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The document provides a comprehensive overview of various fungal infections, including candidiasis, histoplasmosis, coccidioidomycosis, pneumocystosis, cryptococcosis, and aspergillosis. Each infection is outlined with its clinical findings, risk factors, diagnostic methods, and treatment options. The details also emphasize the importance of immunocompromised states in the manifestation and management of these infections.

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Fungal infections DR/ Abdo Wadi Hepatologist, gastroenterologist, Endoscopist
1.CANDIDIASIS 2.HISTOPLASMOSIS 3.COCCIDIOIDOMYCOSIS 4.PNEUMOCYSTOSIS (Pneumocystis jirovecii Pneumonia) 5.CRYPTOCOCCOSIS 6.ASPERGILLOSIS 7.MUCORMYCOSIS 8.BLASTOMYCOSIS
1. CANDIDIASIS ▪ Common normal flora but opportunistic pathogen. ▪ Mucosal disease, particularly vaginitis and esophagitis. ▪ Risk factors for fungemia: neutropenia, intravenous catheter, abdominal surgery, total parenteral nutrition, kidney disease, broad-spectrum antibiotics.
Clinical Findings A. Mucosal Candidiasis ▪ Esophageal involvement is the most frequent type of significant mucosal disease. ▪ Presenting symptoms include substernal odynophagia, gastroesophageal reflux, or nausea without substernal pain. ▪ Oral candidiasis, though often associated, is not invariably present. Diagnosis is best confirmed by endoscopy with biopsy and culture.
B - Vulvovaginal candidiasis occurs in an estimated 75% of women during their lifetime. Risk factors include pregnancy, uncontrolled diabetes mellitus, broad-spectrum antimicrobial treatment, corticosteroid use, and HIV infection. Symptoms include acute vulvar pruritus, burning vaginal discharge, and dyspareunia. Candidal Funguria Most cases of candidal funguria are asymptomatic and represent specimen contamination or bladder colonization. However, symptoms and signs of true Candida urinary tract infections are indistinguishable from bacterial urinary tract infections and can include urgency, hesitancy, fever, chills, or flank pain.
C. Invasive Candidiasis (1) candidemia (bloodstream infection) without deep seated infection; (2) (candidemia with deep-seated infection (typically eyes, kidney, or abdomen); (3) deep-seated candidiasis in the absence of bloodstream infection. Varying ratios of these clinical entities depends on the predominating risk factors for affected patients (ie, neutropenia, dialysis, postsurgical).
▪ The clinical presentation of candidemia varies from minimal fever to septic shock that can resemble a severe bacterial infection. ▪ Hepatosplenic candidiasis can occur following prolonged neutropenia in patients with underlying hematologic cancers, but this entity is less common in the era of widespread antifungal prophylaxis. ▪ Typically, fever and variable abdominal pain present weeks after chemotherapy, when neutrophil counts have recovered
D. Candidal Endocarditis ▪ is a rare infection affecting patients with prosthetic heart valves or prolonged candidemia, such as with indwelling catheters. ▪ The diagnosis is established definitively by culturing Candida from emboli or from vegetations at the time of valve replacement.
Treatment Mucosal Candidiasis Therapy of esophageal candidiasis depends on the severity of disease. fluconazole, itraconazole intravenous voriconazole, intravenous amphotericin B, intravenous caspofungin, intravenous anidulafungin, intravenous micafungin, Posaconazole tablets, -
Vulvovaginal candidiasis topical azole preparations (eg, clotrimazole, miconazole, Fluconazole Candidal Funguria fluconazole, Invasive Candidiasis echinocandin such as caspofungin micafungin or anidulafungin Fluconazole intravenously, A dilated fundoscopic examination is recommended for patients with candidemia to exclude endophthalmitis.
2. HISTOPLASMOSIS ▪ Exposure to bird and bat droppings; common along river valleys (especially Ohio River and the Mississippi River valleys). ▪ Most patients asymptomatic; ▪ respiratory illness most common clinical problem. ▪ Disseminated disease common in AIDS or other immunosuppressed states; with poor prognosis. ▪ Blood and bone marrow cultures and urine polysaccharide antigen are useful in diagnosis of disseminated disease.
Clinical Findings ▪ Most cases of histoplasmosis are asymptomatic or mild and thus go unrecognized. Past infection is recognized by pulmonary and splenic calcification noted on incidental radiographs. ▪ Symptomatic infection may present with mild influenza-like illness, often lasting 1–4 days. Moderately severe infections are frequently diagnosed as atypical pneumonia. These patients have fever, cough, and mild central chest pain lasting 5–15 days. Clinically evident infections occur in several forms:
(1) Acute pulmonary histoplasmosis. ▪ Clinical manifestations can vary from a mild influenza like illness to severe pneumonia. The illness may last from 1 week to 6 months but is almost never fatal. (2) Progressive disseminated histoplasmosis ▪ is commonly seen in patients with underlying HIV infection (with CD4 cell counts usually less than 100 cells/mcL) or other conditions of impaired cellular immunity. ▪ It is characterized by fever and multiple organ system involvement. ▪ Chest radiographs may show a miliary pattern. ▪ Presentation may be fulminant, simulating septic shock, with death ensuing rapidly unless treatment is provided. ▪ Symptoms usually consist of fever, dyspnea, cough, loss of weight, and prostration. ▪ Ulcers of the mucous membranes of the oropharynx may be present.
(3) Chronic pulmonary histoplasmosis is usually seen in older patients who have underlying chronic lung disease. Chest radiographs show various lesions including complex apical cavities, infiltrates, and nodules. (4) Complications of pulmonary histoplasmosis include granulomatous mediastinitis characterized by persistently enlarged mediastinal lymph nodes and fibrosing mediastinitis in which an excessive fibrotic response to Histoplasma infection results in compromise of pulmonary vascular structures.
Laboratory Findings ▪ Most patients with chronic pulmonary disease show anemia of chronic disease. Bone marrow involvement with pancytopenia may be prominent in disseminated forms. ▪ Marked lactate dehydrogenase (LD) and ferritin elevations are also common, as are mild elevations of serum aspartate aminotransferase. ▪ With pulmonary involvement, sputum culture is rarely positive except in chronic disease; antigen testing of bronchoalveolar lavage fluid may be helpful in acute disease. The combination of a first morning urine and serum polysaccharide antigen assays has an 83% sensitivity for the diagnosis of acute pulmonary histoplasmosis. ▪ Blood or bone marrow cultures from immunocompromised patients with acute disseminated disease are positive more than 80% of the time, but may take several weeks for growth. ▪ The urine antigen assay has a sensitivity of greater than 90% for disseminated disease in immunocompromised patients and a declining titer can be used to follow response to therapy. ▪ Diagnosis of CNS disease requires antigen and antibody testing of the cerebrospinal fluid (CSF) and serum as well as urine antigen testing.
Treatment ▪ For progressive localized disease and for mild to moderately severe nonmeningeal disseminated disease in immunocompetent or immunocompromised patients, itraconazole, 200– 400 mg/day orally divided into two doses, ▪ Duration of therapy ranges from weeks to several months depending on the severity of illness. ▪ Intravenous liposomal amphotericin B, 3 mg/kg/day, is used in patients with more severe illness such as meningitis.
3. COCCIDIOIDOMYCOSIS ▪ Influenza-like illness during acute infection: malaise, fever, backache, headache, and cough. ▪ Erythema nodosum common with acute infection. ▪ Dissemination may result in meningitis, bony lesions, or skin and soft tissue abscesses. ▪ Chest radiograph findings vary from pneumonitis to cavitation. ▪ Serologic tests useful; large spherules containing endospores demonstrable in sputum or tissues.
Clinical Findings ▪ Symptoms of primary coccidioidomycosis occur in about 40% of infections. Symptom onset (after an incubation period of 10–30 days) is usually that of a respiratory tract illness with fever and occasionally chills. ▪ Coccidioidomycosis is a common, frequently unrecognized, etiology of community-acquired pneumonia in endemic areas. ▪ Erythema nodosum may appear 2–20 days after onset of symptoms. Persistent pulmonary lesions, varying from cavities and abscesses to parenchymal nodular densities or bronchiectasis, occur in about 5% of diagnosed cases. ▪ Disseminated disease occurs in about 0.1% of white and 1% of nonwhite patients. ▪ Any organ may be involved. Pulmonary findings usually become more pronounced, with mediastinal lymph node enlargement, cough, and increased sputum production. Lung abscesses may rupture into the pleural space, producing an empyema
▪ Complicated skin and bone infections may develop. ▪ Fungemia may occur and is characterized clinically by a diffuse miliary pattern on chest radiograph and by early death. The course may be particularly rapid in immunosuppressed patients. ▪ Meningitis occurs in 30–50% of cases of dissemination and may result in chronic basilar meningitis. Subcutaneous abscesses and verrucous skin lesions are especially common in fulminating cases. ▪ HIV -infected persons with disseminated disease have a higher incidence of miliary infiltrates, lymphadenopathy, and meningitis, but skin lesions are uncommon.
Laboratory Findings ▪ In primary coccidioidomycosis, there may be moderate leukocytosis and eosinophilia. ▪ Serologic testing (ELISA) detect IgM antibodies ▪ Patients in whom coccidioidomycosis is diagnosed should undergo evaluation for meningeal involvement when CNS symptoms or neurologic signs are present. Demonstrable complement-fixing antibodies in spinal fluid are diagnostic of coccidioidal meningitis.. ▪ spinal fluid findings include increased cell count with lymphocytosis and reduced glucose. Spinal fluid culture is positive in approximately 30% of meningitis cases.
