Dr Jenny Robson

Infectious diseases

Podcasts

Q fever – Indications for testing

Prevaccination screen; acute Q fever; post-acute Q fever monitoring (particularly where there is a risk of developing chronic infection)

Sexual health

Clinical Articles

Detecting and treating Mycoplasma genitalium

Mycoplasma genitalium (M. genitalium), is thought to affect up to 400,000 Australians. It causes urethritis in men, and in women it can lead to pelvic inflammatory disease, cervicitis and preterm labour. It is also a recognised cause of anorectal proctitis along with other infections including Chlamydia trachomatis (including the LGV strains), gonorrhoea, syphilis, HSV and shigellosis. Asymptomatic infection is also common. Who to test Only test those with symptoms and their contacts. Screening asymptomatic people for M. genitalium is not currently recommended. Diagnosis Females: PCR on endocervical or vaginal swab, first pass urine (FPU), ThinPrep -collected by cervical brush/swab. Males: PCR on urethral swab (in preference to FPU), anorectal swabs. Throat swabs are not recommended as pharyngeal infection is uncommon. Transport: Ambient temperature; if there is any delay from collection to transport to the laboratory, the sample must be refrigerated Current treatment recommendations Preliminary data from the patient populations suggests resistance rates to macrolides may be as high as 64 per cent. The highest rates are likely to be in the men who have sex with men (MSM) population. Although information regarding fluoroquinolone resistance (moxifloxacin) is not available with this test, some studies suggest resistance to fluoroquinolones is present in 10–15% of infections. Doxycycline alone is ineffective in two-thirds of infections but will lower bacterial load in most cases, increasing the likelihood of cure with a subsequent antibiotic. Pretreating M. genitalium infections with doxycycline for one week and then treating susceptible infections with azithromycin and macrolide-resistant infections with a fluoroquinolone eradicates >90% of infections. Current treatment regimens Macrolide sensitive Doxycycline 100mg bd for seven days followed by azithromycin 1g stat then 500mg daily for three days (total 2.5g) OR Doxycycline 100mg bd for seven days followed by azithromycin 1g single dose. It is not known to what extent the improved outcomes resulting from the use of doxycycline followed by 2.5g azithromycin are due to this dose of azithromycin, rather than simply the pre-treatment with doxycycline. The higher dose of azithromycin requires a private prescription. Macrolide resistant Doxycycline 100mg bd for seven days followed by moxifloxacin 400mg daily for seven days. A longer course of moxifloxacin may be required in women with pelvic inflammatory disease. Moxifloxacin requires a private prescription, cannot be used in pregnancy and is expensive. It is associated with diarrhoea, occasional tendinopathy and rare neurological and cardiac events. Treatment failures following appropriate fluoroquinolone treatment may require specialist advice. Additional actions Advise no sex without condoms until tested for cure (14 days after completion of treatment). Advise no sex with untested previous sexual partners. Test of cure Test of cure by PCR should be done at least two weeks after treatment is completed i.e. four weeks after commencing therapy. Contact tracing In heterosexuals, the risk of PID and reproductive complications suggests a greater need to trace, test and treat infected contacts. The time period for contact tracing is unknown. Asymptomatic infection and macrolide resistance are more common in MSM and there is only limited evidence that this is harmful. As moxifloxacin will probably be required for treatment, contact tracing may be best confined to continuing partners of a symptomatic person. References: Australian STI Management Guidelines for Use in Primary Care http://www.sti.guidelines.org.au/sexually-transmissible-infections/mycoplasma-genitalium#management Australian Contact Tracing Manual contacttracing.ashm.org.au/conditions/when-contact-tracing-is-recommended/mycoplasma-genitalium General Practice Pathology is a new regular column each authored by an Australian expert pathologist on a topic of particular relevance and interest to practising GPs. The authors provide this editorial, free of charge as part of an educational initiative developed and coordinated by Sonic Pathology.

