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Phase 2A > Microbiology 3 > Flashcards

Microbiology 3 Flashcards

1
Q

what are the major categories of fungi? how do they grow?

A
  • yeasts and yeast-like fungi, which reproduce by budding
  • moulds, which grow by branching and longitudinal extension of hyphae
  • dimorphic fungi, which behave as yeasts in the host but as moulds in vitro
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2
Q

what is the behaviour of dimorphic fungi?

A

behave as yeasts in the host but as moulds in vitro

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3
Q

what are examples of dimorphic fungi?

A

Histoplasma capsulatum and Sporothrix schenckii

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4
Q

where are systemic mycoses usually seen?

A

in immunocompromised patients, and in critical care settings; becoming more prevalent as this population of patient increases

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5
Q

how are fungal infections transmitted?

A

by inhalation of spores, by contact with the skin, or by direct inoculation

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6
Q

how can direct inoculation by fungi occur?

A

penetrating injuries, injecting drug use, or iatrogenic procedures

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7
Q

what are categories of fungal infections?

A

systemic, subcutaneous, superficial

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8
Q

what are some common systemic fungal infections?

A
  • Histoplasmosis
  • Cryptococcosis
  • Coccidiodomycosis
  • Blastomycosis
  • Zygomycosis (mucomycosis)
  • Candidiasis
  • Aspergillosis
  • Pneumocystis
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9
Q

what are some common subcutaneous fungal infections?

A
  • Sporotrichosis
  • Subcutaneous zygomycosis
  • Chromoblastomycosis
  • Mycetoma
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10
Q

what are some common superficial fungal infections?

A
  • Dermatophytosis
  • Superficial candidiasis
  • Malassezia infections
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11
Q

what is Candidiasis caused by?

A
  • most common fungal infection in fumans
  • caused by Candida albicans; other species are increasingly recognised
  • Candida are small asexual fungi
  • most species pathogenic to humans are normal oropharyngeal and GI commensals
  • found worldwide
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12
Q

what are clinical features of Candidiasis?

A
  • any organ can be invaded; vaginal infection and oral thrush are most common forms
  • candidal oesophagitis presents with painful dysphagia
  • cutaneous candidiasis typically occurs in intertrignous areas
  • paronychia
  • balanitis and vaginal infection
  • dissemination may lead to haematogenous spread, with meningitis, pulmonary involvement, endocarditis or osteomyelitis
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13
Q

where is oral thrush often seen?

A
  • very young
  • elderly
  • following antibiotic therapy
  • those who are immunosuppressed
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14
Q

what may dissemination of candidiasis lead to?

A
  • haematogenous
  • meningitis
  • pulmonary involvement
  • endocarditis
  • osteomyelitis
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15
Q

what is diagnosis of Candidiasis?

A

demonstrated in scrapings from infected lesions, tissue secretions or in invasive disease, from blood cultures

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16
Q

what is treatment of Candidiasis?

A
  • varies depending on the site and severity of infection
  • oral lesions respond to local nystatin or amphotericin B or systemic fluconazole
  • systemic infections: parenteral therapy with amphotericin B, fluconazole, voriconazole or caspofungin is necessary
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17
Q

what is Histoplasmosis caused by?

A

Histoplasma capsulatum

  • non-encapsulated, dimorphic fungus
  • spores can survive in moist soil for several years, esp. when enriched by bird and bat droppings
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18
Q

where does Histoplasmosis often occur?

A
  • occurs worldwide
  • only commonly seen in Ohio and Mississippi river valleys where over 80% of the population have been subclinically exposed
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19
Q

how is Histoplasmosis transmitted?

A

mainly by inhalation of the spores, esp. when clearing out attics, barns and bird roosts or exploring caves

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20
Q

what is the pathogenesis of Histoplasma infection?

A

spores -> lungs -> budding forms -> granulomatous reaction or caseating necrosis

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21
Q

what are the main clinical forms of Histoplasma infection?

A
  • acute pulmonary histoplasmosis
  • chronic pulmonary histoplasmosis
  • cutaneous
  • ocular
  • disseminated histoplasmosis
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22
Q

what are clinical features of primary pulmonary histoplasmosis?

A
  • usually asymptomatic; only evidence of infection is conversion of a histoplasmin skin test from negative to positive and radiological features similar to those seen with Ghon primary complex of TB
  • calcification in the lungs, spleen and liver in high endemic areas
  • when symptomatic, it presents as a mild influenza like illness, with fever, chills, myalgia and cough
  • systemic symptoms are pronounced in severe disease
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23
Q

what are complications of primary pulmonary histoplasmosis?

A
  • atelectasis
  • secondary bacterial pneumonia
  • pleural effusions
  • erythema nodosum
  • erythema multiforme
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24
Q

what are clinical features of chronic pulmonary histoplasmosis?

A
  • clinically indistinguishable from pulmonary TB
  • usually seen in American white males over 50
  • fever, lymphadenopathy, hepatosplenomegaly, weight loss, leucopenia and thrombocytopenia
  • features of meningitis, hepatitis, hypoadrenalism, endocarditis and peritonitis (rare)
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25
Q

what is the diagnosis of histoplasmosis?

A
  • culturing the fungi (e.g. from sputum) or by demonstrating them on histological secretions
  • H. capsulatum glycoprotein can be detected in urine and serum in those with acute pulmonary and disseminated infection
  • antibodies usually develop within 3 weeks of the onset of illness and are best detected by complement fixation or immunodiffusion (sensitivity of 95% and 90%)
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26
Q

where can H. capsulatum be detected?

A

in urine and serum in those with acute pulmonary and disseminated infection

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27
Q

when do H. capsulatum antibodies develop? how are they detected?

A

antibodies usually develop within 3 weeks of the onset of illness and are best detected by complement fixation or immunodiffusion (sensitivity of 95% and 90%)

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28
Q

what is the sensitivity of complement fixation or immunodiffusion?

A

95% and 90%, respectively

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29
Q

what is the management of of histoplasmosis?

A
  • only symptomatic acute pulmonary histoplasmosis, chronic histoplasmosis and acute disseminated histoplasmosis require treatment
  • itraconazole is effective in mild-moderate disease
  • severe infection treated with IV amphotericin B for 1-2 weeks followed by itraconazole for 12 weeks or with voriconazole
  • methylprednisolone for respiratory complications
  • AIDS: parenteral amphotericin B followed by maintenance therapy with itraconazole 200mg BD where HAART unavailable
  • surgical excision of histoplasmomas or chronic cavitatory lung lesions or adhesions following mediastinits are often required
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30
Q

what is African histoplasmosis caused by?

A

Histoplasma duboisii (spores larger than H. capsulatum)

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31
Q

what are the clinical features of African histoplasmosis?

A
  • skin lesions (e.g. abscesses, nodules, lymph node involvement and lytic bone lesions) are prominent
  • pulmonary lesions do not occur
  • treatment similar to that for H. capsulatum infection
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32
Q

what is Aspergillosis caused by?

A

one of several species of dimorphic fungi of the genus Aspergillus

  • A. fumigatus is most common
  • A. flavus and A. niger are also recognised
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33
Q

how is Asperigillosis transmitted?

A
  • ubiquitous in the environment and are commonly found on decaying leaves and trees
  • infection by inhalation of the spores
  • disease manifestation depends on dose of the spores inhaled and the immune response of the host
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34
Q

what does disease manifestation of Aspergillosis depend on?

A

dose of spores inhaled and immune response of the host

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35
Q

what are the three major forms of Aspergillosis?

A
  • bronchopulmonary allergic aspergillosis
  • aspergilloma
  • invasive aspergilllosis
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36
Q

what is Cryptococcosis caused by?

A
  • yeast like fungus Cryptococcus neoformans

- worldwide distribution

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37
Q

what is Cryptococcosis spread by?

A

birds, esp. pigeons, in their droppings

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38
Q

what is the mechanism of entry of Cryptococcus neoformans entry into the body?

A

spores gain entry into the body through the respiratory tract, where they elicit a granulomatous reaction

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39
Q

what are clinical features of Cryptococcosis?

A
  • pulmonary symptoms are uncommon
  • meningitis is usual mode of presentation and often develops subacutely; HIV infection or lymphoma
  • lung cavitation, hilar lymphadenopathy, pleural effusions and occasionally pulmonary fibrosis
  • skin and bone involvement is rare
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40
Q

what is the diagnosis of Cryptococcosis?

A
  • demonstrating organisms in appropriately stained tissue sections
  • positive latex cryptococcal agglutinin test performed on CSF is diagnostic of cryptococcosis
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41
Q

what is the treatment of Cryptococcosis?

A
  • liposomal amphotericin B alone or in combination with flucytosine for 2 weeks is followed by oral fluconazole 400mg OD
  • therapy continued for 8 weeks if meningitis present
  • fluconazole may be used
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42
Q

when is fluconazole used in treatment of Cryptococcosis?

A
  • has greater CSF penetration
  • used when toxicity is encountered with amphotericin B and flucytosine
  • as maintenance therapy in immunocompromised patients, esp. those with HIV
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43
Q

what is Coccidioidomycosis caused by?

A

non-budding spherical form (spherule) of Coccidioides immitis

  • soil saprophyte
  • found in southern USA, Central America and parts of South America
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44
Q

how are humans infected by Coccidioidomycosis?

A

inhalation of thick-walled barrel-shaped spores called arthrospores
- epidemics of coccidioidomycosis have been documented after dust storms

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45
Q

what are clinical features of Coccidioidomycosis?

A
  • most are asymptomatic
  • acute pulmonary coccidioidomycosis presents after an incubation of 10 days
  • fever, malaise, cough and expectoration
  • erythema nodosum, erythema multiforme, phlyctenular conjunctivitis and pleural effusions may occur
  • pulmonary cavitation with haemoptysis, pulmonary fibrosis, meningitis lytic bone lesions, hepatosplenomegaly, skin ulcers and abscesses in severe disease
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46
Q

what is the diagnosis of Coccidioidomycosis?

A
  • respiratory secretions
  • can be cultured in specialist labs
  • serological test: latex agglutination and precipitin tests (IgM); positive within 2 weeks of infection and decline after
  • complement fixation, ELISA and radioimmunoassay
  • complement fixation test (IgG) on CSF is diagnostic of coccidioidomycosis meningitis; positive within 4-6 weeks
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47
Q

how is coccidioidomycosis detected?

