New risk-scoring system helps GPs with CHF patients
1. How might mumps present?
About one-third of mumps infections are sub-clinical. A smaller subgroup presents with complications in the absence of parotid swelling. In classic mumps, non-
specific prodromal symptoms (low-grade fever, anorexia, malaise, headache), lasting a day or two, herald the onset of parotitis.
The parotid glands are not usually apparent and are deemed to be swollen once visible or palpable. Earache and parotid tenderness commence on one side, becoming bilateral in 75 per cent of cases. Rapid parotid enlargement may be particularly painful and citrus fruits and juices are said to exacerbate symptoms.
Other salivary glands are involved in up to 10 per cent of cases but rarely occur as a sole manifestation of mumps.
Whereas most complications of mumps occur with similar frequency regardless of age, orchitis and oophoritis are largely confined to post-pubertal groups. In 5 per cent of symptomatic cases, parotid swelling is not a feature of mumps, patients instead present with one or more of the complications.
Mumps, therefore, needs to be considered in the differential diagnosis of meningitis, encephalitis, hearing loss, orchitis and pancreatitis, whether or not accompanied by salivary gland swelling.
2. What is the risk of infertility?
Epididymo-orchitis is common, developing in more than 20 per cent of postpubertal males, and may be bilateral in around one in six. Two-thirds of cases arise in the week following onset of parotitis, but orchitis can present earlier, later, or in the absence of parotid swelling.
Onset is usually sudden and associated with constitutional symptoms. The testis is hot, tender, and may be greatly enlarged, usually with epididymitis. While infection leads to some degree of testicular atrophy in 50 per cent of cases, it is rarely implicated as a cause of male sterility.
Oophoritis, associated with fever, nausea, vomiting and lower abdominal pain, is less common, but may mimic acute appendicitis. Mumps has not been implicated in female infertility.
3. How rare is pancreatitis?
Pancreatitis is said to occur in up to 5 per cent of patients, and is manifested by epigastric pain, tenderness and vomiting. Routine blood tests do not differentiate between pancreatic and salivary amylases, so high serum amylase may reflect salivary or pancreatic inflammation or both. Pancreatic/salivary isoenzyme analysis or pancreatic lipase measurements may thus be required for confirmation.
4. How rare is CNS involvement?
The central nervous system is the commonest single site of mumps complications, but sub-clinical involvement must be very common given the presence of CSF pleocytosis in 50 per cent of mumps cases without clinical meningitis.
5. What are the CNS complications?
These include meningitis, encephalitis, temporary or permanent hearing loss, plus, rarely, other neurological syndromes. Mumps was a leading cause of hearing loss in children under 15, and the commonest cause of aseptic meningitis, pre-MMR.
Meningeal symptoms can arise before, during, after or in the absence of parotitis. Almost 50 per cent of cases of mumps meningitis occur in the absence of parotid swelling, but conversely meningitis complicates less than one-10th of cases with parotitis. Curiously, mumps meningitis occurs three times as often in males as females.
CSF typically shows a lymphocytosis, with increased protein and normal glucose. A predominance of neutrophils and/or depressed CNS glucose levels can occur, however, warranting consideration for possible bacterial meningitis. After an illness of up to 10 days, complete recovery without sequelae is the rule.
Mumps encephalitis is a relatively rare complication, presenting with seizures or other focal signs and /or impaired consciousness. Two patterns are seen: acute infectious encephalitis implicating mumps invasion of neural tissue and post-infectious demyelinating disease mediated by an aberrant host response and presenting several days later. The mortality is 1.4 per cent and survivors may suffer permanent sequelae.
6. What about exposure in pregnancy and newborns?
Mumps is not more severe in pregnancy. It has not been associated with congenital malformations but may increase the risk of miscarriage in the first trimester. Mumps is very unusual in infants under one year old, reflecting persistence of passively acquired neutralising antibodies. Premature infants may, however, be susceptible.
7. What should GPs know about transmission?
Mumps is an enveloped virus and therefore does not survive for long outside the host. It is spread by direct contact, droplet spread or fomites. Compared with the notoriously transmissible measles virus, it is moderately infectious.