Imaging ▪ patchy, nodular, and lobar upper lobe pulmonary infiltrates are most common. ▪ Hilar lymphadenopathy may be visible and is seen in localized disease; ▪ mediastinal lymphadenopathy suggests dissemination. Treatment ▪ Itraconazole, ▪ fluconazole, ▪ For progressive pulmonary or extrapulmonary disease, liposomal amphotericin B intravenously is used ▪ lumbar or cisternal intrathecal administration of amphotericin B daily ▪ Systemic therapy with liposomal amphotericin B, 3–5 mg/kg/day intravenously, is generally given concurrently with intrathecal therapy,
4. PNEUMOCYSTOSIS (Pneumocystis jirovecii Pneumonia) ▪ Fever, dyspnea, dry cough, hypoxia. ▪ Often only slight lung physical findings. ▪ Chest radiograph: diffuse interstitial disease or normal. ▪ P jirovecii in sputum, bronchoalveolar lavage fluid, or lung tissue; PCR of bronchoalveolar lavage; (1,3)-beta-D-glucan in blood. ▪
Clinical Findings ▪ Findings are usually limited to the pulmonary parenchyma. In the sporadic form of the disease associated with deficient cell- mediated immunity, the onset may be subacute, characterized by dyspnea on exertion and nonproductive cough, many patients have bibasilar crackles. ▪ Without treatment, the course is usually one of rapid deterioration and death. Adult patients may present with spontaneous pneumothorax, usually in patients with previous episodes or those receiving aerosolized pentamidine prophylaxis. ▪ Patients with AIDS will usually have other evidence of HIV associated disease, including fever, fatigue, and weight loss, for weeks or months preceding the illness.
Laboratory Findings ▪ Chest radiographs most often show diffuse “interstitial” infiltration, ▪ High-resolution chest CT scans may be quite suggestive of P jirovecii pneumonia, helping distinguish it from other causes of pneumonia. ▪ Arterial blood gas determinations usually show hypoxemia with hypocapnia. ▪ (PCR) of bronchoalveolar lavage, negative PCR from bronchoalveolar lavage rules out disease. ▪ Open lung biopsy and needle lung biopsy
Treatment ▪ Trimethoprim-Sulfamethoxazole ▪ Primaquine/Clindamycin ▪ . Pentamidine Isethionate ▪ Atovaquone ▪ Prednisone
5. CRYPTOCOCCOSIS ▪ Most common cause of fungal meningitis. ▪ Predisposing factors: chemotherapy for hematologic malignancies, Hodgkin lymphoma, corticosteroid therapy, transplant recipients, TNF-alpha inhibitor therapy, and HIV infection. ▪ Headache, abnormal mental status; meningismus seen occasionally, though rarely in HIV -infected patients. ▪ Demonstration of capsular polysaccharide antigen or positive culture in CSF is diagnostic.
Clinical Findings ▪ Pulmonary disease ranges from simple nodules to widespread infiltrates leading to respiratory failure. ▪ Disseminated disease may involve any organ, but CNS disease predominates. ▪ Headache is usually the first symptom of meningitis. Confusion and other mental status changes as well as cranial nerve abnormalities, nausea, and vomiting may be seen as the disease progresses. ▪ Nuchal rigidity and meningeal signs occur about 50% of the time but are uncommon in HIV -infected patients. ▪ Communicating hydrocephalus may complicate the course. ▪ Paradoxical clinical worsening associated with improved immunologic status has been reported in HIV -positive and transplant patients with cryptococcosis; this entity has been labeled the immune reconstitution inflammatory syndrome (IRIS).
Laboratory Findings ▪ Respiratory tract disease is diagnosed by culture of respiratory secretions or pleural fluid. ▪ For suspected meningeal disease, lumbar puncture is the preferred diagnostic procedure. Spinal fluid findings include increased opening pressure, variable pleocytosis, increased protein, and decreased glucose, ▪ Gram stain of the CSF usually reveals budding, encapsulated fungi. ▪ Cryptococcal capsular antigen in CSF and culture together establish the diagnosis over 90% of the time.
▪ Patients with AIDS often have the antigen in both CSF and serum, and extrameningeal disease (lungs, blood, urinary tract) is common. ▪ In patients with AIDS, the serum cryptococcal antigen is also a sensitive screening test for meningitis, being positive in over 95% of cases. ▪ MRI is more sensitive than CT in finding CNS abnormalities such as cryptococcomas.
Treatment ▪ Liposomal amphotericin B, 3–4 mg/kg/day intravenously for 14 days, is the preferred agent for induction therapy, followed by an additional 8 weeks of fluconazole, 400 mg/day orally , The addition of flucytosine has been associated with improved survival ▪ Fluconazole (800–1200 mg orally daily) may be given with amphotericin B . ▪ Frequent, repeated lumbar punctures or ventricular shunting should be performed to relieve high CSF pressures or if hydrocephalus is a complication.
6. ASPERGILLOSIS ▪ Most common cause of non-candidal invasive fungal infection in transplant recipients and in patients with hematologic malignancies. ▪ Predisposing factors: leukemia, bone marrow or organ transplant, late HIV infection. ▪ Pulmonary, sinus, and CNS are most common disease sites. ▪ Detection of galactomannan by ELISA or PCR in serum or other body fluids is useful for early diagnosis and treatment.
Clinical Findings 1. Allergic forms of aspergillosis—Allergic bronchopulmonary aspergillosis (ABPA) occurs in patients with preexisting asthma or cystic fibrosis who develop worsening bronchospasm and fleeting pulmonary infiltrates accompanied by eosinophilia, high levels of IgE, and IgG Aspergillus precipitins in the blood. Allergic aspergillus sinusitis produces a chronic sinus inflammation characterized by eosinophilic mucus and noninvasive hyphal elements.
Clinical Findings 2. Chronic aspergillosis—Chronic pulmonary aspergillosis produces a spectrum of disease that usually occurs when there is preexisting lung damage but not significant immunocompromise. Disease manifestations range from aspergillomas that develop in a lung cavity to chronic fibrosing pulmonary aspergillosis in which the majority of lung tissue is replaced with fibrosis. Long-standing (longer than 3 months) pulmonary and systemic symptoms such as cough, shortness of breath, weight loss, and malaise are common.
3. Invasive aspergillosis—Invasive aspergillosis ▪ most commonly occurs in profoundly immunodeficient patients, such as those who have undergone hematopoietic stem cell transplantation or have prolonged, severe neutropenia, but it can occur among critically ill immunocompetent patients as well. ▪ Specific risk factors in patients who have undergone a hematopoietic stem cell transplant include cytopenias, corticosteroid use, iron overload, cytomegalovirus disease, and graft-versus-host disease. ▪ Pulmonary disease is most common, with patchy infiltration leading to a severe necrotizing pneumonia. Invasive sinus disease also occurs.
Laboratory Findings ▪ There is eosinophilia, high levels of total IgE, and IgE and IgG specific for Aspergillus in the blood of patients with ABPA. ▪ Detection of galactomannan by ELISA or Aspergillus DNA by PCR, or both, has been used for the early diagnosis of invasive disease, . ▪ Galactomannan levels and Aspergillus DNA PCR can be tested in serum or in bronchoalveolar lavage fluid, which may be more sensitive than serum. ▪ Higher galactomannan levels are correlated with increased mortality, and failure of galactomannan levels to fall in response to therapy portends a worse outcome. ▪ CT scan of the chest may show characteristics quite suggestive of invasive aspergillosis (eg, “halo sign,” which is a zone of diminution of ground glass around a consolidation).
Treatment 1. Allergic forms of aspergillosis ▪ Itraconazole, corticosteroids or Voriconazole. 2. Chronic aspergillosis ▪ The most effective therapy for symptomatic aspergilloma remains surgical resection, other forms of chronic aspergillosis are generally treated with at least 4–6 months of oral azole , itraconazole , voriconazole or posaconazole 3. Invasive aspergillosis ▪ voriconazole ▪ anidulafungin . ▪ Isavuconazole ▪ voriconazole. ▪ amphotericin B . ▪ caspofungin ▪ posaconazole oral tablets
7. MUCORMYCOSIS ▪ Most common cause of non-Aspergillus invasive mold infection ▪ Predisposing factors: poorly controlled diabetes, leukemia, transplant recipient, wound contamination by soil. ▪ Pulmonary, rhinocerebral, and skin are most common disease sites. ▪ Rapidly fatal without multidisciplinary interventions. Clinical Findings ▪ Invasive disease of the sinuses, orbits, and the lungs may occur. Necrosis is common due to hyphal tissue invasion that may manifest as ulceration of the hard palate or nasal palate or hemoptysis. ▪ Widely disseminated disease can occur. ▪ A reverse “halo sign” (focal area of ground glass diminution surrounded by a ring of consolidation) may be seen on chest CT. ▪ Biopsy of involved tissue remains the cornerstone of
Treatment ▪ Reversal of predisposing conditions (if possible). ▪ surgical debridement, and prompt antifungal therapy. ▪ A prolonged course of a lipid preparation of intravenous liposomal amphotericin B (5 mg/kg with higher doses possibly given for CNS disease) should be started early . ▪ posaconazole
8. BLASTOMYCOSIS ▪ Chronic pulmonary infection is most common and may be asymptomatic. ▪ When dissemination takes place, lesions are most frequently seen in the skin, bones, and urogenital system. ▪ Cough, moderate fever, dyspnea, and chest pain are common. These may resolve or progress, with purulent sputum production, pleurisy, fever, chills, loss of weight, and prostration. ▪ Radiologic studies, either chest radiographs or CT scans, usually reveal lobar consolidation or masses. ▪ Raised, verrucous cutaneous lesions are commonly present in disseminated blastomycosis. ▪ Bones—often the ribs and vertebrae—are frequently involved. Epididymitis, prostatitis, and other involvement of the male urogenital system may occur.
▪ infection in HIV -infected persons may progress rapidly, with dissemination common. Laboratory findings usually include leukocytosis and anemia, though these are not specific. ▪ The organism is found in clinical specimens, It grows readily on culture. ▪ A urinary antigen test is available. ▪ Itraconazole, 200–400 mg/day orally for at least 6–12 months, is the therapy of choice for non meningeal disease, with a response rate of over 80% (Table 36–1). ▪ Liposomal amphotericin B, 3–5 mg/kg/day intravenously, is given initially for severe disease.