A

conversion of a skin test using coccidiodin (extract from a culture of mycelial growth of C. immitis) from negative to positive

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48
Q

what is coccidiodin?

A

extract from a culture of mycelial growth of C. immitis

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49
Q

what is the treatment of coccidioidomycosis?

A
  • mild pulmonary infections are self limiting and need no treatment
  • progressive and disseminated disease needs urgent therapy
  • ketoconazole, itraconazole or fluconazole for 6 months is used for primary pulmonary disease
  • more prolonged courses for cavitating or fibronodular disease
  • fluconazole in high dose (600-1000mg daily) for meningitis
  • voriconazole and posaconazole for poor response
  • surgical excision of cavitatory pulmonary lesions or localised bone lesions may be needed
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50
Q

what is Blastomycosis caused by?

A

systemic infection caused by biphasic fungus Blastomyces dermatitidis
- in North America, South America, India and Middle East

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51
Q

what are clinical features of Blastomycosis?

A
  • involves skin: non-itchy papular lesions that later develop into ulcers with red verrucous margins
  • ulcers initially confined to exposed parts of the body but later involve unexposed parts as well
  • atrophy and scarring may occur
  • pulmonary involvement presents as a solitary lesion resembling a malignancy or gives rise to radiological features similar to TB
  • fever, malaise, cough and weight loss
  • bone lesions common and present as painful swelling
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52
Q

what is the diagnosis of Blastomycosis?

A
  • organism is demonstrated in histological sections or by culture
  • results can be negative in 30-50% of cases
  • enzyme immunoassay may be helpful, but there is some cross-reactivity of antibodies to blastomyces with histoplasma
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53
Q

what is the treatment of Blastomycosis?

A
  • itraconazole for mild to moderate disease in the immunocompetent for up to 6 months
  • ketoconazole or fluconazole also used
  • amphotericin B indicated in severe or unresponsive disease and in the immunocompromised
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54
Q

what are types of Mucormycosis?

A
  • invasive zygomycosis
  • rhinocerebral mucormycosis
  • subcutaneous zygomycosis
  • other forms
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55
Q

what is invasive zygomycosis (mucormycosis) caused by? when does it occur?

A
  • rare
  • caused by several fungi, including Mucor spp., Rhizopus spp. and Absidia spp.
  • severely ill patients
  • vascular invasion with marked haemorrhagic necrosis
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56
Q

what are features of Rhinocerebral mucormycosis?

A
  • most common form of Mucormycosis
  • nasal stuffiness, facial pain and oedema and necrotic, black nasal turbinates
  • rare
  • mainly seen in diabetics with ketoacidosis
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57
Q

what are features of Subcutaneous zygomycosis?

A

brawny, woody infiltration involving the limbs, neck and trunk and rarely the pharynx and orbital regions in immunosuppressed patients

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58
Q

what are other forms of Mucormycosis?

A

pulmonary and disseminated infection (immunosuppressed) and GI infection (in malnutrition)

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59
Q

what is treatment of Mucormycosis?

A
  • amphotericin B and sometimes judicious debridement

- oral saturated postassium iodide has been used in subcutaneous variety

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60
Q

what causes Sporotrichosis?

A
  • caused by saprophytic fungus Sporothrix schenckii

- found worldwide

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61
Q

what are clinical features of Sporotrichosis?

A
  • infection usually follows cutaneous inoculation
  • at site of inoculation, a reddish, non-tender, maculopapular lesion develops (plaque sporotrichosis)
  • pulmonary involvement and disseminated disease rarely occur
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62
Q

what is plaque sporotrichosis?

A

occurs at site of cutaneous inoculation with Sporothrix schenckii; reddish, non-tender, maculopapular lesion develops

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63
Q

what is treatment of Sporotrichosis?

A

itraconazole 100-200mg/day for 3-6 months is usually curative

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64
Q

what is Subcutaneous zygomycosis caused by?

A
  • disease seen in the tropics

- caused by several filamentous fungi of the Basidobolus genus

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65
Q

what are clinical features of Subcutaneous zygomycosis?

A
  • usually remains confined to the subcutaneous tissues and muscle fascia
  • presents as a brawny, woody infiltration involving the limbs, neck and trunk
  • pharyngeal and orbital regions affected in immunocompromised patients and poorly controlled diabetes mellitus (less common)
  • locally erosive
  • may be fatal
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66
Q

what is the treatment of Subcutaneous zygomycosis?

A
  • amphotericin B

- saturated potassium iodide solution given orally

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67
Q

what is Chromoblastomycosis caused by?

A
  • caused by fungus of various genera including Phialophora, Wangella and Fonsecaea
  • found in tropical and subtropical countries
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68
Q

what are the clinical features of Chromoblastomycosis?

A
  • initially as a small papule, at site of previous injury
  • papule persists for months before ulcerating
  • later becomes warty and encrusted and gradually spreads
  • satellite lesions may be present
  • itching
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69
Q

what is treatment of Chromoblastomycosis?

A
  • amphotericin B combined with itraconazole or voriconazole

- cryosurgery used to remove local lesions

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70
Q

what is Mycetoma (Madura foot) caused by?

A
  • subcutaneous infection with fungi (Eumycetes spp.) or bacteria
  • confined to tropics
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71
Q

what are clinical features of Mycetoma (Madura foot)?

A
  • local swelling which may discharge through sinuses

- bone involvement may follow

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72
Q

what is treatment of Mycetoma (Madura foot)?

A

surgical debridement, combined with antimicrobials chosen according to the aetiological agent

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73
Q

what are features of Pneumocystis jiroveci infection?

A
  • P. jiroveci is homologous with fungi

- associated with immunodeficiency states, esp. AIDS

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74
Q

what are features of Dermatophytosis?

A
  • chronic fungal infections of keratinous structures such as the skin, hair or nails
  • Trichophyton spp., Microsporum spp., Epidermophyton spp. and Candida spp. can also infect keratinous structures
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75
Q

what are clinical features of Malassezia infection?

A
  • Malassezia spp. are found on the scalp and greasy skin
  • responsible for seborrhoeic dermatitis, pityriasis versicolor (hypo- or hyperpigmented rash on trunk) and Malassezia folliculitis (itchy rash on back)
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76
Q

what is treatment of Malassezia infection?

A

topical antifungals or oral ketonazole if infection is refractory or more extensive

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77
Q

what is pre-erythrocytic sporogeny?

A
  • sporozites that aren’t destroyed by immune response are taken up by the liver and multiply inside hepatocytes as merozoites
  • infected hepatocytes rupture, releasing merozoites into blood where they’re taken up by erythrocytes
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78
Q

what parasites (malaria) may stay dormant in the liver?

A
  • P. vivax and P. ovale stay dormant in the liver as hypnozoites
  • may reactivate at any time subsequently, causing relapsing infection
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79
Q

what is erythrocytic schizogony?

A

multiply, changing from merozoite, to trophozoite, to schizont and finally appearing as 8-24 new merozoites
- erythrocyte ruptures, releasing the merozoites to infect further cells

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80
Q

how long does erythrocytic schizogony take?

A

48hrs in P. falciparum, P. vivax and P. ovale

72hrs in P. malariae

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81
Q

what cells do different malarial parasites attack?

A
  • P. vivax and P. ovale attack reticulocytes and young erythrocytes
  • P. malariae attacks older cells
  • P. falciparum parasitizes any stage of erythrocyte
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82
Q

what are causes of anaemia in malaria infection?

A
  • haemolysis of infected red cells
  • haemolysis of non-infected red cells (blackwater fever)
  • dyserythropoiesis
  • splenomegaly and sequestration
  • folate depletion
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83
Q

who is typical malaria seen in?

A

non-immune individuals; e.g. children in area, adults in hypoendemic areas and any visitors from non-malarious region

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84
Q

what is the normal incubation period of malaria?

A

10-21 days, but can be longer

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85
Q

what are symptoms of malaria?

A
  • fever
  • general malaise, headache, vomiting or diarrhoea
  • fever may be continual or erratic; classical tertian or quartan fever only appears after a few days
  • temp reaches 41
  • rigors and drenching sweats
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86
Q

what are clinical features of P. vivax or P. ovale infection?

A
  • usually mild illness (P. vivax can cause severe disease)
  • anaemia develops slowly and may be tender hepatosplenomegaly
  • spontaneous recovery in 2-6 weeks
  • hypnozoites in liver can cause relapses
  • repeated infections cause chronic ill health due to anaemia and hyperreactive splenomegaly
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87
Q

what are clinical features of P. malariae infection?

A
  • mild illness
  • runs a more chronic course
  • parasitaemia may persist for years, with or without symptoms
  • associated with glomerulonephritis and nephrotic syndrome in children
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88
Q

what are clinical features of P. falciparum infection?

A
  • causes self-limiting illness
  • may cause serious complications; most deaths are due to this
  • high parasitaemia indicates severe disease
  • cerebral malaria and blackwater fever
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89
Q

what is parasitaemia?

A

> 1% of red cells infection

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90
Q

what are features of cerebral malaria?

A
  • marked by diminished consciousness, confusion and convulsions
  • often progress to coma and death
  • untreated it’s universally fatal
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91
Q

what are features of blackwater fever?

A
  • due to widespread intravascular haemolysis due to malaria

- affects both parasitised and unparasitised red cells, giving rise to dark urine

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92
Q

what is TSS? what are clinical features of it?

A

tropical splenomegaly syndrome/hyperreactive malarial splenomegaly

  • seen in older children and adults in hyperendemic areas
  • associated with exaggerated immune response to repeated malria infections
  • anaemia, massive splenomegaly and elevated IgM levels
  • malaria parasites are absent/scanty
  • usually respond to prolonged treatment with prophylactic antimalarial drugs
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93
Q

when should malaria be considered?

A
  • presenting with febrile illness in, or having left, a malarious area
  • falciparum malaria unlikely to present more than 3 months after exposure, even if patient has been taking prophylaxis
  • vivax malaria may cause symptoms up to a year later
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94
Q

how is malaria clinically diagnosed?

A
  • identifying parasites on a Giemsa-stained thick or thin blood film
  • 3 films should be examined before malaria is declared unlikely
  • rapid antigen detection test for near-patient use
  • serological tests are of no diagnostic value
  • lumbar puncture may be needed to exclude bacterial infection
  • overdiagnosed in endemic areas
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95
Q

what are CNS features of severe falciparum malaria?

A
  • prostration

- cerebral malaria (coma convulsion = 3 seizures in 24hrs)

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96
Q

what are renal features of severe falciparum malaria?