8. Figures vary: how long is the incubation period for mumps?
Various figures have been quoted, the best evidence indicating a period of 15 to 24 days (median 19 days) from exposure to the onset of parotid gland swelling. In practice 14-21 days is a useful rule of thumb.
9. How long is someone infectious?
Virus shedding starts as early as seven days before parotid swelling, and continues for four days afterwards. In the UK, infection control guidance for schools and nurseries advises that children stay away from school for five days from the onset of swollen glands. Exclusion of cases is of limited value in controlling an outbreak because cases are infectious before clinical presentation and because mumps virus can be transmitted by the 30 per cent of individuals with asymptomatic infection.
10. After immunisation, how long does it take to get an antibody response?
Neutralising antibody is generated within two weeks of mumps vaccination. Response rates to a first dose range from 60-90 per cent. A second dose of MMR increases mumps seropositivity to 95 per cent and leads to higher sustained antibody concentrations.
11. What should GPs know about salivary swabs?
Salivary samples can be easily and painlessly collected at home by patients or parents. They are primarily an epidemiological tool designed to generate important information about the efficacy of vaccine programmes and information about circulating virus strains. Following onset of clinical mumps, mumps specific IgM can be detected in saliva after seven days.
The samples can also be used to detect
viral RNA in PCR assays, allowing confirmation of mumps if the specimen has been collected at less than one week. Analysis of the viral RNA also facilitates tracking of viral strains in circulation.
The salivary testing programme is not designed to be an acute diagnostic testing facility. Turnaround times vary, therefore, depending on competing demands and available resources. During the outbreak this year, the Health Protection Agency said GPs did not need to send any more serology tests and in the context of an epidemic a clinical diagnosis was accurate enough for notification.
Where the clinical picture demands a faster turnaround, a test for IgM in blood may be useful. A special request for rapid PCR testing of a saliva sample at the HPA Centre for Infections may be made through your local virology service.
Mumps RNA is also present in urine samples, appearing later and persisting longer than in saliva.
12. Why can't we have direct access to salivary swabs in an epidemic and are they better than blood tests? How long does it take to produce IgM?
Swabs may also be available from your local/regional HPU or virology laboratory.
Advantages include acceptability to patients of all ages, together with ease of collection and delivery. Saliva samples are more useful than blood samples because they are suitable for PCR diagnosis, facilitating detection within seven days of the onset of parotid swelling and molecular epidemiology. In addition, saliva samples can be
taken at the optimal time for IgM detection (one to four weeks after onset), usually when the patient has recovered and is no longer attending the surgery. For this reason, the swabs are usually sent out only once the case has been reported, which avoids swabs being taken too early for IgM detection.
13. If patients have had mumps, are they immune or can they get mumps twice?
As noted above, a clinical diagnosis of mumps has a very low (<10 per="" cent)="" positive="" predictive="" value="" outside="" the="" epidemic="" setting.="" as="" a="" general="" rule,="" natural="" mumps="" infection="" gives="" lifelong="" immunity.="" as="" is="" the="" case="" with="" the="" childhood="" exanthems,="" occasional="" recurrences="" have="" nevertheless="" been="" reported.="" in="" the="" absence="" of="" stored="" samples="" for="" analysis,="" it="" is="" not="" possible="" to="" substantiate="" such="" claims="" in="" most="">10>
Apparent recurrences are not unexpected because bilateral parotid swelling may accompany several other virus infections. Indeed in a recent study of mumps-like illness in vaccinated patients, in whom mumps was excluded serologically, other viral infections were diagnosed in 14 per cent, most commonly Epstein-Barr virus. By analogy, therefore, in at least some of such cases, one or other episode of apparent recurrence will not have been caused by mumps (see table).
Parainfluenza infections are likely to account for some such cases. The viruses are genetically related. Not only do they cause parotitis, they also may manifest cross-reactivity in some serological tests, falsely suggesting reinfection.
There is, nevertheless, some evidence to suggest that mumps reinfection may occur. Serological investigation of a cohort of unvaccinated individuals in France with clinically mild mumps showed features consistent with a secondary, not a primary, immune response. Divergent strains might account for such observations. Indeed, putative reinfection with a mumps virus strain unrecognised by pre-existent neutralising antibodies has been described.