macrogametes are produced; they unite to form a zygote and then an oocyst. Transmission and Epidemiology Fecal–oral transmission of cysts. Human and animal reservoir. Occurs worldwide. Pathogenesis Trophozoites attach to wall of small intestine but do not invade. Laboratory Diagnosis Oocysts visible in stool with acid-fast stain. Treatment No effective therapy; however, paromomycin may reduce symptoms. Prevention None. |
| Trichomonas vaginalis Disease Trichomoniasis. Characteristics Urogenital protozoan. Pear-shaped, flagellated trophozoites. No cysts or other forms. Transmission and Epidemiology Transmitted sexually. Human reservoir. Occurs worldwide. Pathogenesis Trophozoites attach to wall of vagina and cause inflammation and discharge. Laboratory Diagnosis Trophozoites visible in secretions. Treatment Metronidazole for both sexual partners. Prevention Condoms limit transmission. |
| Plasmodium Species (P. vivax, P. ovale, P. malariae, & P. falciparum) Disease Malaria. Characteristics Protozoan that infects red blood cells and tissue, e.g., liver, kidney, and brain. Life cycle: Sexual cycle consists of gametogony (production of gametes) in humans and sporogony (production of sporozoites) in mosquitoes; asexual cycle (schizogony) occurs in humans. Sporozoites in saliva of female Anopheles mosquito enter the human bloodstream and rapidly invade hepatocytes (exoerythrocytic phase). There they multiply and form merozoites (Plasmodium vivax and Plasmodium ovale also form hypnozoites, a latent form). Merozoites leave the hepatocytes and infect red cells (erythrocytic phase). There they form schizonts that release more merozoites, which infect other red cells in a synchronous pattern (3 days for Plasmodium malariae; 2 days for the others). Some merozoites become male and female gametocytes, which, when ingested by female Anopheles, release male and female gametes. These unite to produce a zygote, which forms an oocyst containing many sporozoites. These are released and migrate to salivary glands. Transmission and Epidemiology Transmitted by female Anopheles mosquitoes. Occurs primarily in the tropical areas of Asia, Africa, and Latin America. Pathogenesis Merozoites destroy red cells, resulting in anemia. Cyclic fever pattern is due to periodic release of merozoites. Plasmodium falciparum can infect red cells of all ages and cause aggregates of red cells that occlude capillaries. This can cause tissue anoxia, especially in the brain (cerebral malaria) and the kidney (blackwater fever). Hypnozoites can cause relapses. Laboratory Diagnosis Organisms visible in blood smear. Thick smear is used to detect presence of organism and thin smear to speciate. Treatment Chloroquine if sensitive. For chloroquine-resistant P. falciparum, use mefloquine or quinine plus doxycycline. Primaquine for hypnozoites of P. vivax and P. ovale. In severe cases, use parenteral quinidine or quinine. Prevention Chloroquine in areas where organisms are sensitive. For those in areas with a high risk of chloroquine resistance, mefloquine or doxycycline. Primaquine to prevent relapses. Protection from bites. Control mosquitoes by using insecticides and by draining water from breeding areas. |
| Toxoplasma gondii Disease Toxoplasmosis, including congenital toxoplasmosis. Characteristics Tissue protozoan. Life cycle: Cysts in cat feces or in meat are ingested by humans and differentiate in the gut into forms that invade the gut wall. They infect macrophages and form trophozoites (tachyzoites) that multiply rapidly, kill cells, and infect other cells. Cysts containing bradyzoites form later. Cat ingests cysts in raw meat, and bradyzoites excyst, multiply, and form male and female gametocytes. These fuse to form oocysts in cat gut, which are excreted in cat feces. Transmission and Epidemiology Transmitted by ingestion of cysts in raw meat and in food contaminated with cat feces. Also by passage of trophozoites transplacentally from mother to fetus. Infection of fetus occurs only when mother is infected during pregnancy and when she is infected for the first time, i.e., she has no protective antibody. Cat is definitive host; humans and other mammals are intermediate hosts. Occurs worldwide. Pathogenesis Trophozoites infect many organs, especially brain, eyes, and liver. Cysts persist in tissue, enlarge, and cause symptoms. Severe disease in patients with deficient cell-mediated immunity, e.g., encephalitis in AIDS patients. Laboratory Diagnosis Serologic tests for IgM and IgG antibodies are usually used. Trophozoites or cysts visible in tissue. Treatment Sulfadiazine plus pyrimethamine for congenital or disseminated disease. Prevention Meat should be cooked. Pregnant women should not handle cats, cat litter boxes, or raw meat. |