A
  • haemoglobinuria (blackwater fever)
  • oliguria
  • uraemia (serum creatinine >250umol/L) (acute tubular necrosis)
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97
Q

what blood features of severe falciparum malaria?

A
  • severe anaemia (<50g/L) (haemolysis and dyserythropoiesis)
  • disseminated intravascular coagulation (DIC)
  • bleeding e.g. retinal haemorrhages
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98
Q

what are respiratory features of severe falciparum malaria?

A
  • tachypnoea

- acute respiratory distress syndrome

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99
Q

what are metabolic features of severe falciparum malaria?

A
  • hypoglycaemia (<2mmol/L) (esp. in children)

- metabolic acidosis (blood pH <7.25)

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100
Q

what are GI/liver features of severe falciparum malaria?

A
  • diarrhoea
  • jaundice (bilirubin >50umol/L)
  • splenic rupture
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101
Q

what are other features of severe falciparum malaria?

A
  • shock; hypotensive and Gram-negative septicaemia

- hyperpyrexia

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102
Q

what is drug treatment of uncomplicated malaria P. vivax, P. ovale and P. malariae?

A
  • chloroquine 600mg, 300mg 6hrs later, 300mg 24hrs later and 300mg 24hrs later OR ACT for 3 days
  • plus primaquine 15mg for 2-3 weeks
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103
Q

what is drug treatment of uncomplicated malaria P. falciparum (adults, endemic zone)?

A
  • ACT 3 days OR quinine + doxycycline 7 days

- plus primaquine 0.75mg/kg single dose

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104
Q

what is drug treatment of malaria P. falciparum (pregnant)?

A

1st trimester: quinine + doxycycline 7 days

2nd/3rd trimester: ACT 3 days

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105
Q

what is drug treatment of malaria P. falciparum (infants)?

A
  • ACT 3 days; appropriate dose for body weight

- plus primaquine 0.75mg/kg single dose

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106
Q

what is drug treatment of malaria P. falciparum (returning traveller)?

A

atovaquone-proguanil or quinine + doxycycline 7 days

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107
Q

what is ACT?

A

artemisinin-based combination therapy

- recommended oral treatment for uncomplicated falciparum malaria worldwide

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108
Q

what indicates severe falciparum malaria?

A
  • presence of any complications

- parasite count above 1% in a non-immune patient

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109
Q

what are the latest WHO guidelines for severe falciparum malaria?

A
  • IV artesunate is more effective than IV quinine and should be used when possible; absorption from IM injection is less reliable than from IV injection
  • intensive care facilities may be needed, including mechanical ventilation and dialysis
  • severe anaemia may need transfusion
  • careful monitoring of fluid balance is essential; pulmonary oedema and prerenal failure are common
  • hypoglycaemia can be induced by infection and by quinine treatment
  • superadded bacterial infection is common
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110
Q

what are the fixed dose combination tablets of ACT for malaria?

A
  • artemether-lumefantrine: 4 tablets BD for 3 days
  • artesunate-amodiaquine: 4mg/kg per day artesunate for 3 days
  • dihydroartemisin-piperaquine: 4mg/kg per day dihydroartemisinin for 3 days
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111
Q

what are fixed dose copackaged separate tablets of ACT for malaria?

A
  • artesunate-mefloquine: 4mg/kg per day artesunate for 3 days
  • artesunate-sulfadoxine-pyrimethamine: 4mg/kg per day artesunate for 3 days
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112
Q

what are alternatives where no combination packages of ACT are available for malaria?

A
  • artesunate + clindamycin: 2mg/kg per day + 10mg/kg BD for 7 days
  • artesunate + doxyclycline: 2mg/kg per day + 3.5 mg/kg per day for 7 days
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113
Q

what are strategies for controlling malaria?

A
  1. aggressive control in highly endemic countries, to reduce mortality and decrease transmission
  2. progressive eradication at the endemic margins, to shrink the malaria map
  3. research into new vaccines, new drugs, new diagnostics and better ways of delivering malaria care
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114
Q

what is very heavy malaria infection?

A

parasitaemia >10%

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115
Q

what does control of malaria rely on?

A
  • combination of case treatment
  • vector eradication
  • personal protection from vector bites, e.g. insecticide (permethrin) treated nets
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116
Q

how is mosquito eradication usually achieved?

A
  • insecticides
  • house spraying with DDT
  • manipulation of habitat (e.g. marsh drainage)
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117
Q

what is an example of an insect repellent?

A

diethyltoluamide, DEET, 20-50% in lotions and sprays

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118
Q

what are the options, in order of preference of severe falciparum malaria?

A
  1. IV artesunate
  2. IV quinine
  3. IM artesunate
  4. IM artemether
  5. rectal artesunate
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119
Q

what is the immediate and subsequent dose of IV artesunate in treatment of severe falciparum malaria?

A

immediate: 2.4mg/kg
subsequent: 2.4mg/kg at 12 and 24hrs, then daily (up to 7 days)

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120
Q

what is the immediate and subsequent dose of IV quinine in treatment of severe falciparum malaria?

A

immediate: 20mg/kg
subsequent: 10mg/kg 8 hourly (up to 7 days)

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121
Q

what is the immediate and subsequent dose of IM artesunate in treatment of severe falciparum malaria?

A

immediate: 2.4mg/kg
subsequent: 2.4mg/kg at 12 and 24hrs, then daily (up to 7 days)

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122
Q

what is the immediate and subsequent dose of IM artemether in treatment of severe falciparum malaria?

A

immediate: 3.2mg/kg
subsequent: 1.6mg/kg daily

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123
Q

what is the immediate and subsequent dose of rectal artesunate in treatment of severe falciparum malaria?

A

immediate: 10mg/kg
subsequent: transfer to centre where parenteral therapy available

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124
Q

what is the prophylactic regimen and alternative for visit to areas with no chloroquine resistance?

A
  • chloroquine 300mg weekly

- alternative: proguanil 200mg daily

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125
Q

what is the prophylactic regimen and alternative for

visit to areas with limited chloroquine resistance?

A
  • chloroquine 300mg weekly + proguanil 200mg daily

- alternative: doxycycline 100mg daily OR malarone 1 tablet daily OR mefloquine 250mg weekly

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126
Q

what is the prophylactic regimen and alternative for visit to areas with significant chloroquine resistance?

A
  • mefloquine 250mg weekly

- alternative: doxycycline 100mg daily OR malarone 1 tablet daily

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127
Q

what is sleeping sickness?

A

African trypanosomiasis

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128
Q

what is sleeping sickness caused by?

A
  • caused by trypanosomes transmitted to humans by bite of the tsetse fly (genus Glossina)
  • endemic in a belt across sub-Saharan Africa, extending to 14N and 20S (natural range of tsetse fly)
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129
Q

what are the two subspecies of trypanosome that cause sleeping sickness?

A
  • Tryanosoma bruceigambiense (Gambian sleeping sickness)

- Trypanosoma b. rhodesiense (Rhodesian sleeping sickness)

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130
Q

what causes Gambian sleeping sickness?

A

Trypsanosoma bruceigambiense

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131
Q

what causes Rhodesian sleeping sickness?

A

T. b. rhodesiense

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132
Q

what is the epidemiology of Gambian sleeping sickness?

A
  • found from Uganda in Central Africa, west to Senegal and south as far as Angola
  • man is major reservoir and infection is transmitted by riverine Glossina species (e.g. G. palpalis)
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133
Q

what is the epidemiology of Rhodesian sleeping sickness?

A
  • occurs in East and Central Africa from Ethiopia to Botswana
  • zoonosis of both wild and domestic animals
  • maintained in game animals and transmitted by savanna flies e.g. G. morsitans
  • epidemics usually related to cattle and vectors are riverine flies
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134
Q

what is the parasitology of African trypanosomiasis (sleeping sickness)?

A
  • Tsetse flies bite during the day and both males and females take blood meals
  • an infected insect may deposit metacyclic trypomastigotes (the infective form of the parasite) into the subcutaneous tissue
  • cause local inflammation (trypanosomal chancre) and regional lymphadenopathy
  • invade bloodstream within 2-3 weeks, then spread to all parts of the body including the brain
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135
Q

what is the infective form of African trypanosomiasis?

A

metacyclic trypomastigotes

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136
Q

what is trypanosomal chancre?

A

local inflammation caused by metacyclic trypomastigotes

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137
Q

what drugs are used in the treatment of African trypanosomiasis (T. b. gambiense)?

A

stage 1: pentamidine

stage 2 (CNS): eflornithin + nifurtimox; eflornithine monotherapy (melarsoprol)

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138
Q

what drugs are used in treatment of African trypanosomiasis (T. b. rhodesiense)?

A

stage 1: suramin

stage 2 (CNS): melarsoprol

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139
Q

what are clinical features of T. b. gambiense?

A
  • causes a chronic, slowly progressive illness
  • episodes of fever and lymphadenopathy occur over months or years and hepatosplenomegaly may develop
  • infection eventually reaches the CNS, causing headache, behavioural changes, confusion and daytime somnolence
  • progresses to tremors, ataxia, convulsions and hemiplegias
  • eventually coma and death
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140
Q

what are histological features of T. b. gambiense?

A

lymphocytic meningoencephalitis, with scattered trypanosomes visible in the brain substance

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141
Q

what are clinical features of T. b. rhodesiense?

A
  • more acute
  • early systemic features: myocarditis, hepatitis and serous effusions and patients can die before the onset of CNS disease
  • if they survive, cerebral involvement occurs within weeks of infection and is rapidly progressive
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142
Q

what is the diagnosis of African trypanosomiasis?

A
  • may be seen on Giemsa-stained smears of thick or thin blood films, or of lymph node aspirate
  • blood films usually positive in T. b. gambiense; concentration techniques may increase the yield
  • serological tests useful for screening for infection
  • CATT is robust and easy to use field assay
  • examination of CSF
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143
Q

what is CATT?

A

card agglutination test for trypanosomiasis

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144
Q

what does CNS involvement of African trypanosomiasis cause?

A

causes lymphocytosis and elevated protein in the CSF and parasites may be seen in concentrated specimens

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145
Q

what is Chagas’ disease?

A

South American trypanosomiasis

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146
Q

what is South American trypanosomiasis?

A

Chagas’ disease

147
Q

what causes South American trypanosomiasis (Chagas’ disease)?