Infectious diseases

Clinical Articles

The microbiology laboratory has made great strides in introducing clinically useful diagnostics over the past couple of decades, particularly in recent years with the development of molecular assays that ‘narrow the gap’ and provide early diagnoses. While introducing new tests, it has also been important to evaluate and discard old tests that may not contribute greatly to patient outcomes. One such test that has come under the spotlight is the classic Widal agglutination test in the diagnosis of typhoid. The Widal test, developed by George Fernand Widal in 1896, uses a suspension of killed Salmonella typhi as antigen to detect agglutinating antibodies to somatic O antigens and flagellar H antigens present in serum of typhoid patients. There are many reasons for its lack of clinical utility. Antibodies are not present in the acute illness and take time to develop. Significant cross reactivity can occur with other infectious agents that mimic typhoid including malaria, dengue, endocarditis, tuberculosis and chronic liver disease. Other limitations are of a technical nature and include non-standardisation of the antigen preparation used in the assay, interference with serological responses following typhoid vaccination commonly provided to travellers, and prior exposure and antibodies in patients most susceptible to typhoid, especially those from endemic areas visiting friends and relatives (VFRs). Unless multiple antigens are included, it generally does not detect the other causes of enteric fever, S. Paratyphi A, B and C. It is now time to discontinue this simple agglutination test for typhoid in modern medicine and consider more appropriate diagnostic tests. Typhoid fever Typhoid fever is a life-threatening illness caused by the bacterium Salmonella Typhi. Whereas Salmonellae which cause gastroenteritis are zoonoses, humans are the only reservoir for S.Typhi and S. Paratyphi which cause enteric fever. Typhoid fever is still common in the developing world where it affects about 21.5 million people each year but is much less common in the Lucky Country such as ours where good sanitation prevails. About 100 cases are notified each year in Australia. In 2014, 92% of cases were acquired overseas. India continues to be the most common country of acquisition and in 2014 accounted for more than half of cases. Most transmission occurs through contaminated drinking water or food. Large epidemics are most often related to faecal contamination of water supplies or street-vended foods. A chronic carrier state – excretion of the organism for more than one year – occurs in about 5% of infected persons. Where no travel history is present, the likely source of infection is contaminated food or water from a human carrier akin to ‘Typhoid Mary’. Such an outbreak was reported in Auckland, New Zealand, this year where 20 local cases and one death occurred when a carrier from Samoa helped prepare food at a church community gathering. The incubation period is typically eight to 14 days but may be much longer. Without therapy, the illness may last for three to four weeks and death rates range between 12% and 30%. Increasing resistance to available antimicrobial agents, including fluoroquinolones, has occurred in recent years. Resistance to antimicrobials including amoxycillin, and trimethoprim+sulfamethoxazole has limited the options for treatment; reduced susceptibility to quinolones is common in infections acquired on the Indian subcontinent and in Southeast Asia. While awaiting the results of susceptibility testing, azithromycin or ceftriaxone should be used for initial therapy for infections acquired in these regions. Diagnosis of enteric fevers Two sets of blood cultures are the single most useful diagnostic procedure for diagnosis of enteric fever. Other bodily fluids and tissues may yield positive cultures including faeces, urine, and if seeded, bones and joints, liver and gall bladder. Food handlers, healthcare workers, carers of children, and carers of the elderly, and others who are not able to maintain their own personal hygiene, should further be excluded from working with food or caring for people until two consecutive stool specimens – collected at least 48 hours apart and the first specimen collected not sooner than 48 hours post-cessation of antibiotics – are culture negative. Prevention Both an oral live attenuated multi-dose vaccine and a killed vaccine are available. Booster doses after 3-5 years are generally required if continued exposure occurs. Vaccine efficacy is of the order of only 80%. What to order Blood culture x 2 (Salmonella Typhi and Salmonella Paratyphi) Faeces for Bacterial PCR and MCS; Urine MCS Collection Centres: Faeces and urine samples are accepted at all collection centres. Blood cultures are collected only at designated collection centres. Sample Blood (use blood culture bottles), faeces, urine Transportation Ambient Costs Medicare rebate applies Typhoid Mary Mary Mallon, better known as Typhoid Mary, was an Irish immigrant to New York and the first person in the United States identified as an asymptomatic carrier of the pathogen associated with typhoid fever. Over the course of her career as a cook, she was presumed to have infected 51 people, three of whom died. She was twice forcibly isolated by public health authorities and died after a total of nearly three decades in isolation. General Practice Pathology is a new regular column each authored by an Australian expert pathologist on a topic of particular relevance and interest to practising GPs. The authors provide this editorial, free of charge as part of an educational initiative developed and coordinated by Sonic Pathology.