HELMINTHIC INFECTIONS
▪ TREMATODE (FLUKE) INFECTIONS ✓ SCHISTOSOMIASIS (Bilharziasis) ▪ LIVER, LUNG, & INTESTINAL FLUKES ✓ FASCIOLIASIS ✓ CLONORCHIASIS & OPISTHORCHIASIS ✓ PARAGONIMIASIS ✓ INTESTINAL FLUKES ▪ CESTODE INFECTIONS ▪ NONINVASIVE CESTODE INFECTIONS ✓ Beef Tapeworm ✓ Pork Tapeworm ✓ Fish Tapeworm ✓ Dwarf Tapeworm ▪ INVASIVE CESTODE INFECTIONS ✓ Cysticercosis ✓ Echinococcosis
▪ INTESTINAL NEMATODE (Roundworm) INFECTIONS ✓ ASCARIASIS ✓ TRICHURIASIS ✓ HOOKWORM DISEASE ✓ STRONGYLOIDIASIS ✓ ENTEROBIASIS ▪ INVASIVE NEMATODE (Roundworm) INFECTIONS ✓ TRICHINOSIS ✓ TOXOCARIASIS ✓ CUTANEOUS LARVA MIGRANS (Creeping Eruption) ▪ FILARIASIS ✓ LYMPHATIC FILARIASIS ✓ ONCHOCERCIASIS ✓ LOIASIS
▪ (Bilharziasis) ✓History of freshwater exposure in an endemic area. ✓ Acute schistosomiasis: fever, headache, myalgias, cough, urticaria, diarrhea, and eosinophilia. ✓Intestinal schistosomiasis: abdominal pain, diarrhea, and hepatomegaly, progressing to anorexia, weight loss, and features of portal hypertension. ✓urinary schistosomiasis: hematuria and dysuria, progressing to hydronephrosis and urinary infections. ✓Diagnosis: characteristic eggs in feces or urine; biopsy of rectal or bladder mucosa; positive serology. ✓
▪ clinical features ✓dermatitis—Following cercarial penetration, localized erythema develops in some individuals, which can progress to a pruritic maculopapular rash that persists for some days. ✓Acute schistosomiasis (Katayama syndrome)—A febrile illness may develop 2–8 weeks after exposure in persons without prior infection, most commonly Presenting symptoms and signs include acute onset of fever; headache; myalgias; cough; malaise; urticaria; diarrhea, which may be bloody; hepatosplenomegaly; lymphadenopathy; and pulmonary infiltrates. Localized lesions may occasionally cause severe manifestations, including CNS abnormalities and death. Acute schistosomiasis usually resolves in 2–8 weeks.
▪ Chronic schistosomiasis ✓ Many infected persons have light infections and are asymptomatic, but an estimated 50–60% have symptoms and 5–10% have advanced organ damage. ✓ Symptomatic patients with intestinal schistosomiasis typically experience abdominal pain, fatigue, diarrhea, and hepatomegaly. Over years, anorexia, weight loss, weakness, colonic polyps, and features of portal hypertension develop. ✓ Late manifestations include hematemesis from esophageal varices, hepatic failure, and pulmonary hypertension. ✓ Urinary schistosomiasis may present within months of infection with hematuria and dysuria, . ✓ Fibrotic changes in the urinary tract can lead to hydroureter, hydronephrosis, bacterial urinary infections and, ultimately, kidney disease or bladder cancer.
▪ Laboratory investigation ✓ Microscopic examination of stool or urine for eggs, ✓ serologic tests ✓ Diagnosis can also be made by biopsy of the rectum, colon, liver, or bladder. ✓ Point-of-care assays to detect circulating schistosome antigens in serum and urine are also available;. ✓ In acute schistosomiasis, leukocytosis and marked eosinophilia may occur; ✓ With a diagnosis of schistosomiasis, evaluation for the extent of disease is warranted, including liver function studies and imaging of the liver with intestinal disease and ultrasound or other imaging studies of the urinary system in urinary disease.
▪ Treatment ✓ The drug of choice for schistosomiasis is praziquantel. The drug is administered for 1 day at an oral dose of 40 mg/kg (in one or two doses) for S mansoni, S haematobium, and a dose of 60 mg/kg (in two or three doses) for S japonicum and S mekongi.
FASCIOLIASIS ▪ Infection by Fasciola hepatica, the sheep liver fluke, results from ingestion of encysted metacercariae on watercress or other aquatic vegetables. ▪ Infection is prevalent in sheep-raising areas in many countries, especially parts of South America, the Middle East, and southern Europe, and it has increasingly been recognized in travelers to these areas. ▪ Fasciola gigantica has a more restricted distribution in Asia and Africa and causes similar findings. Eggs are passed from host feces into freshwater, leading to infection of snails, and then deposition of metacercariae on vegetation.
▪ In humans, metacercariae excyst, penetrate into the peritoneum, migrate through the liver, and mature in the bile ducts, where they cause local necrosis and abscess formation. ▪ Two clinical syndromes are seen, related to acute migration of worms and chronic infection of the biliary tract. ▪ Symptoms related to migration of larvae present 6–12 weeks after ingestion. Typical findings are abdominal pain, fever, malaise, weight loss, urticaria, eosinophilia, and leukocytosis. Tender hepatomegaly and elevated liver biochemical tests may be seen. Rarely, migration to other organs may lead to localized disease.
▪ CT and other imaging studies show hypodense migratory lesions of the liver. Definitive diagnosis is made by the identification of characteristic eggs in stool. ▪ In chronic infection, imaging studies show masses obstructing the extrahepatic biliary tract. Serologic assays have sensitivity and specificity greater than 90%, but cannot distinguish between past and current infection. ▪ The treatment of choice is triclabendazole, Standard dosing of 10 mg/kg orally in a single dose or two doses over 12 hours achieves a cure rate of about 80%, but repeat dosing is indicated if abnormal radiologic findings or eosinophilia do not resolve. ▪ The second-line drug for fascioliasis is bithionol (30–50 mg/kg/day orally in three divided doses on alternate days for 10–15 days).
INTESTINAL FLUKES ▪ The large intestinal fluke, Fasciolopsis buski. Eggs shed in stools hatch in freshwater, followed by infection of snails, and release of cercariae that encyst on aquatic plants. Humans are infected by eating uncooked plants, ▪ Adult flukes mature in about 3 months and live in the small intestine attached to the mucosa, leading to local inflammation and ulceration. ▪ Other intestinal flukes that cause similar syndromes include Heterophyes (North Africa and Turkey) and Metagonimus (East Asia) species; these species are transmitted by undercooked freshwater fish. Infections with intestinal flukes are often asymptomatic, although eosinophilia maybe marked.
▪ In symptomatic cases, after an incubation period of 1–2 months, manifestations include epigastric pain and diarrhea. Other gastrointestinal symptoms, ileus, edema, and ascites may be seen uncommonly. ▪ Diagnosis is based on identification of characteristic eggs or adult flukes in the stool. ▪ The drug of choice is praziquantel, 25 mg/kg orally as a single dose. Alternative therapies are triclabendazole and niclosamide (for most species).
NONINVASIVE CESTODE INFECTIONS 1. Beef Tapeworm Infection is most common in cattle breeding areas. Humans are the definitive host. Gravid segments of T saginata are passed in human feces to soil, where they are ingested by grazing animals, especially cattle. The eggs then hatch to release embryos that encyst in muscle as cysticerci. Humans are infected by eating raw or undercooked infected beef. Most individuals infected with T saginata are asymptomatic, but abdominal pain and other gastrointestinal symptoms may be present. Eosinophilia is common. The most common presenting finding is the passage of proglottids in the stool.
2. Pork Tapeworm T solium is transmitted to pigs that ingest human feces. Humans can be either the definitive host (after consuming undercooked pork, leading to tapeworm infection) or the intermediate host (after consuming food contaminated with human feces containing T solium eggs, leading to cysticercosis, which is discussed under Invasive Cestode Infections). As with the beef tapeworm, infection with T solium adult worms is generally asymptomatic, but gastrointestinal symptoms may occur. Infection is generally recognized after passage of proglottids. Autoinfection with eggs can progress to cysticercosis.
3. Fish Tapeworm Infection with D latum follows ingestion of undercooked freshwater fish, most commonly in temperate regions. Eggs from human feces are taken up by crustaceans, these are eaten by fish, which are then infectious to humans. Infection with multiple worms over many years can occur. Infections are most commonly asymptomatic, but nonspecific gastrointestinal symptoms, including diarrhea, may occur. Diagnosis usually follows passage of proglottids. Prolonged heavy infection can lead to megaloblastic anemia and neuropathy from vitamin B12 deficiency, which is due to infection-induced dissociation of the vitamin from intrinsic factor and to utilization of the vitamin by worms.
4. Dwarf Tapeworm H nana is the only tapeworm that can be transmitted between humans. Infections are common in warm areas, especially with poor hygiene and institutionalized populations. Infection follows ingestion of food contaminated with human feces. Eggs hatch in the intestines, where oncospheres penetrate the mucosa, encyst as cysticercoid larvae, and then rupture after about 4 days to release adult worms. Autoinfection can lead to amplification of infection. Infection with H nana, the related rodent tapeworm H diminuta, or the dog tapeworm D caninum can also follow accidental ingestion of infected insects. H nana are dwarf in size relative to other tapeworms but can reach 5 cm in length. Heavy infection is common, especially in children, and can be accompanied by abdominal discomfort, anorexia, and diarrhea.
Diagnosis is usually made based on the identification of characteristic eggs or proglottids in stool. Egg release may be irregular, so examination of multiple specimens or concentration techniques may be needed. Treatment A single dose of praziquantel (5–10 mg/kg orally) is highly effective. The alternative therapy for these infections is niclosamide. A single dose of niclosamide (2 g chewed) is effective For H nana, therapy is continued daily for 1 week.