A
  • caused by Trypanosoma cruzi
  • transmitted to humans in faces of bloodsucking reduviid bugs (cone-nose or assassain bugs)
  • faces infected with T. cruzi trypomastigotes are rubbed in through skin abrasions, mucosa or conjunctiva
  • bugs live in mud or thatch buildings, feed on vertebrate hosts at night, defecate
148
Q

how do Trypanosoma cruzi spread in the human body?

A
  • spread in the bloodstream, before entering host cells and multiplying
  • cell rupture releases them back into the circulation, where they are taken up by a feeding bug
  • further multiplication takes place in the insect gut, completing the trypanosome life cycle
  • human infection can occur via contaminated blood transfusion or by transplacental spread
149
Q

what are clinical features of acute Chagas’ disease?

A
  • usually in children
  • often passes unnoticed
  • firm reddish papule may be seen at site of entry, associated with regional lymphadenopathy
  • in conjunctival infection, there is swelling of the eyelid which may close the eye (Romana’s sign)
  • fever, lymphadenopathy, hepatosplenomegaly and rarely, meningoencephalitis
  • may be fatal in infants
  • full recovery within weeks or months
150
Q

what are clinical features of chronic Chagas’ disease?

A
  • 10-30% of people go on to chronic disease after latent period
  • may be due to autoimmune response triggered by the initial infection
  • heart affected; conduction abnormalities, arrhythmias, aneurysm formation and cardiac dilation
  • GI involvement -> progressive dilation of parts of the GI tract -> megaoesophagus and megacolon
151
Q

what is the diagnosis of Chagas’ disease?

A
  • trypanosomes seen on stained blood film during acute illness
  • in chronic disease, parasites may be detected by xenodiagnosis: infection-free reduviid bugs feed on patient and the insect gut examined for parasites
  • serological tests can detect acute and chronic Chagas’ disease
152
Q

what is the management of Chagas’ disease?

A
  • nifurtimox and benznidazole; effective in acute infection (cure rate of 90%), less effective in chronic disease
  • toxic with adverse reactions in up to 40% of patients
  • antiarrhythmic drugs and pacemakers may be needed in cardiac disease
  • surgical treatment for GI complications
153
Q

how is Chagas’ disease prevented?

A
  • improved housing and living conditions
  • local vector control programmes
  • spraying houses with insecticide
  • impregnated bed nets with pyrethoid and insect repellents
154
Q

what are types of Leishmania?

A
  • visceral leishmania
  • cutaneous leishmania
  • mucocutaneous leishmania
155
Q

what species complex and species cause visceral leishmania?

A

species complex
- L. donovani

species

  • L. donovani
  • L. infantum
  • L. chagasi
156
Q

what species complex and species cause cutaneous leishmania?

A

species complex

  • L. tropica
  • L. major
  • L. aethiopica
  • L. mexicana
  • L. braziliensis

species

  • L. tropica
  • L. major
  • L. aethiopica
  • L. mexicana
  • L. amazonensis
  • L. garnhami
  • L. pifanoi
  • L. venezuelensis
  • L. braziliensis
  • L. guyanesis
  • L. panamanensis
  • L. peruviana
157
Q

what are species that cause mucocutaneous leishmania?

A

L. braziliensis

158
Q

what causes Leishmaniasis? where is it commonly seen?

A
  • caused by protozoa of the genus Leishmania
  • transmitted by bite of the female phlebotomine sandfly
  • seen in localised areas of Africa, Asia, Europe, the Middle East and South and Central America
159
Q

what are clinical features of Leishmaniasis?

A
  • asymptomatic infection: parasite suppressed by a strong immune response; common in endemic areas (high incidence of positive skin tests)
  • symptomatic infection: combined to the skin or through the body (visceral)
  • relapse of previously asymptomatic infection is seen in patients who become immunocompromised
160
Q

what is the behaviour of Leishmaniasis organisms in the body?

A
  • parasites found as oval amastigotes (Leishman-Donovan bodies)
  • parasites multiply inside the macrophages and cells of the reticuloendothelial system and are released into the circulation as the cells rupture
  • parasites are taken into the gut of a feeding sandfly (genus Phlebotomus in Old World, Lutzomyia in New), wherre they develop into flagellate promastigote form
  • migrate to salivary glands of the insect, then inoculated into new host
161
Q

what are clinical features of visceral leishmaniasis?

A
  • kala azar
  • caused by L. donovani, L. infantum or L. chagasi
  • prevalent in localised areas of Asia, Africa, Mediterranean and South America
  • incubation period usually 1-2 months, can be years
  • onset of symptoms is insidious
  • fever, enlargement of liver and spleen, lymphadenopathy, rough and pigmented skin, pancytopenia, wasting and immunosuppression
  • death within a year due to bacterial infection or uncontrolled bleeding
162
Q

what is diagnosis of visceral leishmaniasis?

A
  • demonstrating parasite in stained smears of aspirates of bone marrow, lymph node, spleen or liver
  • organism can be cultured from these specimens
  • specific serological tests are positive in 95% of cases
  • pancytopenia, hypoalbuminaemia and hypergammaglobulinaemia are common
  • leishmanin skin test is negative, indicating poor cell mediated immune response
163
Q

what is the management of visceral leishmaniasis?

A
  • pentavalent antimony salts (e.g. sodium stibogluconate and meglumine antimoniate)
  • IV amphotericin B effective but expensive
  • IM paromomycin is cheaper and has good cure rate
  • miltefosine
  • combination therapy
  • PKDL
164
Q

what is PKDL?

A

post-kala azar dermal leishmaniasis

  • skin eruption after successful treatment of visceral leishmaniasis
  • starts as a macular maculopapular nodular rash which spreads over the body
  • most often seen in Sudan and India
  • reports of it after miltefosine
165
Q

what causes cutaneous leishmaniasis?

A

number of geographically localised species which may be zoonotic or anthroponotic

166
Q

how does cutaneous leishmaniasis spread within the body?

A
  • sandfly bite
  • leishmania amastigotes multiply in dermal macrophages
  • local response depends on species of leishmania, size of the inoculum and the host immune response
  • single or multiple painless nodules occur on exposed areas within 1 week to 3 months
  • nodules enlarge and ulcerate with a characteristic erythematous raised border
  • overlying crust may develop
  • lesions heal slowly over months or years
167
Q

where are L. major and L. tropica found? what are their reservoirs?

A
  • Russia and Eastern Europe, Middle East, Central Asia, Mediterranean littoral and sub-Saharan Africa
  • reservoir for L. major is desert rodents
  • L. tropica has a mainly urban distribution with dogs and humans as reservoirs
168
Q

where is L. aethiopica found? what is its reservoir?

A
  • highlands of Ethiopia and Kenya

- animal reservoir is the hyrax

169
Q

what is Leishmaniasis recidivans?

A

rare chronic relapsing form caused by L. tropica

170
Q

where is L. mexicana found?

A

Mexico, Guatemala, Brazil, Venezuela and Panama

- infection usually runs a benign course with spontaneous healing within 6 months

171
Q

where is L. braziliensis found?

A

tropical South America

- infections heal spontaneously, but may take longer

172
Q

what is diagnosis of cutaneous leishmaniasis?

A
  • endemic area
  • Giemsa stain on a split-skin smear will demonstrate leishmania parasites in 80% of cases
  • biopsy tissue from edge of lesion can be examined histologically and parasites identified by PCR
  • leishmanin skin test positive in 90% of cases; doesn’t distinguish between active and resolved infection
  • serology unhelpful
173
Q

what is treatment of cutaneous leishmaniasis?

A
  • small lesions usually require no treatment
  • large lesions or those in cosmetically sensitive sites can be treated locally, by curettage, cryotherapy or topical antiparasitic agents
  • systemic treatment may be needed
174
Q

what are clinical features of mucocutaneous leishmaniasis?

A
  • 3-10% of infections with L. b. braziliensis
  • commonest in Bolivia and Peru
  • cutaneous sores are followed months or years later by indurated or ulcerating lesions affecting mucosa or cartilage, on lips or nose
  • may remain static
  • may be progression affecting nasopharynx, uvula, palate and upper airways
175
Q

how is mucocutaneous leishmaniasis diagnosed?

A
  • biopsies show scanty organisms
  • parasites can be detected by PCR
  • serological tests frequently positive
176
Q

what is treatment of mucocutaneous leishmaniasis?

A
  • amphotericin B
  • systemic antimonial compounds
  • relapses are common
  • patients may die due to secondary bacterial infection or laryngeal obstruction
177
Q

how is mucocutaneous leishmaniasis prevented?

A
  • relies on control of vectors/reservoirs of infection
  • insecticide spraying, control of host animals and treating infected humans
  • personal protection against sandfly bites
  • sandflies are poor fliers and sleeping off the ground helps prevent bites
178
Q

what is Toxoplasmosis caused by?

A
  • intracellular protozoan parasite Toxoplasma gondii
  • sexual form of the parasite lives in the gut of the definitive host, the cat, where it produces oocysts
  • after maturation, oocysts become source of infection for secondary hosts
179
Q

what is the definitive host of Toxoplasma gondii?

A

cat

180
Q

what are secondary hosts of Toxoplasma gondii?

A

man, cattle, sheep, pigs, rodents and birds

- disseminated infection

181
Q

how are humans infected by Toxoplasma gondii?

A

from contaminated cat faces, or by eating undercooked infected meat; transplacental infection may occur

182
Q

when is the life cycle of Toxoplasma gondii completed?

A

when carnivorous felines eat infected animal tissue

183
Q

what is the seroprevalence in adults of Toxoplasmosis?

A

in UK about 25%, rising to 90% in some parts of Europe

184
Q

what are clinical features of Toxoplasmosis?

A
  • most are asymptomatic or trivial
  • symptomatic patients: lymphadenopathy in head and neck, fever, myalgia, general malaise
  • hepatitis, pneumonia, myocarditis, choroidoretinitis
  • congenital toxoplasmosis: microcephaly, hydrocephalus, encephalitis, convulsions and mental retardation
  • affects immunocompromised aptients
185
Q

what is the diagnosis of Toxoplasmosis?

A
  • IgG antibodies detectable by Sabin-Feldman dye test remain positive for years
  • acute infection confirmed by demonstrating a rising titre of specific IgM
186
Q

what is the management of Toxoplasmosis?

A
  • acquired toxoplasmosis in an immunocompetent host rarely requires treatment
  • severe disease: sulfadiazine 2-4g daily and pyrimethamine 25mg daily given for 4 weeks, with folinic acid
  • infected infants treated from birth
187
Q

what is Babesiosis?