Dermatology

Clinical Articles

In Australia the commonest encounter with fungi in a medical sense is with superficial and cutaneous fungal infections such as those infecting the skin, scalp or nails.

Tinea or ringworm of the scalp, skin and nails

Fungal infection of the scalp (tinea capitus), skin (tinea) and nails (tinea unguium, onychomycosis) is usually caused by dermatophytes which have a unique ability to utilise keratin as a nutrient source due to the presence of the enzyme keratinase allowing colonisation of the stratum corneum. The presence of the fungus and its metabolic products can occasionally induce an allergic or inflammatory response in the host. The type and severity of the host response is often related to the species and strain of dermatophyte causing the infection. Following is a list of the dermatophytes that have been identified in our laboratories:

SPECIES	NATURAL HABITAT	INCIDENCE
Epidermophyton floccosum	Humans	Common
Trichophyton rubrum [worldwide]	Humans	Very common
Trichophyton interdigitale [anthropophilic]	Humans	Very common
Trichophyton tonsurans	Humans	Common
Trichophyton violaceum	Humans	Less common
Trichophyton concentricum	Humans	Rare
Trichophyton schoenleinii	Humans	Rare
Trichophyton soudanense	Humans	Rare
Trichophyton rubrum [African]	Humans	Rare
Microsporum audouinii	Humans	Less common

SPECIES	NATURAL HABITAT	INCIDENCE
Trichophyton interdigitale [zoophilic]	Mice, rodents	Common
Trichophyton erinacei	Hedgehogs	Rare
Microsporum canis	Cats	Common

SPECIES	NATURAL HABITAT	INCIDENCE
Microsporum gypseum	Soil	Common
Microsporum nanum	Soil/pigs	Rare
Microsporum cookei	Soil	Rare

Mycotic infections

Despite the majority of work done by mycology laboratories being concerned with superficial and cutaneous fungal infections, in recent years there has been an increase in fungal subcutaneous and systemic disease. Mycotic infections are usually classified according to the level of tissue involvement in the patient. The following table includes examples of such mycotic infections, their classification and an indication of their incidence.

LEVEL OF INFECTION	MYCOSIS	CAUSATIVE ORGANISM	INCIDENCE
Superficial	Pityriasis versicolor Seborrhoeic dermatitis including dandruff and follicular pityriasis	Malassezia furfur (a lipophilic yeast)	Common
	Tinea nigra	Hortaea werneckii	Rare
	White Piedra	Trichosporon sp	Common
	Black Piedra	Piedraia hortaea	Rare
Cutaneous	Dermatophytosis	Trichophyton, Epidermophyton, Microsporum
	Dermatomycosis	Fungi other than dermatophytes
	Candidiasis	Candida species
	Other yeasts	Geotrichum, Trichosporon
Subcutaneous	Sporotrichosis	Sporothrix schenckii	Rare
	Chromoblastomycosis	Fonsecaea, Phialophora, Cladophialophora etc	Rare
	Phaeohyphomycosis	Cladophialophora, Exophiala, Bipolaris, Exserohilum, Curvularia	Rare
Dimorphic Systemic Mycoses	Histoplasmosis	Histoplasma capsulatum	Rare
Opportunistic Systemic Mycoses	Candidiasis	Candida albicans and related species	Common
	Cryptococcosis	Cryptococcus neoformans	Rare/Common
	Aspergillosis	Aspergillus fumigatus etc	Rare

Specimen Collection

Laboratory diagnosis requires collection of an adequate amount of material for both microscopy and culture. The site needs to be cleaned with an alcohol wipe, which helps lower the contamination rate from bacteria, saprophytic moulds and yeasts that may overgrow a dermatophyte. As a health and safety precaution, scalpel blades should not be enclosed with specimen.