Cysticercosis ▪ Exposure to T solium through fecal contamination of food. Focal CNS lesions; seizures, headache. ▪ Brain imaging shows cysts; positive serologic tests. Clinical Findings ▪ Neurocysticercosis can cause intracerebral, subarachnoid, and spinal cord lesions and intraventricular cysts. Single or multiple lesions may be present. Lesions may persist for years before symptoms develop, generally due to local inflammation or ventricular obstruction. Presenting symptoms include seizures, focal neurologic deficits, altered cognition, and psychiatric disease. Symptoms develop more quickly with intraventricular cysts, with findings of hydrocephalus and meningeal irritation, including severe headache, vomiting,
A particularly aggressive form of the disease, racemose cysticercosis, involves proliferation of cysts at the base of the brain, leading to alterations of consciousness and death. Spinal cord lesions can present with progressive focal findings. Cysticercosis of other organ systems is usually clinically benign. Involvement of muscles can uncommonly cause discomfort and is identified by radiographs of muscle showing multiple calcified lesions. Subcutaneous involvement presents with multiple painless palpable skin lesions. Involvement of the eyes can present with ptosis due to extraocular muscle involvement or intraocular abnormalities.
Laboratory Findings and Imaging Diagnosis ▪ CSF examination may show lymphocytic or eosinophilic pleocytosis, decreased glucose, and elevated protein ▪ Serology. ▪ With neuroimaging by CT or MRI, multiple parenchymal cysts are most typically seen. Parenchymal calcification is also common. Treatment ▪ albendazole (10–15 mg/kg/day orally for 8 days) ▪ praziquantel (50 mg/kg/day orally for 15–30 days). Combining albendazole plus praziquantel improved outcomes compared to albendazole alone in patients with multiple viable intraparenchymal cysts. ▪ Corticosteroids ▪ Anticonvulsant therapy is provided if needed. ▪ shunting is performed if required for elevated intracranial pressure. ▪ Surgical removal of cysts may be helpful for some difficult cases of neurocysticercosis and for symptomatic non-neurologic disease.
Echinococcosis History of exposure to dogs or wild canines in an endemic area. Large cystic lesions, most commonly of the liver or lung. Positive serologic tests. Clinical Findings Infections are commonly asymptomatic and may be noted incidentally on imaging studies or present with symptoms caused by an enlarging or superinfected mass. Findings may include abdominal or chest pain, biliary obstruction, cholangitis, portal hypertension, cirrhosis, bronchial obstruction leading to segmental lung collapse, and abscesses. Cyst leakage or rupture may be accompanied by a severe allergic reaction, including fever and hypotension.
Laboratory Findings ➢Serologic tests. Imaging ultrasonography, CT, and MRI. Treatment ✓ albendazole often with cautious surgical resection of cysts. ✓ When used alone, as in cases where surgery is not possible, albendazole (10–15 mg/kg/day orally) for 3 months or longer duration ✓ Mebendazole (40–50 mg/kg/day orally) is an alternative drug, and praziquantel may also be effective. In some cases, medical therapy is begun, with surgery performed if disease persists after some months of therapy. ✓ Another approach, in particular with inoperable cysts, is percutaneous aspiration, injection, and reaspiration (PAIR).
ASCARIASIS ▪ Transient cough, urticaria, pulmonary infiltrates, eosinophilia. ▪ Nonspecific abdominal symptoms. ▪ Eggs in stool; adult worms occasionally passed. Clinical Findings ▪ Most persons with Ascaris infection are asymptomatic. ▪ In a small proportion of patients, symptoms develop during migration of worms through the lungs, with fever, nonproductive cough, chest pain, dyspnea, and eosinophilia, occasionally with eosinophilic pneumonia. Rarely, larvae lodge ectopically in the brain, kidney, eye, spinal cord, and other sites and may cause local symptoms. Light intestinal infections usually produce no symptoms.
▪ With heavy infection,abdominal discomfort may be seen. Adult worms may also migrate and be coughed up, be vomited, or may emerge through the nose or anus. They may also migrate into the common bile duct, pancreatic duct, appendix, and other sites, which may lead to cholangitis, cholecystitis, pyogenic liver abscess, pancreatitis, obstructive jaundice, or appendicitis. With very heavy infestations, masses of worms may cause intestinal obstruction, volvulus, intussusception, or death. ▪ The diagnosis of ascariasis is made after adult worms emerge from the mouth, nose, or anus, or by identifying characteristic eggs in the feces, ▪ Eosinophilia is marked during worm migration but may be absent during intestinal infection.
▪ Treatment ▪ All infections should ideally be treated. Treatments of choice are ▪ albendazole (single 400-mg oral dose), ▪ mebendazole (single 500-mg oral dose or 100 mg twice daily for 3 days), or ▪ pyrantel pamoate (single 11-mg/kg oral dose, maximum 1 g). ▪ An alternative is ivermectin (single 200 mcg/kg oral dose). ▪ Surgery may be required for appendicitis and other gastrointestinal complications.
Enterobius vermicularis Clinical features Due to migration of worm -Perianal, perineal & vaginal itching (pruritis) worsens at night. Insomnia and restlessness Nocturnal enuresis Laboratory Diagnosis & Treatment Detection of adult worms in Feces Perianal region scrapings from perianal region Microscopy – non bile stained eggs Treatment Mebendazole, pyrantel pamoate
Trichuris trichiura (Whip Worm) o Site of localization Large intestine caecum Clinical features Infection – Trichuriasis Symptoms depend on worm burden Less than 10 worms – asymptomatic Heavier infections – 1. chronic profuse mucus and bloody diarrhea with abdominal pains and edematous rectum 2. malnutrition, weight loss and anemia Laboratory diagnosis & Treatment Stool examination – bile stained eggs with bipolar mucus plugs Treatment – albendazole / mebendazole
HOOK WORM DISEASE ▪ Transient pruritic skin rash and lung symptoms. ▪ Anorexia, diarrhea, abdominal discomfort. ▪ Iron deficiency anemia. ▪ Characteristic eggs and occult blood in the stool. Symptoms and Signs ▪ Most infected persons are asymptomatic. ▪ A pruritic maculopapular rash (ground itch) may occur at the site of larval penetration ▪ Pulmonary symptoms may be seen during larval migration through the lungs, with dry cough, wheezing, and low-grade fever, ▪ About 1 month after infection, as maturing worms attach to the small intestinal mucosa, gastrointestinal symptoms may develop, with epigastric pain, anorexia, and diarrhea,, and findings of marked iron-deficiency anemia and protein malnutrition.
▪ Anemia can lead to pallor, weakness, dyspnea, and heart failure, and protein loss can lead to hypoalbuminemia, edema, and ascites. ▪ Infection with the dog hookworm Ancylostoma caninum can uncommonly lead to abdominal pain, diarrhea, and eosinophilia, with intestinal ulcerations and regional lymphadenitis. Laboratory Findings ▪ eggs in feces; ▪ Microcytic anemia, occult blood in the stool, and hypoalbuminemia, esinophilia Treatment ▪ albendazole (single 400-mg oral dose) or mebendazole (100 mg orally twice daily for 3 days). ▪ Pyrantel pamoate and levamisole.
Treatment Potentially life threatening disease – treat even if its asymptomatic Thiabendazole for 2 days Disseminated strongyloidosis – 5 to 7 days
LYMPHATIC FILARIASIS ▪ Episodic attacks of lymphangitis, lymphadenitis, and fever. ▪ Chronic progressive swelling of extremities and genitals; hydrocele; chyluria; lymphedema. ▪ Microfilariae in blood, chyluria, or hydrocele fluid; ▪ positive serologic tests.
symptoms and Signs ▪ Many infections remain asymptomatic ▪ The initial manifestation of infection is often acute lymphangitis, with fever, painful lymph nodes, edema, and inflammation spreading peripherally from involved lymph nodes (in contrast to bacterial lymphangitis, which spreads centrally). ▪ Lymphangitis and lymphadenitis of the upper and lower extremities is common ▪ genital involvement, including epididymitis and orchitis, with scrotal pain and tenderness, occurs principally only with W bancrofti infection.
▪ The most common chronic manifestation of lymphatic filariasis is swelling of the extremities or genitals due to chronic lymphatic inflammation and obstruction. Extremities become increasingly swollen, with a progression over time from pitting edema, to nonpitting edema, to sclerotic changes of the skin that are referred to as elephantiasis. ▪ Tropical pulmonary eosinophilia is a distinct syndrome , it is characterized by asthma-like symptoms, with cough, wheezing, dyspnea, and low-grade fevers, usually at night. Without treatment, tropical pulmonary eosinophilia can progress to interstitial fibrosis and chronic restrictive lung disease.
Laboratory Findings ▪ microfilariae, usually in blood, but microfilariae may be absent, especially early in the disease progression (first 2–3 years) or with chronic obstructive disease. To increase yields, blood samples are obtained at about midnight in most areas, ▪ Microfilariae may also be identified in hydrocele fluid or chylous urine. ▪ Serologic tests may be helpful but cannot distinguish past and active infections. ▪ Adult worms may also be found in lymph node biopsy specimens (although biopsy is not usually clinically indicated) or by ultrasound of a scrotal hydrocele .
Treatment ▪ Single annual doses of diethylcarbamazine (6 mg/kg orally), alone or with ivermectin (400 mcg/kg orally) or albendazole (400 mg orally) may be as effective as longer courses of diethylcarbamazine. A single dose of all three drugs cleared parasites in more than 95% of persons for 3 years . ▪ doxycycline (100–200 mg/day orally for 4–6 weeks), which kills obligate intracellular Wolbachia bacteria, leading to death of adult filarial worms. ▪ Secondary bacterial infections must be treated. ▪ Surgical correction may be helpful in some cases.
Thank you

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Fungal infections to medicinestudent.pdf

  • 1.
    Fungal infections DR/ AbdoWadi Hepatologist, gastroenterologist, Endoscopist
  • 2.
  • 3.
    1. CANDIDIASIS ▪ Commonnormal flora but opportunistic pathogen. ▪ Mucosal disease, particularly vaginitis and esophagitis. ▪ Risk factors for fungemia: neutropenia, intravenous catheter, abdominal surgery, total parenteral nutrition, kidney disease, broad-spectrum antibiotics.