A
  • tick-borne parasitic disease
  • North America and Europe
  • zoonosis in rodents and cattle and may be transmitted to humans
  • infection more common in immunocompromised
188
Q

what organisms cause Babesiosis?

A

plasmodium-like Babesia microti (rodents) and B. divergins (cattle)

189
Q

what is the incubation period of Babesiosis?

A

around 10 days

190
Q

what are clinical features of Babesiosis?

A
  • in patients with normal splenic function, illness is mild
  • in splenoctomised individuals, systemic symptoms are more pronounced and haemolysis is associated with haemoglobinuria, jaundice and acute kidney injury
191
Q

what is diagnosis of Babesiosis?

A

examination of a peripheral blood smear may reveal the characteristic plasmodium-like organisms

192
Q

what is the treatment of Babesiosis?

A
  • combination of quinine 650mg and clindamycin 600mg orally TDS for 7 days
  • atovaquone and azithromycin plus doxycycline used for persistent or relapsing disease
193
Q

what are the main pathogenic human intestinal protozoa?

A

Amoebae
- Entamoeba histolytica

Flagellates
- Giardia intestinalis

Ciliates
- Balantidium coli

Coccidia

  • Cryptosporidium parvum
  • Isospora belli
  • Sarcocystis spp.
  • Cyclospora cayetanensis

Microspora

  • Enterocytozoon bieneusi
  • Encephalitozoon spp.
194
Q

what is Amoebiasis caused by?

A

Entamoeba histolytica

195
Q

what are the three species of Entamoeba histolytica?

A
  • E. histolytica (pathogen)
  • E. dispar (non-pathogenic)
  • E. moshkovskii (uncertain significance)
196
Q

how can cysts of the three Entamoeba histolytica be distinguished from eachother?

A
  • identical
  • can be distinguished by molecular techniques after culture of the trophozoite
  • E. histolytica can be distinguished from all other amoebae and other intestinal protozoa by microscopic appearance
197
Q

how does Entamoeba histolytica exist? how is it transmitted to humans?

A
  • motile trophozoite and as a cyst that can survive outside the body
  • cysts are transmitted by ingestion of contaminated food or water, or spread directly by person-to-person contact
  • trophozoites emerge from cysts in small intestine and pass to the colon, where they multiply
198
Q

what are asymptomatic cyst passers?

A

many individuals can carry the pathogen without obvious evidence of clinical disease

199
Q

how does E. histolytica behave in the body?

A
  • E. histolytica trophozoites invade the colonic epithelium, with the aid of their own cytotoxins and proteolytic enzymes
  • parasites continue to multiply and finally frank ulceration of the mucosa occurs
  • if penetration continues, trophozoites may enter the portal vein, and reach the liver and cause intrahepatic abscesses
200
Q

what are clinical features of Amoebiasis?

A
  • incubation period is variable
  • usual course is chronic, with mild intermittent diarrhoea and abdominal discomfort
  • may progress to bloody diarrhoea with mucus and may have systemic symptoms e.g. headache, nausea and anorexia
  • infection may present as acute amoebic dysentry, resembling baillary dysentry or acute UC (less common)
201
Q

what are complications of Amoebiasis?

A
  • toxic dilatation of the colon
  • chronic infection with stricture formation
  • severe haemorrhage
  • amoeboma
  • amoebic liver abscess
  • tender hepatomegaly
  • high swinging fever
  • profound malaise
202
Q

what is the diagnosis of Amoebiasis?

A
  • microscopic examination of fresh stool or colonic exudate obtained at sigmoidoscopy
  • motile trophozoites containing erythrocytes must be identified
  • presence of amoebic cysts alone doesn’t imply disease
  • sigmoidoscopy and barium enema may show colonic ulceration but aren’t diagnostic
  • amoebic fluorescent antibody test is positive in 90% of patients with liver abscess and in 60-70% with active colitis
  • seropositivity low in asymptomatic cyst passers
203
Q

what is management of Amoebiasis?

A
  • metronidazole 800mg TDS for 5 days (amoebic colitis)
  • lower dose (400mg TDS for 5 days) in liver abscess
  • tinidazole effective
  • bowel should be cleaned of parasites with a luminal amoebicide e.g. diloxanide furoate after treatment of invasive disease
204
Q

how can Amoebiasis be prevented?

A
  • difficult to eradicate due to substantial human reservoir of infection
  • improved standards of hygiene, sanitation and better access to clean water
  • cysts are destroyed by boiling, but chlorine and iodine sterilizing tablets not always effective
205
Q

what is Giardiasis? where is it found?

A
  • caused by Giardia intestinalis (flagellate)
  • small intestinal disease, with diarrhoea and malabsorption
  • prevalence high in developing countries and is most common parasitic infection in travellers returning to the UK
  • Europe and North america
  • person-to-person spread in day nurseries and residential institutions
  • exists as a trophozoite and cyst
206
Q

what is the behaviour of Giardiasis in the human body?

A
  • organism may colonise the small intestine and may remain there without causing detriment
  • severe malabsorption may occur and is related to morphological damage to the small intestine
  • mild partial villous atrophy; subtotal villous atrophy is rare
  • damage may be immune mediated
  • bacterial overgrowth has been found in association with giardiasis and may contribute to fat malabsorption
207
Q

what are clinical features of Giardiasis?

A
  • many ingesting Giardia cysts have no symptoms
  • may become ill within 1-3 weeks after ingesting cysts
  • watery diarrhoea, nausea, anorexia, abdominal discomfort and bloating
  • symptoms usually resolve, but may persist
  • stools become paler, with features of steatorrhoea
  • weight loss
208
Q

what is diagnosis of Giardiasis?

A
  • cysts and trophozoites can be found in stool
  • negative stool examination doesn’t exclude the diagnosis since parasite may be excreted at irregular intervals
  • parasite can be seen in duodenal aspirates (obtained at endoscopy or with a luminal capsule) and in histological sections of jejunal mucosa
209
Q

what is managemnt of Giardiasis?

A
  • metronidazole 2g as a single does on three successive days
  • second/third dose may be needed
  • alternative drugs are tinidazole, mepacrine and albendazole
210
Q

what is the cause and transmission of Cryptosporidiosis?

A
  • organism found worldwide
  • cattle is major natural reservoir
  • demonstrated in supplies of drinking water in the UK
  • reproduces sexually and asexually
  • transmitted by oocysts excreted in the faeces
211
Q

what are the clinical features of Cryptosporidiosis?

A
  • self-limiting in healthy individuals
  • acute watery diarrhoea associated with fever and general malaise
  • lasts 7-10 days
  • severe and intractable diarrhoea in immunocompromised patients, esp. with HIV
212
Q

what is diagnosis and treatment of Cryptosporidiosis?

A
  • faecal microscopy; can be detected in intestinal biopsies

- no reliable treatment; nitazoxanide may benefit

213
Q

what is Balantidiasis caused by? where is it commonly seen?

A
  • Balantidium coli; only ciliate that produces clinically significant infection in humans
  • found throughout the tropics, in Central and South America, Iran, Papua New Guinea and the Philippines
  • carried by pigs
  • most common in communities living closely with swine
  • identical lifecycle to E. histolytica
214
Q

what is diagnosis and treatment of Balantidiasis?

A
  • diarrhoea and a dysenteric illness with invasion of the distal ileal and colonic mucosa
  • trophozoites rather than cysts are found in the stool
  • treatment with tetracycline or metronidazole
215
Q

what is Blastocystis hominis?

A

strictly anaerobic protozoan pathogen that inhabits the colon

216
Q

what is Cyclospora cayetanensis?

A
  • coccidian protozoal parasite
  • cause of diarrhoea in travellers to Nepal
  • has been detected in stool specimens from immunocompetent and immunodeficient people worldwide
  • infection is usually self-limiting
  • treated with co-trimoxazole
217
Q

what is Microsporidiosis?

A

protozoa of the phylum Microsporea can cause diarrhoea in patients with HIV/AIDS

218
Q

what are characteristics of Helminths?

A
  • largest internal human parasite
  • reproduce sexually, generating millions of eggs or larvae
  • nematodes and trematodes have a mouth and intestinal tract
  • cestodes absorb nutrients directly through the outer tegument
  • all worms are motile, however as adults they rarely migrate further
  • adult helminths live up to 30yrs
219
Q

what categories can nemotodes (roundworms) be divided into?

A
  • tissue dwelling worms
  • intestinal human nematodes
  • zoonotic nematodes
220
Q

what is the Guinea worm?

A

Dracunculus medinensis

221
Q

what is the common roundworm?

A

Ascaris lumbricoides

222
Q

what are some tissue-dwelling worms? what diseases do they cause?

A
  • Wuchereria bancrofti; filariasis
  • Brugia malayi/timori; filariasis
  • Loa loa; loiasis
  • Onchocerca volvulus; river blindness
  • Dracunculus medinensis; dracunculiasis
  • Mansonella perstans; mansonellosis
223
Q

what are some intestinal human nematodes? what diseases do they cause?

A
  • Enterobius vernicularis; threadworm
  • Acaris lumbricoides; roundworm
  • Trichuris trichiura; whipworm
  • Necator americanus; hookworm
  • Ancylostoma duodenale; hookworm
  • Strongyloides stercoralis; strongyloidosis
224
Q

what are some zoonotic nematodes? what diseases do they cause?

A
  • Toxocara canis; toxocariasis

- Trichinella spiralis; trichinellosis

225
Q

what are some types of trematodes (flukes)?

A
  • blood flukes
  • lung flukes
  • intestinal/hepatic flukes
226
Q

what are some blood flukes?

A

Schistosoma species; causes schistosomiasis

227
Q

what are some lung flukes? what diseases do they cause?

A

Paragonimus species; paragonimiasis

228
Q

what are some intestinal/hepatic flukes?

A
  • Fasciolopsis buski
  • Fasciola hepatica
  • Clonorchis sinensis
  • Opisthorchis felineus
229
Q

what are types of cestodes (tapeworms)?

A

intestinal adult worms and larval tissue cysts

230
Q

what are some intestinal adult worms and what are their common names?

A
  • Taenia saginata; beef tapeworm
  • Taenia solium; pork tapeworm
  • Diphyllobothrium latum; fish tapeworm
  • Hymenolepis nana; dwarf tapeworm
231
Q

what are some larval tissue cysts and what are they commonly called/what disease do they cause?