| Pneumocystis carinii Disease Pneumonia. Characteristics Respiratory pathogen. Reclassified in 1988 as a yeast based on molecular evidence but medically has several attributes of a protozoan. Life cycle: uncertain. Transmission and Epidemiology Transmitted by inhalation. Humans are reservoir. Occurs worldwide. Most infections asymptomatic. Pathogenesis Organisms in alveoli cause inflammation. Immunosuppression predisposes to disease. Laboratory Diagnosis Organisms visible in silver stain of lung tissue or lavage fluid. Treatment Trimethoprim-sulfamethoxazole, pentamidine. Prevention Trimethoprim-sulfamethoxazole or aerosolized pentamidine in immunosuppressed individuals. |
| Trypanosoma cruzi Disease Chagas' disease. Characteristics Blood and tissue protozoan. Life cycle: Trypomastigotes in blood of reservoir host are ingested by reduviid bug and form epimastigotes and then trypomastigotes in the gut. When the bug bites, it defecates and feces containing trypomastigotes contaminate the wound. Organisms enter the blood and form amastigotes within cells; these then become trypomastigotes. Transmission and Epidemiology Transmitted by reduviid bugs. Humans and many animals are reservoirs. Occurs in rural Latin America. Pathogenesis Amastigotes kill cells, especially cardiac muscle leading to myocarditis. Also neuronal damage leading to megacolon and megaesophagus. Laboratory Diagnosis Trypomastigotes visible in blood, but bone marrow biopsy, culture in vitro, xenodiagnosis, or serologic tests may be required. Treatment Nifurtimox or benznidazole for acute disease. No effective drug for chronic disease. Prevention Protection from bite. Insect control. |
| Trypanosoma gambiense & Trypanosoma rhodesiense Disease Sleeping sickness (African trypanosomiasis). Characteristics Blood and tissue protozoan. Life cycle: Trypomastigotes in blood of human or animal reservoir are ingested by tsetse fly. They differentiate in the gut to form epimastigotes and then metacyclic trypomastigotes in salivary glands. When fly bites, trypomastigotes enter the blood. Repeated variation of surface antigen occurs, which allows the organism to evade the immune response. Transmission and Epidemiology Transmitted by tsetse flies. Trypanosoma gambiense has a human reservoir and occurs primarily in west Africa. Trypanosoma rhodesiense has an animal reservoir (especially wild antelope) and occurs primarily in east Africa. Pathogenesis Trypomastigotes infect brain, causing encephalitis. Laboratory Diagnosis Trypomastigotes visible in blood in early stages and in cerebrospinal fluid in late stages. Serologic tests useful. Treatment Suramin in early disease. Suramin plus melarsoprol if central nervous system symptoms exist. Prevention Protection from bite. Insect control. |
| Leishmania donovani Disease Kala-azar (visceral leishmaniasis). Characteristics Blood and tissue protozoan. Life cycle: Human macrophages containing amastigotes are ingested by sandfly. Amastigotes differentiate in fly gut to promastigotes, which migrate to pharynx. When fly bites, promastigotes enter blood macrophages and form amastigotes. These can infect other reticuloendothelial cells, especially in spleen and liver. Transmission and Epidemiology Transmitted by sandflies (Phlebotomus or Lutzomyia). Animal reservoir (chiefly dogs, small carnivores, and rodents) in Africa, Middle East, and parts of China. Human reservoir in India. Pathogenesis Amastigotes kill reticuloendothelial cells, especially in liver, spleen, and bone marrow. Laboratory Diagnosis Amastigotes visible in bone marrow smear. Serologic tests useful. Skin test indicates prior infection. Treatment Sodium stibogluconate. Prevention Protection from bite. Insect control. |