  • 4.
    Clinical Findings A. MucosalCandidiasis ▪ Esophageal involvement is the most frequent type of significant mucosal disease. ▪ Presenting symptoms include substernal odynophagia, gastroesophageal reflux, or nausea without substernal pain. ▪ Oral candidiasis, though often associated, is not invariably present. Diagnosis is best confirmed by endoscopy with biopsy and culture.
  • 5.
    B - Vulvovaginalcandidiasis occurs in an estimated 75% of women during their lifetime. Risk factors include pregnancy, uncontrolled diabetes mellitus, broad-spectrum antimicrobial treatment, corticosteroid use, and HIV infection. Symptoms include acute vulvar pruritus, burning vaginal discharge, and dyspareunia. Candidal Funguria Most cases of candidal funguria are asymptomatic and represent specimen contamination or bladder colonization. However, symptoms and signs of true Candida urinary tract infections are indistinguishable from bacterial urinary tract infections and can include urgency, hesitancy, fever, chills, or flank pain.
  • 6.
    C. Invasive Candidiasis (1)candidemia (bloodstream infection) without deep seated infection; (2) (candidemia with deep-seated infection (typically eyes, kidney, or abdomen); (3) deep-seated candidiasis in the absence of bloodstream infection. Varying ratios of these clinical entities depends on the predominating risk factors for affected patients (ie, neutropenia, dialysis, postsurgical).
  • 7.
    ▪ The clinicalpresentation of candidemia varies from minimal fever to septic shock that can resemble a severe bacterial infection. ▪ Hepatosplenic candidiasis can occur following prolonged neutropenia in patients with underlying hematologic cancers, but this entity is less common in the era of widespread antifungal prophylaxis. ▪ Typically, fever and variable abdominal pain present weeks after chemotherapy, when neutrophil counts have recovered
  • 8.
    D. Candidal Endocarditis ▪is a rare infection affecting patients with prosthetic heart valves or prolonged candidemia, such as with indwelling catheters. ▪ The diagnosis is established definitively by culturing Candida from emboli or from vegetations at the time of valve replacement.
  • 9.
    Treatment Mucosal Candidiasis Therapy ofesophageal candidiasis depends on the severity of disease. fluconazole, itraconazole intravenous voriconazole, intravenous amphotericin B, intravenous caspofungin, intravenous anidulafungin, intravenous micafungin, Posaconazole tablets, -
  • 10.
    Vulvovaginal candidiasis topical azolepreparations (eg, clotrimazole, miconazole, Fluconazole Candidal Funguria fluconazole, Invasive Candidiasis echinocandin such as caspofungin micafungin or anidulafungin Fluconazole intravenously, A dilated fundoscopic examination is recommended for patients with candidemia to exclude endophthalmitis.
  • 11.
    2. HISTOPLASMOSIS ▪ Exposureto bird and bat droppings; common along river valleys (especially Ohio River and the Mississippi River valleys). ▪ Most patients asymptomatic; ▪ respiratory illness most common clinical problem. ▪ Disseminated disease common in AIDS or other immunosuppressed states; with poor prognosis. ▪ Blood and bone marrow cultures and urine polysaccharide antigen are useful in diagnosis of disseminated disease.
  • 12.
    Clinical Findings ▪ Mostcases of histoplasmosis are asymptomatic or mild and thus go unrecognized. Past infection is recognized by pulmonary and splenic calcification noted on incidental radiographs. ▪ Symptomatic infection may present with mild influenza-like illness, often lasting 1–4 days. Moderately severe infections are frequently diagnosed as atypical pneumonia. These patients have fever, cough, and mild central chest pain lasting 5–15 days. Clinically evident infections occur in several forms:
  • 13.
    (1) Acute pulmonaryhistoplasmosis. ▪ Clinical manifestations can vary from a mild influenza like illness to severe pneumonia. The illness may last from 1 week to 6 months but is almost never fatal. (2) Progressive disseminated histoplasmosis ▪ is commonly seen in patients with underlying HIV infection (with CD4 cell counts usually less than 100 cells/mcL) or other conditions of impaired cellular immunity. ▪ It is characterized by fever and multiple organ system involvement. ▪ Chest radiographs may show a miliary pattern. ▪ Presentation may be fulminant, simulating septic shock, with death ensuing rapidly unless treatment is provided. ▪ Symptoms usually consist of fever, dyspnea, cough, loss of weight, and prostration. ▪ Ulcers of the mucous membranes of the oropharynx may be present.
  • 14.
    (3) Chronic pulmonaryhistoplasmosis is usually seen in older patients who have underlying chronic lung disease. Chest radiographs show various lesions including complex apical cavities, infiltrates, and nodules. (4) Complications of pulmonary histoplasmosis include granulomatous mediastinitis characterized by persistently enlarged mediastinal lymph nodes and fibrosing mediastinitis in which an excessive fibrotic response to Histoplasma infection results in compromise of pulmonary vascular structures.
  • 15.
    Laboratory Findings ▪ Mostpatients with chronic pulmonary disease show anemia of chronic disease. Bone marrow involvement with pancytopenia may be prominent in disseminated forms. ▪ Marked lactate dehydrogenase (LD) and ferritin elevations are also common, as are mild elevations of serum aspartate aminotransferase. ▪ With pulmonary involvement, sputum culture is rarely positive except in chronic disease; antigen testing of bronchoalveolar lavage fluid may be helpful in acute disease. The combination of a first morning urine and serum polysaccharide antigen assays has an 83% sensitivity for the diagnosis of acute pulmonary histoplasmosis. ▪ Blood or bone marrow cultures from immunocompromised patients with acute disseminated disease are positive more than 80% of the time, but may take several weeks for growth. ▪ The urine antigen assay has a sensitivity of greater than 90% for disseminated disease in immunocompromised patients and a declining titer can be used to follow response to therapy. ▪ Diagnosis of CNS disease requires antigen and antibody testing of the cerebrospinal fluid (CSF) and serum as well as urine antigen testing.
  • 16.
    Treatment ▪ For progressivelocalized disease and for mild to moderately severe nonmeningeal disseminated disease in immunocompetent or immunocompromised patients, itraconazole, 200– 400 mg/day orally divided into two doses, ▪ Duration of therapy ranges from weeks to several months depending on the severity of illness. ▪ Intravenous liposomal amphotericin B, 3 mg/kg/day, is used in patients with more severe illness such as meningitis.
  • 17.
    3. COCCIDIOIDOMYCOSIS ▪ Influenza-likeillness during acute infection: malaise, fever, backache, headache, and cough. ▪ Erythema nodosum common with acute infection. ▪ Dissemination may result in meningitis, bony lesions, or skin and soft tissue abscesses. ▪ Chest radiograph findings vary from pneumonitis to cavitation. ▪ Serologic tests useful; large spherules containing endospores demonstrable in sputum or tissues.
  • 18.
    Clinical Findings ▪ Symptomsof primary coccidioidomycosis occur in about 40% of infections. Symptom onset (after an incubation period of 10–30 days) is usually that of a respiratory tract illness with fever and occasionally chills. ▪ Coccidioidomycosis is a common, frequently unrecognized, etiology of community-acquired pneumonia in endemic areas. ▪ Erythema nodosum may appear 2–20 days after onset of symptoms. Persistent pulmonary lesions, varying from cavities and abscesses to parenchymal nodular densities or bronchiectasis, occur in about 5% of diagnosed cases. ▪ Disseminated disease occurs in about 0.1% of white and 1% of nonwhite patients. ▪ Any organ may be involved. Pulmonary findings usually become more pronounced, with mediastinal lymph node enlargement, cough, and increased sputum production. Lung abscesses may rupture into the pleural space, producing an empyema
  • 19.
    ▪ Complicated skinand bone infections may develop. ▪ Fungemia may occur and is characterized clinically by a diffuse miliary pattern on chest radiograph and by early death. The course may be particularly rapid in immunosuppressed patients. ▪ Meningitis occurs in 30–50% of cases of dissemination and may result in chronic basilar meningitis. Subcutaneous abscesses and verrucous skin lesions are especially common in fulminating cases. ▪ HIV -infected persons with disseminated disease have a higher incidence of miliary infiltrates, lymphadenopathy, and meningitis, but skin lesions are uncommon.
  • 20.
    Laboratory Findings ▪ Inprimary coccidioidomycosis, there may be moderate leukocytosis and eosinophilia. ▪ Serologic testing (ELISA) detect IgM antibodies ▪ Patients in whom coccidioidomycosis is diagnosed should undergo evaluation for meningeal involvement when CNS symptoms or neurologic signs are present. Demonstrable complement-fixing antibodies in spinal fluid are diagnostic of coccidioidal meningitis.. ▪ spinal fluid findings include increased cell count with lymphocytosis and reduced glucose. Spinal fluid culture is positive in approximately 30% of meningitis cases.
  • 21.
    Imaging ▪ patchy, nodular,and lobar upper lobe pulmonary infiltrates are most common. ▪ Hilar lymphadenopathy may be visible and is seen in localized disease; ▪ mediastinal lymphadenopathy suggests dissemination. Treatment ▪ Itraconazole, ▪ fluconazole, ▪ For progressive pulmonary or extrapulmonary disease, liposomal amphotericin B intravenously is used ▪ lumbar or cisternal intrathecal administration of amphotericin B daily ▪ Systemic therapy with liposomal amphotericin B, 3–5 mg/kg/day intravenously, is generally given concurrently with intrathecal therapy,
  • 22.
    4. PNEUMOCYSTOSIS (Pneumocystisjirovecii Pneumonia) ▪ Fever, dyspnea, dry cough, hypoxia. ▪ Often only slight lung physical findings. ▪ Chest radiograph: diffuse interstitial disease or normal. ▪ P jirovecii in sputum, bronchoalveolar lavage fluid, or lung tissue; PCR of bronchoalveolar lavage; (1,3)-beta-D-glucan in blood. ▪
  • 23.