A
  • Taenia solium; cysticercosis
  • Echinococcus granulosus; Hyatid disease
  • Echinococcus multilocularis; Hyatid disease
  • Spirometra mansoni; sparganosis
232
Q

what is the action of zoonotic nematodes?

A
  • accidentally infect man and are not able to complete their normal life cycle
  • often become trapped in the tissues, causing a potentially severe local inflammatory response
233
Q

what are characteristics of Filariasis?

A
  • Filarioidea superfamily
  • adult worms are long and threadlike, from 2 to 50cm in length
  • females longer than males
  • larval stages inoculated into humans by various species of biting flies (each specific to a particular parasite)
234
Q

what is the life cycle of Filariasis?

A
  • inoculated into humans by species of biting flies
  • adult worms develop from larvae mate
  • produce millions of offspring (microfilariae), which migrate in the blood or skin
  • ingested by feeding flies, where the remainder of the life cycle takes place
235
Q

how does Filariasis cause disease?

A
  • may be caused by adult worms or by microfilariae

- caused by host immune response to the parasite and is characterised by massive eosinophilia

236
Q

what is the life cycle of Filariasis?

A

adult worms are long lived (10-15yrs) and reinfection is common; disease is chronic and progressive

237
Q

what are drugs used in mass treatment of helminths?

A
  • diethylcarbamazine (DEC)
  • ivermectin
  • albendazole
  • praziquantel
238
Q

what infections is diethylcarbamazepine (DEC) used for?

A
  • loiaisis

- filariasis

239
Q

what infections is ivermectin used for?

A
  • loiaisis
  • filariasis
  • onchocerciasis
  • strongyloidiasis
240
Q

what infections is albendazole used for?

A
  • filariasis (with DEC)

- intestinal helminths

241
Q

what infection is praziquantel used for?

A

schistosomiasis

242
Q

what are filarial worms?

A
  • Wuchereria bancrofti
  • Brugia timori/malayi
  • Loa loa
  • Onchocerca
  • Mansonella perstans
243
Q

what is the site of the adult worm, microfilariae, major vector, clinical signs and distribution of Wuchereria bancrofti?

A 
adult worm: lymphatics
microfilariae: blood
major vector: Culex species
clinical signs: fever, lymphangitis, elephantiasis
distribution: tropics
244
Q

what is the site of the adult worm, microfilariae, major vector, clinical signs and distribution of Brugia timori/malayi?

A

adult worm: lymphatics
microfilariae: blood
major vector: Mansonia species
clinical signs: fever, lymphangitis, elephantiasis
distribution: East and South-east Asia, South India, Sri Lanka

245
Q

what is the site of the adult worm, microfilariae, major vector, clinical signs and distribution of Loa loa?

A 
adult worm: subcutaneous
microfilariae: blood
major vector: Chrysops species
clinical signs: Calabar swellings, urticaria
distribution: West and Central Africa
246
Q

what is the site of the adult worm, microfilariae, major vector, clinical signs and distribution of Onchocerca?

A 
adult worm: subcutaneous
microfilariae: skin, eye
major vector: Simulium species
clinical signs: subcutaneous nodules, eye disease
distribution: Africa, South America
247
Q

what is the site of the adult worm, microfilariae, major vector, clinical signs and distribution of Mansonella perstans?

A 
adult worm: retroperitoneal
microfilariae: blood
major vector: Culicoides species
clinical signs: allergic eosinophilia
distribution: Sub-Saharan Africa, South America
248
Q

what is the transmission of Wuchereria bancrofti?

A
  • by different mosquito species, mainly Culex fatigans
  • adult female worms (5-10cm long) live in lymphatics, releasing large numbers of microfilariae into the blood
  • occurs at night, so coinciding with nocturnal feeding pattern of C. fatigans
249
Q

where are non-periodic forms of W. bancrofti found?

A
  • transmitted by day-biting species

- found in South Pacific

250
Q

what is the periodicity of Brugia malayi and B. timori?

A
  • similar to W. bancrofti
  • nocturnal periodicity
  • Mansonia mosquitos
251
Q

what are clinical features of lymphatic filariasis?

A
  • larvae enter lymphatics and are carried to regional lymph nodes
  • grow and mature for 6-18 months
  • adult worms produce allergic lymphangitis
  • asymptomatic infection in endemic areas
  • early infection marked by bouts of fever with pain, tenderness and erythema along course of affected lymphatics
  • involvement of spermatic cord and epididymis common in Bancroftian filariasis
  • recurrent episodes cause intermittent lymphatic obstruction, which can become fibrotic and irreversible
  • obstructive lymphatics may rupture, causing cellulitis and further fibrosis
  • progressive enlargement, coarsening and fissuring of the skin, leading to elephantiasis
  • adult worms die, but lymphatic obstruction remains and tissue damage continues
  • microfilariae can be trapped in pulmonary capillaries, generating intense local allergic response; pneumonitis, cough, fever, weight loss and shifting radiological changes
252
Q

what is tropical pulmonary eosinophilia?

A

high peripheral eosinophil count associated with pneumonitis caused by Filariasis

253
Q

how long does elephantiasis take to develop?

A

many years; only seen in association with recurrent infection in endemic areas

254
Q

what is diagnosis of Filariasis?

A
  • detecting microfilariae in blood films or skin snips

- rapid and sensitive near-patient antigen detection tests

255
Q

what is treatment of Filariasis?

A
  • DEC kills adult worms and microfilariae
  • serious allergic responses may occur as parasites are killed
  • mass treatment programmes using combinations of DEC, ivermectin and albendazole
256
Q

what causes Loiasis?

A
  • found in humid forests of West and Central Africa
  • caused by Loa loa; small (3-7cm filarial worm), found in subcutaneous tissues
  • microfilariae circulate in blood during day but cause no direct symptoms
  • vectors are day-biting flies of genus Chrysops
257
Q

what is the behaviour of Loa loa in the body?

A
  • adult worms migrate around the body in subcutaneous tissue planes
  • worms may be present for years w/out causing symptoms
258
Q

what are clinical features of Loiasis?

A
  • localised, tender, hot, soft tissue swellings occur due to hypoersensitivity (Calabar swellings) often near a joint; produced in response to passage of a worm
  • urticaria and pruitus
  • worm may be seen crossing eye under conjunctiva
  • may enter the retroorbital tissue; severe pain
259
Q

what are Calabar swellings?

A
  • occur in Loiasis due to passage of a worm

- localised, tender, hot, soft tissue swellings occur due to hypoersensitivity, often near a joint

260
Q

what is diagnosis of Loiasis?

A
  • microfilariae may be seen on stained blood films (often negative)
  • serological tests relatively insensitive and cross-react with other microfilariae
  • massive eosinophilia
261
Q

what is treatment of Loiasis?

A
  • DEC may cause severe allergic reactions associated with parasite killing
  • ivermectin in single doses of 200-400ug/kg is effective; may cause severe reactions
  • albendazole may be used in heavily-infected patients
  • mass treatment with DEC or ivermectin can decrease transmission
262
Q

what is Onchocerciasis? what is it caused by?

A
  • river blindness
  • 37 million people worldwide; 250k are blind and 500k visually impaired
  • West and Central Africa, small foci in Yemen and Central and South America
  • Onchocerca volvulus
  • day-biting flies of genus Simulium
263
Q

what is the pathogenesis of Onchocerciasis?

A
  • larvae inoculated by bite of infected fly
  • worms mature in 2-4 months, live more than 15 years
  • adult worms 50cm and <0.5mm diameter
  • live in subcutaneous tissues
264
Q

what are clinical features of Onchocerciasis?

A
  • fibrotic nodules, esp. over bone and trauma sites
  • microfilariae distributed in skin; may invade eyes
  • live microfilariae cause little harm, dead parasites may cause severe allergic reactions, with hyaline necrosis and loss of tissue collagen and elastin
  • conjunctivitis, sclerosing keratitis, uveitis and secondary glaucoma, and choroidoretinitis
  • pruitus, urticaria and fleeting oedema
  • subcutaneous nodules, hypo/hyperpigmentation from excoriation and inflammatory changes
  • roughened, inelastic skin
  • hanging groin
265
Q

what is diagnosis of Onchocerciasis?

A
  • eosinophilia on blood film
  • skin snips taken from iliac crest or shoulder placed in saline under cover slip
  • after 4hrs, microscopy shows microfilariae
  • if this is negative, DEC applied topically under occlusive dressing; provokes an allergic rash (modified Mazzotti reaction)
  • slit lamp examination of eyes may show microfilariae
266
Q

what is the modified Mazzotti reaction?

A
  • used to diagnose Onchocerciasis
  • if microscopy is negative, DEC is applied topically under an occlusive dressing
  • provokes allergic rash in most infected people
267
Q

what is management of Onchocerciasis?

A

Ivermectin, 150ug/kg

  • kills microfilariae and prevents return for 6-12 months
  • little effect on adult worms
  • annual retreatment is needed
  • in patients coinfected with Loa loa, it may induce severe allergic reactions, including toxic encephalopathy
268
Q

what are features of Mansonellosis?

A

Mansonella perstans

  • filarial worm
  • transmitted by biting midges of genus Culicoides
  • small numbers of microfilariae are in blood
  • don’t cause serious disease
  • may be minor allergic reactions and an eosinophilia
269
Q

what causes Dracunculiasis? how is it transmitted?

A

Dracunculus medinensis (Guinea worm)

  • water fleas (copepods) containing the parasite larvae are swallowed in contaminated drinking water
  • ingested larvae mature and the female worm (up to 1m in length) migrates through connective and subcutaneous tissue for 9-18 months
  • surfaces on skin
  • uterus of worm rupture, releasing larvae which are ingested by small crustacean water fleas; cycle is completed
270
Q

what is treatment of Dracunculiasis?

A
  • extracting worm over several days by winding it round a stick
  • worm should not be damaged
  • antibiotics for secondary infection
271
Q

how is infection of human intestinal nematodes spread?

A
  • two main types of life cycle, both including a soil based phase
  • ingestion of eggs (require period of maturation in environment) OR
  • eggs hatch in soil and larvae penetrate directly through the skin of a new host
272
Q

what is Ascariasis? what causes it? how is it transmitted?

A

roundworm infection; Ascaris lumbricoides

  • pale yellow worm, 20-35cm long
  • found worldwide, common in poor rural communities with faecal contamination
  • larvae migrate through tissues to the lungs
  • expectorated and swallowed
  • adult worms are found in small intestine
  • ova are deposited in faeces and need 2-4 month maturation in soil before infected
273
Q

what are clinical features of Ascariasis?

