Scarlet fever is on the rise. According to the latest issue of The Lancet Infectious Diseases, cases of scarlet fever in the UK reached a 50 year high last year with a seven fold increase in new cases in the last five years. In addition, similar increases having been reported in a number of Asian countries including Vietnam, China, South Korea and Hong Kong. But public health authorities remain perplexed as to why the disease appears to be making a comeback. Detailed analysis of the causative organism shows different strains of the strep bacteria have been responsible for the UK and Asian outbreaks, so they are unsure if they are linked at all or whether the resurgence has to do with external factors such as the immune status of the population or environmental factors. So far it would seem that Australia is yet to be affected by this increased incidence however experts are warning we should not be complacent. Unlike in England, scarlet fever is not a notifiable disease in this country except in WA. And even in the UK, data suggests marked under-reporting. Scarlet fever is highly contagious and usually affects children under the age of 10, although it can occur in adults as well. While the bacterial infection, caused by Streptococcus pyogenes or group A Streptococcus (GAS) was a common cause of death in the 1800s, these days it is readily treated with antibiotics usually penicillin. However, failure to recognise the condition and treat it appropriately can lead to complications such as pneumonia, and liver and kidney damage. Children with the infection typically experience sore throat, headache and fever along with the characteristic popular pink-red rash that feels like sandpaper and the so-called strawberry tongue. Diagnosis is usually made via a throat swab. In an accompanying comment, Australian infectious diseases researchers Professor Mark Walker and Stephan Brouwer from the University of Queensland said, “Scarlet fever epidemics have yet to abate in the UK and northeast Asia. Thus, heightened global surveillance for the dissemination of scarlet fever is warranted.” In other words, be alert, people! Ref: Lancet Infect Dis 2017 Published Online November 27, 2017 http://dx.doi.org/10.1016/ S1473-3099(17)30693-X Online/Comment http://dx.doi.org/10.1016/ S1473-3099(17)30694-1

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.

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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.