Scalp

In general, zoophilic fungi e.g. M.canis tend to cause ectothrix or involvement of the outside of the hair shaft and the lesions tend to be inflammatory, while anthropophilic fungi e.g. T.tonsurans result in endothrix or involvement of the hair shaft itself. The lesions are less inflammatory. Lustreless, broken, infected hairs should be sampled from the edge of a lesion. It is important to collect hair roots, as this is where fungal elements are detected. A scalpel blade may be used to dislodge crusts or scales in which hair stumps may be embedded.

Skin

Skin scrapings should be obtained by scraping the active border of the infection which usually is typically scaly, red and elevated and where the hyphae are present. In cases of kerion, swabs of the exudates should be collected. Separate specimens should be taken from the representative lesions on various parts of the body. When scraping feet, the site of most common involvement is between the fourth and fifth toes.

Nails

Scrape under the nail plate until the crumbling white degenerative portion is reached. All the keratin debris from under the nail should be collected directly onto a black collection card. The distal portion of the nail may need to be trimmed with nail clippers. Fungal elements remain viable for weeks at room temperature. Nail scrapings showing hyaline septate hyphae are diagnostic for a dermatophyte.

Transportation

Glass or plastic bottles with screw tops are not recommended since high relative humidity encourages proliferation of bacteria and reduces the chances of isolating fungi. Specimens for mycological studies are best submitted within the special black fungal scrapings cards provided by the laboratory or, if these are not available, within a folded paper (preferably dark) packet. Although delays are to be avoided, fungi are generally resistant to drying and survive transportation well at room temperature.

Negative Laboratory Report

The reasons for negative microscopy and/or culture include: • Incorrect clinical diagnosis • Sampling variation associated with an inadequate specimen • Splitting the sample to perform microscopy and culture • Presence of non-viable hyphae in the distal portion of nails • Uneven fungal colonisation of nails • Overgrowth by contaminant saprophytic fungi Careful recollection obtaining sufficient material may be necessary to confirm results. Adequate/Inadequate collection

General Practice Pathology is a new regular column each authored by an Australian expert pathologist on a topic of particular relevance and interest to practising GPs. The authors provide this editorial, free of charge as part of an educational initiative developed and coordinated by Sonic Pathology.

Dermatology

Clinical Articles

Focus on dermatophytes

Once specimens are received in the laboratory, microscopy is performed. An interim report is then released. Specimens are then set up on specialised agar containing antibiotics and cycloheximide to inhibit the growth of bacteria and saprophytic fungi. Cultures are incubated at 28°C for three weeks. If microscopy is positive (M+) and no pathogen (C-) has grown in the interim, specimens are held an extra week. Infrequently, where microscopy and culture of nail scrapings is negative and the diagnosis is still suspected, nails can be examined for fungal elements using special stains.

Results:

Specimen types have been subdivided into three anatomical categories (nails, hair and skin) based broadly on the three clinical presentations of onychomycosis, tinea capitis, and tinea corporis/ cruris/pedis. Onychomycosis refers to fungal infections of the nails and includes tinea unguium caused by dermatophytes but also non-dermatophyte fungi and yeasts, predominantly Candida spp.

Negative laboratory report:

A common reason for negative microscopy and /or culture is an incorrect clinical diagnosis. More than 50% of dystrophic nails do not have a fungal cause, so it is important to establish a correct laboratory diagnosis before treating a patient with an antifungal agent. Other reasons for false negative results include sampling variation associated with an inadequate specimen and/or splitting the sample to perform microscopy and culture; the presence of nonviable hyphae in the distal portion of the nail; uneven colonisation of the nail by fungus; and overgrowth by contaminant saprophytic fungi. Careful re-collection to obtain sufficient material may be necessary to confirm negative results.