A
  • usually asymptomatic
  • heavy infections: nausea, vomiting, abdominal discomfort, anorexia
  • worms may obstruct small intestine, esp. at ileocaecal valve
  • may invade appendix, causing acute appendicitis, or bile duct, obstructing it and suppurative cholangitis
  • larvae in lung may cause pulmonary eosinophilia
  • heavy infection in children effects nutrition and development
274
Q

what is diagnosis of Ascariasis?

A
  • eggs identified in stool
  • adult worms may emerge from mouth or anus
  • barium enema studies
275
Q

what is treatment of Ascariasis?

A
  • piperazine, pyrantel pamoate, oxantel pamoate, albendazole, mebendazole, levamisole
  • surgical or endoscopic intervention for intestinal or biliary obstruction
276
Q

what are drugs used for treating human intestinal nematodes and their doses?

A
  • piperazine 75mg/kg
  • pyrantel pamoate 10mg/kg
  • oxantel pamoate 10mg/kg
  • albendazole 400mg
  • mebendazole 500mg
  • tiabendazole 25mg/kg
  • levamisole 2.5mg/kg
  • ivermectin 200ug/kg
277
Q

what is threadworm? what does it do? how is it transmitted?

A

Enterobius vermicularis

  • small (2-12mm) worm
  • common throughout world
  • larval development occurs in small intestine and adult worms are normally found in the colon
  • gravid female deposits eggs around the anus causing intense itching, esp. at night
  • do not need a maturation period in soil and infection often directly transmitted from anus to mouth via hands
  • eggs deposited on clothing and bed linen and are ingested/inhaled
  • usually harmless
278
Q

what is diagnosis of threadworm (Enterobius vermicularis)?

A
  • ova collected using moistened perianal swab
  • applying adhesive cellophane tape to perianal skin
  • identified by microscopy
279
Q

what is the treatment of threadworm (Enterobius vermicularis)?

A
  • mebendazole and piperazine
  • isolated treatment of affected person often ineffective
  • other family members may need to be treated and advised about personal hygeine
  • two course of treatment 2 weeks apart may break cycle of autoinfection
280
Q

what is Whipworm? what do they do? how are they transmitted?

A

Trichuris trichiura

  • common worldwide, esp. in poor communities with inadequate sanitation
  • adult worms are 3-5cm long
  • inhabit terminal ileum and caecum
  • found throughout large bowel in heavy infection
  • head of worm embedded in intestinal mucosa
  • ova deposited in faeces and require maturation period of 3-4 weeks in soil before becoming infective
281
Q

what are clinical features of whipworm (Trichuris trichiura)?

A

usually asymptomatic, but mucosal damage may be so severe that there is colonic ulceration, dysentery or rectal prolapse

282
Q

what is diagnosis of whipworm (Trichuris trichiura)?

A

finding ova on stool microscopy, or by seeing adult worms on sigmoidoscopy

283
Q

what are hookworm infections caused by? where are they found?

A

human hookworms Ancylostoma duodenale and Necator americanus

  • A. duodenale found mainly in East Asia, North Africa and Mediterranean
  • N. americanus found in South and Central America, South-east Asia and sub-Saharan Africa
284
Q

how do hookworms behave in the human body?

A
  • adult worms are 1cm long
  • live in the duodenum and upper jejunum (found in large numbers)
  • attach firmly to the mucosa using the buccal plate, feeding on blood
  • eggs passed in the faeces develop in warm moist soil, producing infective filariform larvae
  • filariform penetrate directly through the skin of a new host and are carried in the bloodstream to the lungs
  • cross the alveoli and parasites are expectorated and then swallowed, arriving at their definitive home
285
Q

what are clinical features of hookworm infection?

A
  • local irritation as the larvae penetrate the skin (ground itch)
  • transient pulmonary signs and symptoms, with eosinophilia
  • light infections often asymptomatic
  • heavier worm loads associated with epigastric pain and nausea, esp. with malnourishment; may cause iron deficiency anaemia and hypoproteinaemia
  • heavy infection in children associated with delays in physical and mental development
286
Q

what is diagnosis of hookworm infection?

A

finding eggs on faecal microscopy; in infections heavy enough to cause anaemia, they present in large numbers

287
Q

what is treatment of hookworm infection?

A
  • aim of treatment in endemic areas is reduction of worm burden rather than complete eradication
  • albendazole given as a single dose
  • WHO is promoting treatment programmes for school children in many parts of the world, with treatment of schistosomiasis where appropriate
288
Q

what causes Strongyloidiasis?

A

Strongyloides stercoralis

  • small (2mm long) worm
  • lives in small intestine
  • found in many parts of the tropics and subtropics; esp. common in Asia
289
Q

what is the behaviour of Strongyloides stercoralis in the human body?

A
  • eggs hatch in the bowel
  • larvae found in the stool
  • non-infective rhabditiform larvae
  • require further period of maturation in soil before becoming infective
  • maturation can occur in large bowel
  • infective filariform larvae can penetrate directly through the perianal skin, reinfecting the host
  • after skin penetration, life cycle is similar to hookworm
  • adult worms may burrow into intestinal mucosa, causing a local inflammatory response
290
Q

what are clinical features of Strongyloidiasis?

A
  • local dermatitis (in autoinfection, this manifests as a migratory linear weal around the buttocks and lower abdomen (cutaenous larva currens))
  • heavy infections; damage to small intestinal mucosa causes malabsorption, diarrhoea and perforation
  • persistent eosinophilia
  • immunocompromised patients: filariform larvae may penetrate directly though the bowel wall, causing an overwhelming and usually fatal generalised infection
  • complicated by Gram-negative septicaemia due to bowel organsms
291
Q

what is strongyloidiasis hyperinfestation syndrome?

A
  • occurs in immunosuppressed patients (by corticosteroids or intercurrent illness)
  • filariform larvae may penetrate directly through the bowel wall in huge numbers
  • causes an overwhelming and usually fatal generalised infection
292
Q

what is the diagnosis and treatment of Strongyloidiasis?

A
  • motile larvae seen on stool microscopy, esp. after incubation
  • serological tests
  • ivermectin (200ug/kg daily for 2 days)
  • albendazole (15mg/kg 12 hourly for 3 days)
293
Q

what causes Trichinosis?

A

Trichinella spiralis

  • normal hosts are pigs, bears and warthogs
  • humans infected by eating undercooked meat from these animals
294
Q

how does Trichinella spiralis infect the human body?

A
  • eating undercooked meat from pigs, bears and warthogs
  • ingested larvae mature in the small intestine
  • adults release new larvae which penetrate the bowel wall and migrate through the tissues
  • larvae encyst in striated muscle
295
Q

what are clinical features of Trichinosis?

A
  • light infections usually asymptomatic
  • heavier loads of worms produce GI symptoms as adults establish themselves in the small intestine, followed by systemic symptoms as larvae invade
  • systemic symptoms: fever, oedema and myalgia
  • massive infection could be fatal
296
Q

what is diagnosis and treatment of Trichinosis?

A
  • clinical picture, associated eosinophilia and serological tests
  • muscle biopsy a few weeks after infection
  • albendazole (20mg/kg for 7 days) given early will kill adult worms and decrease load of larvae reaching the tissues
  • analgesia and steroids for symptomatic relief
297
Q

what causes Toxocariasis (visceral larva migrans)?

A

Toxocara canis

  • dog roundworm
  • may be ingested by humans, esp. children
298
Q

what is the behaviour of Toxocara canis in the human body?

A
  • eggs hatch and larvae penetrate small intestinal wall and enter the mesenteric circulation
  • unable to complete their life cycle in a foreign host
  • held up in liver capillaries, generating a granulomatous response
  • may migrate into lungs, striated muscle, heart, brain or eye
299
Q

what are clinical features of Toxocariasis?

A
  • infection usually asymptomatic; larvae die without causing serious problems
  • generalised symptoms (fever and urticaria) and eosinophilia, and focal signs in heavy infections
  • pulmonary involvement may cause bronchospasm and chest x-ray changes
  • ocular infection may produce granulomatous swelling mimicking retinoblastoma
  • cardiac or neurological involvement may be fatal
300
Q

what is diagnosis and treatment of Toxxocariasis?

A
  • isolation of larvae is difficult and diagnosis usually made serologically
  • albendazole 400mg daily (5-10mg/kg in children) for a week
301
Q

what is CLM?

A

cutaneous larva migrans

302
Q

what causes cutaneous larva migrans?

A

non-human hookworms Ancylostoma braziliense and A. canium

303
Q

how is cutaneous larva migrans transmitted?

A
  • hatch in warm moist soil and penetrate the skin
  • in man they’re unable to complete a normal life cycle
  • migrate under the skin for days or weeks until death
304
Q

what are clinical features of cutaneous larva migrans?

A
  • wandering of the larva accompanied by clearly defined, serpiginous, itchy rash; progresses 1cm per day
  • no systemic symptoms
305
Q

what is the diagnosis and treatment of cutaneous larva migrans?

A
  • diagnosis purely clinical
  • single larvae treated with 15% solution of topical tiabendazole
  • multiple lesions treated with systemic therapy; single dose of albendazole 400mg or ivermectin 150-200ug/kg
306
Q

what are trematodes? how do they cause disease?

A
  • flukes
  • flat leaf-shaped worms
  • complex life cycles, often involving fresh water snails and intermediate mammalian hosts
  • disease caused by inflammatory response to eggs or to adult worms
307
Q

what is the epidemiology of Schistosomiasis?

A
  • affects over 200 million people in the tropics and subtropics, mostly in sub-Saharan Africa
  • chronic infection causes significant morbidity
  • socioeconomic impact
  • disease of rural poor, but also with major development projects e.g. dams and irrigation schemes
308
Q

what are the species of schistosome that cause disease in humans?

A
  • Schistosoma mansoni
  • S. haematobium
  • S. japonicum
  • S. mekongi
  • S. intercalatum
309
Q

how do Schistosomes multiply?

A
  • eggs are passed in the urine or faces of an infected person and hatch in fresh water to release miracidia
  • ciliated organisms penetrate tissue of intermediate host, a species of water snail specific to each species of schistosome
  • multiply in snail, then fork-tailed cercariae are released back into the water, and survive for 2-3 days
310
Q

how do Schistosomes behave in the human body?