    Clinical Findings ▪ Findingsare usually limited to the pulmonary parenchyma. In the sporadic form of the disease associated with deficient cell- mediated immunity, the onset may be subacute, characterized by dyspnea on exertion and nonproductive cough, many patients have bibasilar crackles. ▪ Without treatment, the course is usually one of rapid deterioration and death. Adult patients may present with spontaneous pneumothorax, usually in patients with previous episodes or those receiving aerosolized pentamidine prophylaxis. ▪ Patients with AIDS will usually have other evidence of HIV associated disease, including fever, fatigue, and weight loss, for weeks or months preceding the illness.
  • 24.
    Laboratory Findings ▪ Chestradiographs most often show diffuse “interstitial” infiltration, ▪ High-resolution chest CT scans may be quite suggestive of P jirovecii pneumonia, helping distinguish it from other causes of pneumonia. ▪ Arterial blood gas determinations usually show hypoxemia with hypocapnia. ▪ (PCR) of bronchoalveolar lavage, negative PCR from bronchoalveolar lavage rules out disease. ▪ Open lung biopsy and needle lung biopsy
  • 25.
    Treatment ▪ Trimethoprim-Sulfamethoxazole ▪ Primaquine/Clindamycin ▪. Pentamidine Isethionate ▪ Atovaquone ▪ Prednisone
  • 26.
    5. CRYPTOCOCCOSIS ▪ Mostcommon cause of fungal meningitis. ▪ Predisposing factors: chemotherapy for hematologic malignancies, Hodgkin lymphoma, corticosteroid therapy, transplant recipients, TNF-alpha inhibitor therapy, and HIV infection. ▪ Headache, abnormal mental status; meningismus seen occasionally, though rarely in HIV -infected patients. ▪ Demonstration of capsular polysaccharide antigen or positive culture in CSF is diagnostic.
  • 27.
    Clinical Findings ▪ Pulmonarydisease ranges from simple nodules to widespread infiltrates leading to respiratory failure. ▪ Disseminated disease may involve any organ, but CNS disease predominates. ▪ Headache is usually the first symptom of meningitis. Confusion and other mental status changes as well as cranial nerve abnormalities, nausea, and vomiting may be seen as the disease progresses. ▪ Nuchal rigidity and meningeal signs occur about 50% of the time but are uncommon in HIV -infected patients. ▪ Communicating hydrocephalus may complicate the course. ▪ Paradoxical clinical worsening associated with improved immunologic status has been reported in HIV -positive and transplant patients with cryptococcosis; this entity has been labeled the immune reconstitution inflammatory syndrome (IRIS).
  • 28.
    Laboratory Findings ▪ Respiratorytract disease is diagnosed by culture of respiratory secretions or pleural fluid. ▪ For suspected meningeal disease, lumbar puncture is the preferred diagnostic procedure. Spinal fluid findings include increased opening pressure, variable pleocytosis, increased protein, and decreased glucose, ▪ Gram stain of the CSF usually reveals budding, encapsulated fungi. ▪ Cryptococcal capsular antigen in CSF and culture together establish the diagnosis over 90% of the time.
  • 29.
    ▪ Patients withAIDS often have the antigen in both CSF and serum, and extrameningeal disease (lungs, blood, urinary tract) is common. ▪ In patients with AIDS, the serum cryptococcal antigen is also a sensitive screening test for meningitis, being positive in over 95% of cases. ▪ MRI is more sensitive than CT in finding CNS abnormalities such as cryptococcomas.
  • 30.
    Treatment ▪ Liposomal amphotericinB, 3–4 mg/kg/day intravenously for 14 days, is the preferred agent for induction therapy, followed by an additional 8 weeks of fluconazole, 400 mg/day orally , The addition of flucytosine has been associated with improved survival ▪ Fluconazole (800–1200 mg orally daily) may be given with amphotericin B . ▪ Frequent, repeated lumbar punctures or ventricular shunting should be performed to relieve high CSF pressures or if hydrocephalus is a complication.
  • 31.
    6. ASPERGILLOSIS ▪ Mostcommon cause of non-candidal invasive fungal infection in transplant recipients and in patients with hematologic malignancies. ▪ Predisposing factors: leukemia, bone marrow or organ transplant, late HIV infection. ▪ Pulmonary, sinus, and CNS are most common disease sites. ▪ Detection of galactomannan by ELISA or PCR in serum or other body fluids is useful for early diagnosis and treatment.
  • 32.
    Clinical Findings 1. Allergicforms of aspergillosis—Allergic bronchopulmonary aspergillosis (ABPA) occurs in patients with preexisting asthma or cystic fibrosis who develop worsening bronchospasm and fleeting pulmonary infiltrates accompanied by eosinophilia, high levels of IgE, and IgG Aspergillus precipitins in the blood. Allergic aspergillus sinusitis produces a chronic sinus inflammation characterized by eosinophilic mucus and noninvasive hyphal elements.
  • 33.
    Clinical Findings 2. Chronicaspergillosis—Chronic pulmonary aspergillosis produces a spectrum of disease that usually occurs when there is preexisting lung damage but not significant immunocompromise. Disease manifestations range from aspergillomas that develop in a lung cavity to chronic fibrosing pulmonary aspergillosis in which the majority of lung tissue is replaced with fibrosis. Long-standing (longer than 3 months) pulmonary and systemic symptoms such as cough, shortness of breath, weight loss, and malaise are common.
  • 34.
    3. Invasive aspergillosis—Invasiveaspergillosis ▪ most commonly occurs in profoundly immunodeficient patients, such as those who have undergone hematopoietic stem cell transplantation or have prolonged, severe neutropenia, but it can occur among critically ill immunocompetent patients as well. ▪ Specific risk factors in patients who have undergone a hematopoietic stem cell transplant include cytopenias, corticosteroid use, iron overload, cytomegalovirus disease, and graft-versus-host disease. ▪ Pulmonary disease is most common, with patchy infiltration leading to a severe necrotizing pneumonia. Invasive sinus disease also occurs.
  • 35.
    Laboratory Findings ▪ Thereis eosinophilia, high levels of total IgE, and IgE and IgG specific for Aspergillus in the blood of patients with ABPA. ▪ Detection of galactomannan by ELISA or Aspergillus DNA by PCR, or both, has been used for the early diagnosis of invasive disease, . ▪ Galactomannan levels and Aspergillus DNA PCR can be tested in serum or in bronchoalveolar lavage fluid, which may be more sensitive than serum. ▪ Higher galactomannan levels are correlated with increased mortality, and failure of galactomannan levels to fall in response to therapy portends a worse outcome. ▪ CT scan of the chest may show characteristics quite suggestive of invasive aspergillosis (eg, “halo sign,” which is a zone of diminution of ground glass around a consolidation).
  • 36.
    Treatment 1. Allergic formsof aspergillosis ▪ Itraconazole, corticosteroids or Voriconazole. 2. Chronic aspergillosis ▪ The most effective therapy for symptomatic aspergilloma remains surgical resection, other forms of chronic aspergillosis are generally treated with at least 4–6 months of oral azole , itraconazole , voriconazole or posaconazole 3. Invasive aspergillosis ▪ voriconazole ▪ anidulafungin . ▪ Isavuconazole ▪ voriconazole. ▪ amphotericin B . ▪ caspofungin ▪ posaconazole oral tablets
  • 37.
    7. MUCORMYCOSIS ▪ Mostcommon cause of non-Aspergillus invasive mold infection ▪ Predisposing factors: poorly controlled diabetes, leukemia, transplant recipient, wound contamination by soil. ▪ Pulmonary, rhinocerebral, and skin are most common disease sites. ▪ Rapidly fatal without multidisciplinary interventions. Clinical Findings ▪ Invasive disease of the sinuses, orbits, and the lungs may occur. Necrosis is common due to hyphal tissue invasion that may manifest as ulceration of the hard palate or nasal palate or hemoptysis. ▪ Widely disseminated disease can occur. ▪ A reverse “halo sign” (focal area of ground glass diminution surrounded by a ring of consolidation) may be seen on chest CT. ▪ Biopsy of involved tissue remains the cornerstone of
  • 38.
    Treatment ▪ Reversal ofpredisposing conditions (if possible). ▪ surgical debridement, and prompt antifungal therapy. ▪ A prolonged course of a lipid preparation of intravenous liposomal amphotericin B (5 mg/kg with higher doses possibly given for CNS disease) should be started early . ▪ posaconazole
  • 39.
    8. BLASTOMYCOSIS ▪ Chronicpulmonary infection is most common and may be asymptomatic. ▪ When dissemination takes place, lesions are most frequently seen in the skin, bones, and urogenital system. ▪ Cough, moderate fever, dyspnea, and chest pain are common. These may resolve or progress, with purulent sputum production, pleurisy, fever, chills, loss of weight, and prostration. ▪ Radiologic studies, either chest radiographs or CT scans, usually reveal lobar consolidation or masses. ▪ Raised, verrucous cutaneous lesions are commonly present in disseminated blastomycosis. ▪ Bones—often the ribs and vertebrae—are frequently involved. Epididymitis, prostatitis, and other involvement of the male urogenital system may occur.
  • 40.
    ▪ infection inHIV -infected persons may progress rapidly, with dissemination common. Laboratory findings usually include leukocytosis and anemia, though these are not specific. ▪ The organism is found in clinical specimens, It grows readily on culture. ▪ A urinary antigen test is available. ▪ Itraconazole, 200–400 mg/day orally for at least 6–12 months, is the therapy of choice for non meningeal disease, with a response rate of over 80% (Table 36–1). ▪ Liposomal amphotericin B, 3–5 mg/kg/day intravenously, is given initially for severe disease.
  • 41.
  • 42.