Nails:

The analysis of nail specimens from the hands and feet. Fingernails: Of 1202 specimens processed, 59% were negative by both microscopy and culture; 11% had hyphae seen on microscopy but were negative by culture; 27% of all finger and thumbnail cultures grew a yeast, predominantly Candida albicans (88% of all positive nail/hand cultures). Only 3% of all fingernail specimens grew a dermatophyte.

Toenails:

57% of 5097 toenail cultures were negative by both microscopy and culture. 22% were positive by microscopy but culture negative for reasons stated previously. As the literature would suggest, yeast infection of toenails is rare. Dermatophytes (20%) predominate as the main cause of onychomycosis of the lower limbs. Transmission of these dermatophytes is usually via the feet and toe web spaces, which are the major reservoir on the human body. Onychomycosis can be regarded as the end stage of tinea pedis. Desquamated skin scales containing hyphae are shed and survive for months to years on floors and carpets. Infrequently non-dermatophyte moulds are implicated in toenail infections such as Aspergillus. There is some uncertainty as to the significance of these cultures, and repeat culture may be indicated.

Treatment options:

With tinea unguium, topical treatment is successful only with surgical removal of the nail combined with oral therapy. First-line treatment for all types of nail tinea consists of: 1. terbinafine (child < 20 kg: 62.5 mg; 20 to 40 kg: 125 mg) 250 mg orally, daily for six weeks for fingernails and 12 weeks for toenails or (if terbinafine is not tolerated) 2. itraconazole 200 mg orally, twice daily for seven days every month for 2-4 months or 3. fluconazole 150 to 450 mg orally, once weekly for 12 to 52 weeks. Successful management of candidiasis of the nail requires removal of risk factors e.g. water immersion.

Tinea capitis:

Of 414 hair samples submitted over this period, 329 (80%) were negative by both microscopy and culture. Dermatophytes isolated include M. canis (46%); T. tonsurans (42%); M. gypseum (5%); T. mentagrophytes (5%) and T. rubrum (2.5%). This condition afflicts predominantly prepubertal children. Clinically it can present as alopecia or a more inflammatory lesion (kerion). It is noteworthy that T. tonsurans, an anthropophilic fungus, is emerging as a common cause of tinea capitis in children and spreads easily from child to child.

Treatment options:

Tinea capitis often requires oral therapy to eradicate the infection. Treatment options include 1. griseofulvin fine particle (child: 20 mg/kg up to) 500 mg orally, daily for 4-8 weeks, or 2. terbinafine (child< 20 kg: 62.5 mg; 20 to 40 kg: 125 mg) 250 mg orally, daily for four weeks.

Tinea corporis/cruris/pedis:

Of the 7406 specimens received from skin sites, 73% were both microscopy and culture negative; 5% were positive only by microscopy. Of the 22% culture positive specimens, 19% grew a dermatophyte and 3% a yeast.

Treatment options:

When topical treatments have failed, recommended oral therapy includes: 1. griseofulvin fine particle (child: 10 to 20 mg/kg up to) 500 mg orally, daily for at least four weeks or 2. terbinafine (child <20 kg: 62.5 mg; 20 to 40 kg: 125mg) 250 mg orally, daily for at least two weeks, depending on the response or 3. itraconazole capsules 200 mg orally, twice daily for one week for tinea of the feet or hands or 4. itraconazole capsules 200 mg orally, once daily for one week for tinea elsewhere.