A
  • cercariae penetrate skin or mucous membranes of human
  • transform into schistosomulae
  • pass through lungs
  • reach portal vein, where they mature into adult worms (20+mm long)
  • worms pair in portal vein before migrating to final destination
  • remain in final destination for many years, producing many eggs, which are released in urine or faeces, or in the bladder, bowel wall, liver/distant sites
311
Q

what are the final destinations in the human body of the schistosomes?

A

S. mansoni and S. japonicum: mesenteric veins

S. haematobium: vesicular plexus

312
Q

what are clinical features of Schistosome infection?

A
  • local and systemic allergic reactions to migrating parasites in early stages
  • local inflammatory response in bowel or bladder when eggs are produced
  • ectopic eggs may produce granulomatous lesions anywhere in the body
  • chronic heavy infection (many eggs accumulate in the tissues); fibrosis, calcifications, dysplasia and malignant change
  • cerianal penetration may cause local dermatitis
  • symptom free period of 3-4 weeks
  • systemic allergic features: fever, rash, myalgia and pneumonitis (Katayama fever)
313
Q

what is drug treatment of Schistosoma mansoni?

A

praziquantel 40mg/kg single dose

314
Q

what is drug treatment of S. haematobium?

A

praziquantel 40mg/kg single dose

315
Q

what is drug treatment of S. japonicum?

A

praziquantel 60mg/kg single dose

316
Q

what is drug treatment of Paragonimus spp.?

A

praziquantel 25mg/kg 8hrly for 3 days

317
Q

what is drug treatment of Clonorchis sinensis?

A

praziquantel 25mg/kg 8hrly for 1-3 days

318
Q

what is drug treatment of Opisthorchis spp.?

A

praziquantel 25mg/kg 8hrly for 1-3 days

319
Q

what is drug treatment of Fasciolopsis buski?

A

praziquantel 25mg/kg 8hrly for 1 day

320
Q

what is drug treatment of Fasciola hepatica?

A

triclabendazole 10mg/kg single dose

321
Q

what are clinical features of S. haematobium infection (bilharzia)?

A
  • painless terminal haematuria
  • bladder inflammation progresses -> increased urinary frequency and groin pain
  • obstrucive uropathy -> hydronephrosis, CKD and recurrent urinary infection
  • association between chronic urinary schistosomiasis and squamous cell bladder carcinoma
  • genitalia may be affected
  • ectopic eggs may cause pulmonary or neurolgical disease
322
Q

what are clinical features of S. mansoni infection?

A
  • affects large bowel
  • early disease produces superficial mucosal changes, with blood-stained diarrhoea
  • marked mucosal damage with rectal polyps, deeper ulceration and fibrosis and stricture formation
  • ectopic eggs carried to liver, where they cause intense granulomatous response
  • hepatitis followed by progressive periportal fibrosis -> portal hypertension, oesophageal varices and splenomegaly
323
Q

what are clinical features of S. japonicum?

A
  • infects many mammals apart from man
  • infects large and small bowel
  • produces more eggs than S. mansoni
  • severe and rapidly progressive
  • hepatic involvement more common and neurological involvement in 5% of cases
324
Q

what is diagnosis of Schistosomiasis?

A
  • suggested by relevant symptoms following fresh water exposure in an endemic area
  • characteristic eggs (terminal spine in S. haematobium and lateral spine in other species) seen in microscopy
  • S. haematobium seen in a filtered mid-day urine sample, semen and rectal snips
  • S. mansoni and S. japonicum eggs found in faces or rectal snip
    0 serological tests
  • xray, ultrasound and endoscopy may show abnormal bowel/urinary tract in chronic disease
  • liver biopsy may show periportal fibrosis
325
Q

what is the aim of management of Schistosomiasis?

A
  • aim in endemic areas is to decrease worm load and minimise chronic effects of egg deposition
  • may not be possible to eradicate adult worms completely
  • reinfection common
  • 90% reduction in egg output has been achieved in mass treatment programmes
326
Q

what are food-borne flukes?

A

many flukes infect man via ingestion of an intermediate host, often fresh water fish

327
Q

what causes Paragonimiasis?

A

Paragonimus

  • major species is P. westermani
  • adult worms live in the lungs, producing eggs which are expectorated or swallowed and passed in the faeces
328
Q

how do Paragonimus species infect humans?

A
  • adult worms live in the lungs, producing eggs which are expectorated or swallowed and passed in the faeces
  • miracidia emerging from the eggs penetrate the first intermediate host, a fresh water snail
  • larvae released from snail, and encyst as metacercariae in fresh water crustacea
  • humans become infected after consuming uncooked shellfish
  • cercariae penetrate small intestinal wall and migrate directly from the peritoneum to lungs across the diaphragm
329
Q

how do Paragonimus species move within the human body?

A
  • humans become infected after consuming uncooked shellfish
  • cercariae penetrate small intestinal wall and migrate directly from the peritoneum to lungs across the diaphragm
  • establish themselves in lungs
  • can survive up to 20yrs
330
Q

what are clinical features of Paragonimiasis?

A
  • fever
  • cough
  • mild haemoptysis
  • pneumonia or pulmonary TB
  • ectopic worms may cause signs in the abdomen or brain
331
Q

what is diagnosis of Paragonimiasis?

A
  • detection of ova on sputum or stool microscopy
  • radiological appearances are variable and nonspecific
  • treatment with praziquantel and avoidance of inadequately cooked shellfish
332
Q

what are the human liver flukes?

A
  • Clonorchis sinensis
  • Opisthorchis felineus
  • O. viverrini
333
Q

what is the cycle of human liver flukes? what hosts do they need? how do they live in the human body?

A
  • adults live in bile ducts, releasing eggs into faeces
  • parasite requires two intermediate hosts, a fresh water snail and fish
  • humans infected by consumption of raw fish
  • cycle completed when excysted worms migrate from small intestine into bile ducts
334
Q

what are clinical features, diagnosis and treatment of liver flukes?

A
  • infection often asymptomatic, but may be associated with cholangitis and biliary carcinoma
  • diagnosis made by identifying eggs on stool microscopy
  • treatment with praziquantel and cooking fish adequately
335
Q

what are features of Fasciola hepatica and Fasciolopsis buski?

A
  • liver and intestinal flukes
  • require water snail as an intermediate host
  • cercariae encyst on aquatic vegetation and are consumed by animals or man
  • F. hepatica penetrates the intestinal wall before migrating to the liver
  • F. buski doesn’t migrate causes mainly bowel symptoms
336
Q

what are cestodes?

A
  • tapeworms
  • ribbon-shaped worms
  • mm to several m in length
337
Q

how do cestodes (tapeworms) develop in the human body?

A
  • adult worms live in intestine
  • attach to epithelium using suckers on anterior portion (scolex)
  • proglottids (progressively developing segments) arise from scolex
  • mature distal segments contain eggs and are released directly into faces or are carried out with an intact detached proglottid
  • eggs consumed by intermediate hosts
  • hatch into larvae (oncospheres)
  • penetrate intestinal wall of the host (pig or cattle) and encyst in the tissues
338
Q

what is the beef tapeworm?

A

Taenia saginata

  • few if any symptoms
  • infection discovered when proglottids are found in faeces or on underclothing
  • praziquantel (10mg/kg)
339
Q

what is the pork tapeworm?

A

Taenia solium

  • can reach 6m in length
  • South America, South Africa, China and South-east Asia
340
Q

what causes cysticercosis?

A
  • ingestion of cysts of Taenia solium rather than the adult worm; follows ingestion of eggs from contaminated food or water
  • patients with tapeworms do not usually develop cysticercosis and patients with cysticercosis do not harbour tapeworms
341
Q

what are cysticerci?

A

cysts, 0.5-1cm in diameter, containing scolex of a new adult worm
- common sites are subcutaneous tissue, skeletal muscle and brain

342
Q

what is the fish tapeworm?

A

Diphyllobothrium latum

  • Europe and Japan
  • consumption of raw fish
  • no symptoms
  • megaloblastic anaemia (due to competetive utilisation of B12 by the parasite)
343
Q

what is the dog tapeworm?

A

Echinococcus granulosus

344
Q

what is Hyatid disease?

A
  • occurs when humans become an intermediate host of the dog tapeworm Echinococcus granulosus
  • adult worm lives in gut of domestic and wild canines
  • larval stages in sheep, cattle and camels
  • excyst, penetrate the small intestine wall and are carried to the liver
  • life cycle cannot be completed unless cyst is eaten by a dog
345
Q

what are symptoms of Hyatid disease?

A
  • depend on site of cyst
  • liver is most common organ affected, then lung, kidneys, brain and bone
  • pressure on bile ducts -> jaundice
  • rupture into abdominal cavity, pleural cavity or biliary tree
  • intermittent jaundice, abdominal pain, fever with eosinophilia
  • focal seizures if cysts in brain
  • renal involvement produces lumbar pain and haematuria
  • calcification of cyst
  • cyst rupturing into bronchus may result in expectoration and spontaneous cure
346
Q

what is a parasite of foxes?

A

Echinococcus multilocularis

347
Q

what is fish tapeworm?

A

Diphyllobothrium latum

348
Q

what is dwarf tapeworm?

A

Hymenolepis nana

349
Q

what causes Cysticercosis?

A

Taenia solium

350
Q

what organisms cause Hyatid disease?

A
  • Echinococcus granulosus

- E. multilocularis

351
Q

what causes Sparganosis?

A

Spirometra mansoni

352
Q

what causes Trichinellosis?

A

Trichinella spiralis

353
Q

what causes Toxocariasis?

A

Toxocara canis

354
Q

what are species of hookworm?

A
  • Necator americanus

- Ancylostoma duodenale

355
Q

what organisms cause Filariasis?

A
  • Wucheria bancrofti

- Brugia malayi/timori

356
Q

what organism cause Loiasis?

A

Loa loa

357
Q

what organism causes river blindness?

A

Onchocerca volvulus

358
Q

what organism causes Dracunculiasis?

A

Dracunculus medinensis

359
Q

what organism causes Mansonellosis?

A

Mansonella perstans

360
Q

what is an example of a threadworm?

A

Enterobius vermicularis

361
Q

what is an example of a roundworm?

A

Ascaris lumbicoides

362
Q

what is an example of a whipworm?

A

Trichuris trichiura

363
Q

what organism causes Strongyloidosis?

A

Strongyloides stercoralis

Phase 2A (28 decks)

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