    ▪ TREMATODE (FLUKE)INFECTIONS ✓ SCHISTOSOMIASIS (Bilharziasis) ▪ LIVER, LUNG, & INTESTINAL FLUKES ✓ FASCIOLIASIS ✓ CLONORCHIASIS & OPISTHORCHIASIS ✓ PARAGONIMIASIS ✓ INTESTINAL FLUKES ▪ CESTODE INFECTIONS ▪ NONINVASIVE CESTODE INFECTIONS ✓ Beef Tapeworm ✓ Pork Tapeworm ✓ Fish Tapeworm ✓ Dwarf Tapeworm ▪ INVASIVE CESTODE INFECTIONS ✓ Cysticercosis ✓ Echinococcosis
  • 43.
    ▪ INTESTINAL NEMATODE(Roundworm) INFECTIONS ✓ ASCARIASIS ✓ TRICHURIASIS ✓ HOOKWORM DISEASE ✓ STRONGYLOIDIASIS ✓ ENTEROBIASIS ▪ INVASIVE NEMATODE (Roundworm) INFECTIONS ✓ TRICHINOSIS ✓ TOXOCARIASIS ✓ CUTANEOUS LARVA MIGRANS (Creeping Eruption) ▪ FILARIASIS ✓ LYMPHATIC FILARIASIS ✓ ONCHOCERCIASIS ✓ LOIASIS
  • 44.
    ▪ (Bilharziasis) ✓History offreshwater exposure in an endemic area. ✓ Acute schistosomiasis: fever, headache, myalgias, cough, urticaria, diarrhea, and eosinophilia. ✓Intestinal schistosomiasis: abdominal pain, diarrhea, and hepatomegaly, progressing to anorexia, weight loss, and features of portal hypertension. ✓urinary schistosomiasis: hematuria and dysuria, progressing to hydronephrosis and urinary infections. ✓Diagnosis: characteristic eggs in feces or urine; biopsy of rectal or bladder mucosa; positive serology. ✓
  • 45.
    ▪ clinical features ✓dermatitis—Followingcercarial penetration, localized erythema develops in some individuals, which can progress to a pruritic maculopapular rash that persists for some days. ✓Acute schistosomiasis (Katayama syndrome)—A febrile illness may develop 2–8 weeks after exposure in persons without prior infection, most commonly Presenting symptoms and signs include acute onset of fever; headache; myalgias; cough; malaise; urticaria; diarrhea, which may be bloody; hepatosplenomegaly; lymphadenopathy; and pulmonary infiltrates. Localized lesions may occasionally cause severe manifestations, including CNS abnormalities and death. Acute schistosomiasis usually resolves in 2–8 weeks.
  • 46.
    ▪ Chronic schistosomiasis ✓Many infected persons have light infections and are asymptomatic, but an estimated 50–60% have symptoms and 5–10% have advanced organ damage. ✓ Symptomatic patients with intestinal schistosomiasis typically experience abdominal pain, fatigue, diarrhea, and hepatomegaly. Over years, anorexia, weight loss, weakness, colonic polyps, and features of portal hypertension develop. ✓ Late manifestations include hematemesis from esophageal varices, hepatic failure, and pulmonary hypertension. ✓ Urinary schistosomiasis may present within months of infection with hematuria and dysuria, . ✓ Fibrotic changes in the urinary tract can lead to hydroureter, hydronephrosis, bacterial urinary infections and, ultimately, kidney disease or bladder cancer.
  • 47.
    ▪ Laboratory investigation ✓Microscopic examination of stool or urine for eggs, ✓ serologic tests ✓ Diagnosis can also be made by biopsy of the rectum, colon, liver, or bladder. ✓ Point-of-care assays to detect circulating schistosome antigens in serum and urine are also available;. ✓ In acute schistosomiasis, leukocytosis and marked eosinophilia may occur; ✓ With a diagnosis of schistosomiasis, evaluation for the extent of disease is warranted, including liver function studies and imaging of the liver with intestinal disease and ultrasound or other imaging studies of the urinary system in urinary disease.
  • 48.
    ▪ Treatment ✓ Thedrug of choice for schistosomiasis is praziquantel. The drug is administered for 1 day at an oral dose of 40 mg/kg (in one or two doses) for S mansoni, S haematobium, and a dose of 60 mg/kg (in two or three doses) for S japonicum and S mekongi.
  • 49.
    FASCIOLIASIS ▪ Infection byFasciola hepatica, the sheep liver fluke, results from ingestion of encysted metacercariae on watercress or other aquatic vegetables. ▪ Infection is prevalent in sheep-raising areas in many countries, especially parts of South America, the Middle East, and southern Europe, and it has increasingly been recognized in travelers to these areas. ▪ Fasciola gigantica has a more restricted distribution in Asia and Africa and causes similar findings. Eggs are passed from host feces into freshwater, leading to infection of snails, and then deposition of metacercariae on vegetation.
  • 50.
    ▪ In humans,metacercariae excyst, penetrate into the peritoneum, migrate through the liver, and mature in the bile ducts, where they cause local necrosis and abscess formation. ▪ Two clinical syndromes are seen, related to acute migration of worms and chronic infection of the biliary tract. ▪ Symptoms related to migration of larvae present 6–12 weeks after ingestion. Typical findings are abdominal pain, fever, malaise, weight loss, urticaria, eosinophilia, and leukocytosis. Tender hepatomegaly and elevated liver biochemical tests may be seen. Rarely, migration to other organs may lead to localized disease.
  • 51.
    ▪ CT andother imaging studies show hypodense migratory lesions of the liver. Definitive diagnosis is made by the identification of characteristic eggs in stool. ▪ In chronic infection, imaging studies show masses obstructing the extrahepatic biliary tract. Serologic assays have sensitivity and specificity greater than 90%, but cannot distinguish between past and current infection. ▪ The treatment of choice is triclabendazole, Standard dosing of 10 mg/kg orally in a single dose or two doses over 12 hours achieves a cure rate of about 80%, but repeat dosing is indicated if abnormal radiologic findings or eosinophilia do not resolve. ▪ The second-line drug for fascioliasis is bithionol (30–50 mg/kg/day orally in three divided doses on alternate days for 10–15 days).
  • 52.
    INTESTINAL FLUKES ▪ Thelarge intestinal fluke, Fasciolopsis buski. Eggs shed in stools hatch in freshwater, followed by infection of snails, and release of cercariae that encyst on aquatic plants. Humans are infected by eating uncooked plants, ▪ Adult flukes mature in about 3 months and live in the small intestine attached to the mucosa, leading to local inflammation and ulceration. ▪ Other intestinal flukes that cause similar syndromes include Heterophyes (North Africa and Turkey) and Metagonimus (East Asia) species; these species are transmitted by undercooked freshwater fish. Infections with intestinal flukes are often asymptomatic, although eosinophilia maybe marked.
  • 53.
    ▪ In symptomaticcases, after an incubation period of 1–2 months, manifestations include epigastric pain and diarrhea. Other gastrointestinal symptoms, ileus, edema, and ascites may be seen uncommonly. ▪ Diagnosis is based on identification of characteristic eggs or adult flukes in the stool. ▪ The drug of choice is praziquantel, 25 mg/kg orally as a single dose. Alternative therapies are triclabendazole and niclosamide (for most species).
  • 54.
    NONINVASIVE CESTODE INFECTIONS 1.Beef Tapeworm Infection is most common in cattle breeding areas. Humans are the definitive host. Gravid segments of T saginata are passed in human feces to soil, where they are ingested by grazing animals, especially cattle. The eggs then hatch to release embryos that encyst in muscle as cysticerci. Humans are infected by eating raw or undercooked infected beef. Most individuals infected with T saginata are asymptomatic, but abdominal pain and other gastrointestinal symptoms may be present. Eosinophilia is common. The most common presenting finding is the passage of proglottids in the stool.
  • 55.
    2. Pork Tapeworm Tsolium is transmitted to pigs that ingest human feces. Humans can be either the definitive host (after consuming undercooked pork, leading to tapeworm infection) or the intermediate host (after consuming food contaminated with human feces containing T solium eggs, leading to cysticercosis, which is discussed under Invasive Cestode Infections). As with the beef tapeworm, infection with T solium adult worms is generally asymptomatic, but gastrointestinal symptoms may occur. Infection is generally recognized after passage of proglottids. Autoinfection with eggs can progress to cysticercosis.
  • 56.
    3. Fish TapewormInfection with D latum follows ingestion of undercooked freshwater fish, most commonly in temperate regions. Eggs from human feces are taken up by crustaceans, these are eaten by fish, which are then infectious to humans. Infection with multiple worms over many years can occur. Infections are most commonly asymptomatic, but nonspecific gastrointestinal symptoms, including diarrhea, may occur. Diagnosis usually follows passage of proglottids. Prolonged heavy infection can lead to megaloblastic anemia and neuropathy from vitamin B12 deficiency, which is due to infection-induced dissociation of the vitamin from intrinsic factor and to utilization of the vitamin by worms.
  • 57.
    4. Dwarf Tapeworm Hnana is the only tapeworm that can be transmitted between humans. Infections are common in warm areas, especially with poor hygiene and institutionalized populations. Infection follows ingestion of food contaminated with human feces. Eggs hatch in the intestines, where oncospheres penetrate the mucosa, encyst as cysticercoid larvae, and then rupture after about 4 days to release adult worms. Autoinfection can lead to amplification of infection. Infection with H nana, the related rodent tapeworm H diminuta, or the dog tapeworm D caninum can also follow accidental ingestion of infected insects. H nana are dwarf in size relative to other tapeworms but can reach 5 cm in length. Heavy infection is common, especially in children, and can be accompanied by abdominal discomfort, anorexia, and diarrhea.
  • 58.
    Diagnosis is usually madebased on the identification of characteristic eggs or proglottids in stool. Egg release may be irregular, so examination of multiple specimens or concentration techniques may be needed. Treatment A single dose of praziquantel (5–10 mg/kg orally) is highly effective. The alternative therapy for these infections is niclosamide. A single dose of niclosamide (2 g chewed) is effective For H nana, therapy is continued daily for 1 week.
  • 59.