Pathology

Clinical Articles

Testing options for H. pylori

Identified in 1983 by Australian Nobel prize winners Marshall and Warren, H. pylori is linked to a spectrum of disease including non-ulcer dyspepsia, peptic ulcer, gastric cancer and mucosa-associated lymphoid tissue lymphoma. Infection is estimated to be present in about 30% of adult Australians, though not uniformly distributed in the population. Prevalence is higher in immigrants, those of lower socioeconomic status and the institutionalised. It has been conventionally treated with a standard first-line triple therapy including a proton pump inhibitor (PPI), clarithromycin and amoxicillin or metronidazole administered for seven days. However, in the past decade the effectiveness of this triple therapy, although still recommended in Therapeutic Guidelines, has declined mainly due to the development of antibiotic resistance. A recent meta-analysis¹ of treatment, which reviewed 15,565 studies worldwide, highlighted the geographically localised nature of resistance profiles. It concluded that one single ‘most effective’ treatment was unlikely to be identified across the world, as the treatments needed to be tailored to regional resistance profiles. The range of tests, both non-invasive and invasive, following endoscopy are outlined below.

Pylori serology

This detects organism-specific IgG. It requires the collection of 5 mL of serum. No special preparation of the patient is required. Antibodies may take 5–10 weeks to develop after infection and may remain positive long term. A positive result may indicate present or past infection. Epidemiologic evidence now indicates that most infections are acquired during childhood, even in developed countries, and the frequency of H. pylori infection for any age group in any locality reflects that particular cohort's rate of bacterial acquisition during childhood years.

Urea breath test (UBT)

The UBT requires the patient to drink 13C-labelled or 14C-labelled urea, which is converted to labelled CO₂ by the urease in H. pylori. The labelled gas is measured in a breath sample. Sullivan Nicolaides Pathology currently utilises the nonradioactive 13C-labelled isotope. The test has a sensitivity of 95% and a specificity of 98%. It is generally not suitable for children under five years because of the difficulty in following test instructions. This test has an out-of-pocket fee to the patient of $60.

Faecal antigen test

Active H. pylori infection can be detected by identifying H. pylori–specific antigens in a stool sample with the use of monoclonal antibodies. This assay has similar sensitivity and specificity to the UBT and has no additional out-of-pocket expenses for the patient.

Rapid urease test (CLO test)

If endoscopy is indicated, a biopsy specimen can be placed into a CLO tube containing urea and a pH indicator. If H. pylori is present, the urease will convert the urea to ammonia, leading to a colour change in the pH indicator. This is a reliable and cheap method for identifying H. pylori infection with reported excellent sensitivity and specificity in excess of 90%. The colour change usually occurs within minutes and the clinician can record the results the same day. If the inoculated CLO tube is forwarded to the laboratory the results can be recorded in the pathology Laboratory Information System, but must be read within 72 hours of the tube being inoculated for the result to be valid.

Histology

Histology is slightly more sensitive and specific than the rapid urease test and provides additional information on the type of gastritis, atrophy, intestinal metaplasia and malignancy. If proton pump inhibitors (PPIs) have been taken, biopsies from the gastric body in addition to the antrum can improve the diagnostic yield. The organism can be identified with conventional stains including haematoxylin and eosin and Giemsa. Immunohistochemistry increases sensitivity and specificity further and is of most use in cases of assumed low density colonisation.

Culture and susceptibility testing

Culturing of the organism is available for those who fail therapy. This is done from a gastric biopsy and permits testing for sensitivity to antimicrobial agents. Specialised transport media Portagerm pylori (PORT-PYL – Item 25016) is available to improve organism viability. Susceptibility guided versus empirical antibiotic treatment for H. pylori infection has been shown to be superior to empirical 7–10 day triple therapy for first line treatment. The recent meta-analysis showed that the worst-ranking treatment is standard triple therapy (proton pump inhibitor, clarithromycin and amoxycillin or metronidazole) administered for seven days. Over the past 10 years our microbiology laboratory has cultured H. pylori from 108 endoscopic biopsies and 102 patients. Most of these cultures were performed because patients had failed therapy, introducing significant sample bias. For 24% of episodes, despite the organism being cultured, it did not remain viable to complete susceptibility testing. Susceptibility results for 76 isolates that remained viable for testing indicate that antibiotic resistance (clarithromycin – 59.7%; metronidazole – 51.3%; ampicillin – 22.4%) is a significant cause of treatment failure. Ref:

Li Bao-Zhu, Threapleton DE et al Comparative effectiveness and tolerance of treatments for Helicobacter pylori: systematic review and network meta-analysis. BMJ 2015;351:h4052 http://www.bmj.com/content/351/bmj.h4052

Infectious diseases

Clinical Articles

Schistosomiasis

Schistosomiasis, also known as bilharzia, is the second most prevalent tropical disease after malaria and is a leading cause of morbidity in many parts of the world. It is not uncommon in Australia because of the many travellers who visit endemic areas and swim or bathe in freshwater lakes and streams. Places commonly implicated include Lake Kariba and Lake Malawi in Africa. Immigrants and refugees from bilharzia endemic countries are also likely to present with untreated infection. With increasing travel to and migration from Africa and the Americas knowledge of the dangers and means of avoiding schistosomiasis is essential. Schistosomiasis is caused by trematodes of the genus Schistosoma. The principal schistosomes of medical importance, S japonicum, S mansoni, S mekongi (intestinal schistosomiasis) and S haematobium (urinary schistosomiasis), infect people who enter water in which infected snails (intermediate hosts) are living. The larval cercariae shed by the snail actively penetrate unbroken skin and develop into schistosomulae that migrate through the lungs to the liver where they mature into adults. Female worms lay eggs that pass through the vessels and tissues to the lumen of the gut or bladder (depending on localisation of worms). A proportion of eggs escape from the host and may be found in faeces or urine. The host's immune response to eggs that become lodged in the tissues is largely responsible for disease, Figure 1.

Geographic distribution

This is governed by the distribution of the intermediate host snail. S haematobium Africa, Middle East, India (only Maharashtra) S japonicum Philippines, Indonesia (only Sulawesi), parts of China S mansoni Africa, Middle East, some Caribbean Islands, parts of South America (Brazil, Surinam, Venezuela) S mekongi Laos and Cambodia S intercalatum 10 countries within the rainforest belt of West Africa.

At-risk groups

Owing to the absence of suitable snail hosts, transmission cannot occur in Australia. A history of overseas travel or residence is essential for this diagnosis. Chronic schistosomiasis is more likely to be seen in migrants and refugees from endemic areas. In Australia, where the definitive host is freshwater and marine birds, non-human trematodes may cause schistosomal dermatitis (cercarial dermatitis, swimmer's itch). Onset is usually within 15 minutes of skin contact with cercariae.

Clinical presentation

Disease due to schistosomiasis depends on the infecting species and the intensity of infection. Acute schistosomiasis occurs two to 12 weeks post infection and symptoms last for periods varying from one day to a month or more; recurrence of symptoms 2-3 weeks later is common. Between 40-95% of individuals, not previously exposed to infection, develop symptoms which include fever, malaise, headache, abdominal pain, diarrhoea and urticaria. Many have eosinophilia. After the initial acute onset, most become asymptomatic, although those with S haematobium infections may develop microscopic or macroscopic haematuria. Rare complications result from ectopic deposition of eggs in the spinal cord and brain. Most travellers are only mildly infected and are therefore often asymptomatic and unlikely to develop the severe manifestations of chronic schistosomiasis. Severe disease occurs in patients with heavy and prolonged infection. Hepatosplenomegaly, portal hypertension, ascites and oesophageal varices may result from intestinal schistosomiasis. And frank haematuria with varying degrees of impairment of the urinary bladder and ureters may occur with S haematobium infections.

Diagnosis

The prepatent period of S japonicum, S mansoni and S mekongi is 6-8 weeks, and for S. haematobium 10-12 weeks. Examination of faeces or urine before this time often yields false negative results. Similarly, with serology, testing too early may result in false negative results. Antibody development occurs slightly before eggs are detected. Eosinophilia (greater than 0.60 x10³/mL) is present in up to 80% of patients with infections; however, its absence does not exclude infection.

Parasitologic examination

Diagnosis is by demonstration of eggs of S japonicum, S mansoni and S mekongi in faeces, or eggs of S haematobium in urine. At least two stool or urine specimens should be submitted for examination over a period of 10 days. Whilst eggs may be found in all specimens of urine, there is some evidence of a diurnal periodicity with a peak of excretion around midday. Collection of the terminal portion of urine collected between noon and 2 pm is therefore recommended. Schistosome eggs can also be demonstrated in rectal snips or bladder biopsies. Viability of eggs can be assessed if the biopsies are received fresh.

Serologic examination

At our laboratory, antibodies are detected by enzyme immunoassay (EIA) using purified egg S mansoni antigen. Antibodies to this antigen may be undetectable in the pre-patent period lasting 8-10 weeks. The test detects genus specific antibodies. In the absence of a diagnosis based on egg identification, travel history provides the best assessment of likely species.

Interpretation

Parasitologic Faeces is concentrated (modified formalin-ethyl acetate) and urine either centrifuged or filtered; all of the concentrate or sediment is examined. Because of the low sensitivity of these techniques, a negative faecal or urine examination does not exclude schistosomiasis. Microscopic examination of eggs enables the species of parasite to be determined. At least two examinations on different days are recommended. Serologic Schistosome serology cannot distinguish between past or current infection nor differentiate the species of infection. Clinical history and further investigations should be considered when establishing the diagnosis. Recent infections may be serologically negative.

Preventative measures

Cercariae can burrow through the mucosa of the mouth as well as through unbroken skin. All fresh water in endemic areas should be considered suspect, although snails tend to live in slow-flowing and stagnant waters, rather than in rapids and fast-flowing waters. If freshwater contact is unavoidable, bathing water should be heated to 50°C for five minutes or treated with iodine or chlorine as for the treatment of drinking water. Water can also be strained through paper filters, or allowed to stand for 2-3 days before use. This exceeds the usual life span of the cercariae. Of course, the container must be kept free of snails. High waterproof boots or hip waders are recommended if wading through streams or swamps. It is wise to carry a pair of rubber gloves to protect hands when contact with fresh water is anticipated. Vigorous towel drying, and rubbing alcohol on exposed skin immediately after contact with untreated water, may also help reduce cercarial penetration. Vegetables should be well cooked and salads avoided as these may have been washed in infected water, allowing cercariae to attach themselves to the leaves.

Treatment

Praziquantel (Biltricide) 20 mg/kg bodyweight every four hours for 2-3 doses depending upon the species is recommended. In travellers, this is likely to achieve cure rates in the order of 90%. Tablets are scored and available as a 600mg dose dispensed six per pack. In patients at risk of chronic disease, such as refugees and migrants, it is important to be aware of complications that may arise from chronic infection: liver fibrosis, portal hypertension and its sequelae, and colorectal malignancy in the intestinal forms; obstructive uropathy, superimposed bacterial infection, infertility and possibly bladder cancer.

Follow-up

Follow-up schistosomiasis serology is recommended in 12 to 36 months after treatment. Follow-up serology may differ between immigrants and returned travellers. Travellers may show a more rapid serological decline post-treatment due to a shorter duration of infection and lower parasite burden. Immigrants may even show a rise in titre within the first 6-12 months post-treatment. Persisting titres should not automatically justify retreatment, this should be based on symptoms, parasite identification or eosinophilia. Viable eggs may continue to be excreted for up to one month after successful treatment. Non-viable and degenerate eggs can be found in tissue biopsies for years after infection has occurred.

Microbiologist; Sullivan Nicolaides Pathology's, department of Microbiology and Molecular Pathology

More from this expert

Prevaccination screen; acute Q fever; post-acute Q fever monitoring (particularly where there is a risk of developing chronic infection)

In Australia the commonest encounter with fungi in a medical sense is with superficial and cutaneous fungal infections such as those infecting the skin, scalp or nails.