    Cysticercosis ▪ Exposure toT solium through fecal contamination of food. Focal CNS lesions; seizures, headache. ▪ Brain imaging shows cysts; positive serologic tests. Clinical Findings ▪ Neurocysticercosis can cause intracerebral, subarachnoid, and spinal cord lesions and intraventricular cysts. Single or multiple lesions may be present. Lesions may persist for years before symptoms develop, generally due to local inflammation or ventricular obstruction. Presenting symptoms include seizures, focal neurologic deficits, altered cognition, and psychiatric disease. Symptoms develop more quickly with intraventricular cysts, with findings of hydrocephalus and meningeal irritation, including severe headache, vomiting,
  • 60.
    A particularly aggressiveform of the disease, racemose cysticercosis, involves proliferation of cysts at the base of the brain, leading to alterations of consciousness and death. Spinal cord lesions can present with progressive focal findings. Cysticercosis of other organ systems is usually clinically benign. Involvement of muscles can uncommonly cause discomfort and is identified by radiographs of muscle showing multiple calcified lesions. Subcutaneous involvement presents with multiple painless palpable skin lesions. Involvement of the eyes can present with ptosis due to extraocular muscle involvement or intraocular abnormalities.
  • 61.
    Laboratory Findings andImaging Diagnosis ▪ CSF examination may show lymphocytic or eosinophilic pleocytosis, decreased glucose, and elevated protein ▪ Serology. ▪ With neuroimaging by CT or MRI, multiple parenchymal cysts are most typically seen. Parenchymal calcification is also common. Treatment ▪ albendazole (10–15 mg/kg/day orally for 8 days) ▪ praziquantel (50 mg/kg/day orally for 15–30 days). Combining albendazole plus praziquantel improved outcomes compared to albendazole alone in patients with multiple viable intraparenchymal cysts. ▪ Corticosteroids ▪ Anticonvulsant therapy is provided if needed. ▪ shunting is performed if required for elevated intracranial pressure. ▪ Surgical removal of cysts may be helpful for some difficult cases of neurocysticercosis and for symptomatic non-neurologic disease.
  • 62.
    Echinococcosis History of exposureto dogs or wild canines in an endemic area. Large cystic lesions, most commonly of the liver or lung. Positive serologic tests. Clinical Findings Infections are commonly asymptomatic and may be noted incidentally on imaging studies or present with symptoms caused by an enlarging or superinfected mass. Findings may include abdominal or chest pain, biliary obstruction, cholangitis, portal hypertension, cirrhosis, bronchial obstruction leading to segmental lung collapse, and abscesses. Cyst leakage or rupture may be accompanied by a severe allergic reaction, including fever and hypotension.
  • 63.
    Laboratory Findings ➢Serologic tests. Imaging ultrasonography,CT, and MRI. Treatment ✓ albendazole often with cautious surgical resection of cysts. ✓ When used alone, as in cases where surgery is not possible, albendazole (10–15 mg/kg/day orally) for 3 months or longer duration ✓ Mebendazole (40–50 mg/kg/day orally) is an alternative drug, and praziquantel may also be effective. In some cases, medical therapy is begun, with surgery performed if disease persists after some months of therapy. ✓ Another approach, in particular with inoperable cysts, is percutaneous aspiration, injection, and reaspiration (PAIR).
  • 64.
    ASCARIASIS ▪ Transient cough,urticaria, pulmonary infiltrates, eosinophilia. ▪ Nonspecific abdominal symptoms. ▪ Eggs in stool; adult worms occasionally passed. Clinical Findings ▪ Most persons with Ascaris infection are asymptomatic. ▪ In a small proportion of patients, symptoms develop during migration of worms through the lungs, with fever, nonproductive cough, chest pain, dyspnea, and eosinophilia, occasionally with eosinophilic pneumonia. Rarely, larvae lodge ectopically in the brain, kidney, eye, spinal cord, and other sites and may cause local symptoms. Light intestinal infections usually produce no symptoms.
  • 65.
    ▪ With heavyinfection,abdominal discomfort may be seen. Adult worms may also migrate and be coughed up, be vomited, or may emerge through the nose or anus. They may also migrate into the common bile duct, pancreatic duct, appendix, and other sites, which may lead to cholangitis, cholecystitis, pyogenic liver abscess, pancreatitis, obstructive jaundice, or appendicitis. With very heavy infestations, masses of worms may cause intestinal obstruction, volvulus, intussusception, or death. ▪ The diagnosis of ascariasis is made after adult worms emerge from the mouth, nose, or anus, or by identifying characteristic eggs in the feces, ▪ Eosinophilia is marked during worm migration but may be absent during intestinal infection.
  • 66.
    ▪ Treatment ▪ Allinfections should ideally be treated. Treatments of choice are ▪ albendazole (single 400-mg oral dose), ▪ mebendazole (single 500-mg oral dose or 100 mg twice daily for 3 days), or ▪ pyrantel pamoate (single 11-mg/kg oral dose, maximum 1 g). ▪ An alternative is ivermectin (single 200 mcg/kg oral dose). ▪ Surgery may be required for appendicitis and other gastrointestinal complications.
  • 67.
    Enterobius vermicularis Clinical features Dueto migration of worm -Perianal, perineal & vaginal itching (pruritis) worsens at night. Insomnia and restlessness Nocturnal enuresis Laboratory Diagnosis & Treatment Detection of adult worms in Feces Perianal region scrapings from perianal region Microscopy – non bile stained eggs Treatment Mebendazole, pyrantel pamoate
  • 68.
    Trichuris trichiura (WhipWorm) o Site of localization Large intestine caecum Clinical features Infection – Trichuriasis Symptoms depend on worm burden Less than 10 worms – asymptomatic Heavier infections – 1. chronic profuse mucus and bloody diarrhea with abdominal pains and edematous rectum 2. malnutrition, weight loss and anemia Laboratory diagnosis & Treatment Stool examination – bile stained eggs with bipolar mucus plugs Treatment – albendazole / mebendazole
  • 69.
    HOOK WORM DISEASE ▪Transient pruritic skin rash and lung symptoms. ▪ Anorexia, diarrhea, abdominal discomfort. ▪ Iron deficiency anemia. ▪ Characteristic eggs and occult blood in the stool. Symptoms and Signs ▪ Most infected persons are asymptomatic. ▪ A pruritic maculopapular rash (ground itch) may occur at the site of larval penetration ▪ Pulmonary symptoms may be seen during larval migration through the lungs, with dry cough, wheezing, and low-grade fever, ▪ About 1 month after infection, as maturing worms attach to the small intestinal mucosa, gastrointestinal symptoms may develop, with epigastric pain, anorexia, and diarrhea,, and findings of marked iron-deficiency anemia and protein malnutrition.
  • 70.
    ▪ Anemia canlead to pallor, weakness, dyspnea, and heart failure, and protein loss can lead to hypoalbuminemia, edema, and ascites. ▪ Infection with the dog hookworm Ancylostoma caninum can uncommonly lead to abdominal pain, diarrhea, and eosinophilia, with intestinal ulcerations and regional lymphadenitis. Laboratory Findings ▪ eggs in feces; ▪ Microcytic anemia, occult blood in the stool, and hypoalbuminemia, esinophilia Treatment ▪ albendazole (single 400-mg oral dose) or mebendazole (100 mg orally twice daily for 3 days). ▪ Pyrantel pamoate and levamisole.
  • 72.
    Treatment Potentially life threateningdisease – treat even if its asymptomatic Thiabendazole for 2 days Disseminated strongyloidosis – 5 to 7 days
  • 73.
    LYMPHATIC FILARIASIS ▪ Episodicattacks of lymphangitis, lymphadenitis, and fever. ▪ Chronic progressive swelling of extremities and genitals; hydrocele; chyluria; lymphedema. ▪ Microfilariae in blood, chyluria, or hydrocele fluid; ▪ positive serologic tests.
  • 74.
    symptoms and Signs ▪Many infections remain asymptomatic ▪ The initial manifestation of infection is often acute lymphangitis, with fever, painful lymph nodes, edema, and inflammation spreading peripherally from involved lymph nodes (in contrast to bacterial lymphangitis, which spreads centrally). ▪ Lymphangitis and lymphadenitis of the upper and lower extremities is common ▪ genital involvement, including epididymitis and orchitis, with scrotal pain and tenderness, occurs principally only with W bancrofti infection.
  • 75.
    ▪ The mostcommon chronic manifestation of lymphatic filariasis is swelling of the extremities or genitals due to chronic lymphatic inflammation and obstruction. Extremities become increasingly swollen, with a progression over time from pitting edema, to nonpitting edema, to sclerotic changes of the skin that are referred to as elephantiasis. ▪ Tropical pulmonary eosinophilia is a distinct syndrome , it is characterized by asthma-like symptoms, with cough, wheezing, dyspnea, and low-grade fevers, usually at night. Without treatment, tropical pulmonary eosinophilia can progress to interstitial fibrosis and chronic restrictive lung disease.
  • 76.
    Laboratory Findings ▪ microfilariae,usually in blood, but microfilariae may be absent, especially early in the disease progression (first 2–3 years) or with chronic obstructive disease. To increase yields, blood samples are obtained at about midnight in most areas, ▪ Microfilariae may also be identified in hydrocele fluid or chylous urine. ▪ Serologic tests may be helpful but cannot distinguish past and active infections. ▪ Adult worms may also be found in lymph node biopsy specimens (although biopsy is not usually clinically indicated) or by ultrasound of a scrotal hydrocele .
  • 77.
    Treatment ▪ Single annualdoses of diethylcarbamazine (6 mg/kg orally), alone or with ivermectin (400 mcg/kg orally) or albendazole (400 mg orally) may be as effective as longer courses of diethylcarbamazine. A single dose of all three drugs cleared parasites in more than 95% of persons for 3 years . ▪ doxycycline (100–200 mg/day orally for 4–6 weeks), which kills obligate intracellular Wolbachia bacteria, leading to death of adult filarial worms. ▪ Secondary bacterial infections must be treated. ▪ Surgical correction may be helpful in some cases.
  • 78.