Journal

of Hospital

Infection (1990)

16, 191-221

REVIEW

Control

of viral

infections

J. Breuer Department

of Virology,

ARTICLE

and D. J. Jeffries

St Mary’s Hospital Medical London W2 1PG

Accepted for publication Keywords:

in hospitals

Nosocomial;

viruses,

21 May control

School, Norfolk

Place,

1990 of infection.

Introduction In recent years, certain viruses, in particular hepatitis B and human immunodeficiency virus (HIV), have come to play an increasingly important role in the spectrum of hospital disease and infection. In addition, extensive vaccination programmes and better living conditions have altered the populations at risk from other viruses, e.g. measles and polio. Severe disease due to measles and mumps, although occurring rarely, is almost as common amongst hospital patients, notably the immunosuppressed, as in the healthy population (Moore et al., 1982; Badenoch, 1988). Outbreaks of viral diarrhoea also occur with equal, if not increased, frequency in hospitals, particularly amongst the young and elderly. Clear and practical policies are necessary to enable safe and efficient control of viral infections in hospitals.

Viruses spread by the respiratory

route (see Tables I, II)

Measles Despite the availability in the last 20 years of measles vaccination, the uptake in Britain has been only about 70% (DHSS, 1987). As a result, measles epidemics involving over 50 000 children have occurred annually (Badenoch, 1988). As many as 20-40 children have died each year (Badenoch, 1988), up to a third of whom were immunosuppressed (Miller, Correspondence 0195-6701/91/070191+31

to: Dr J. Breuer. $03.00/0

0 1990 The Hospital

191

Infection

Society

7 days

3-7 days

1-4

3-8 days

14-21

6-8 days 1-3 days

RSV

Influenza

Parainfluenza Rubella

Parvovirus Rotavirus

days

days

days

of infectivity

to 10 days

following

10 days prior to appearance of rash Adults for duration of symptoms. Children up to 5 days after symptoms have finished

before

3-10 days

14-24

Zoster Mumps

days

and available

cross-infection

of infectivity

rash

4 days before to 2 days after rash appears 4 days before to 5 days after rash appears 5 to 7 days after rash appears 2 days prior to 4 days after parotitis appears 3 days prior to onset of symptoms to cessation of upper respiratory symptoms 1 day before to 4 days after onset of symptoms

Duration

times, periods

10-21

Incubation period

of the incubation

Varicella

Summary

7-14 days

I.

Measles

Virus

Table

kg-’

(see text)

HNIG* None

None None

Ribavirin 0.82 mgkg-’ hour by inhalation 60 hours Amantadine (Influenza 100 mg bd for 5-7

Acyclovir None

Acyclovir

treatment (see text)

per

A) days

for

causing hospital

ribavirin

Antiviral

viruses

Possibly

or treatment for

(1) Vaccination (Influenza A + B) (2) Amantadine (Influenza A) 100 mg bd for 7-10 days None (1) Vaccination (see text) (2) HNIG* HNIG* None

None

(1) HNIG* (2) Vaccination (1) ZIG O-1 ml (2) Acyclovir Acyclovir Vaccination

Prophylaxis

prophylaxis

k!

b

LI

simplex

Herpes

* Human

normal

Hepatitis (Enteric NANB) Hepatitis (Parenteral NANB) Viral haemorrhagic fever viruses (see text)

days

2221

14 days following onset of symptoms but may be as long as 2 months

Variable

weeks

Lifelong

S-10

immunoglobulin.

h

days prior to and up to 2 weeks after symptoms 3 weeks prior to onset to 1 week after onset of jaundice Primary infection 3%4 weeks Secondary infection 3-5 days Up to 10 days following onset of symptoms Variable (Seeff & Hoofnagle, 1979)

34

2448

Uncertain

months

days

days

weeks

days

to 48 hours

to 6 months before sero-conversion 4-8 weeks

Up

2-6

Hepatitis

HIV

S-10

Adenovirus

B

2-6

A

Hepatitis

2-11

2-35

Up

Other viruses causing diarrhoea Enterovirus

Ribavirin hourly (Lassa

HNIG*

None

500 mg 6 for 7 days fever)

(1) Hepatitis B immunoglobulin (2) Vaccination AZT

200 mg orally

Ribavirin 10 days

in

agents

in

5 times

15 mgkg-’ for (Lassa fever)

Trials of interferon progress

None

AZT; many other under evaluation

Trials of interferon progress

Acyclovir a day None

qid

Acyclovir orally None

200 mg

None

HNIG+

Vaccination (Polio) HNIG*

None

194 Table

J. Breuer II.

Isolation

and Disinfection

Virus

See Lowbury

precautions for viruses transmitted respiratory route Isolation

Measles Varicella zoster Mumps Respiratory syncytial virus Influenza Parainfluenza Rubella Parvovirus

and D. J. Jeffries

precautions

Standard isolation with respiratory precautions. Single room at relative negative pressure desirable. Gloves and gowns to be worn. Restrict staff attending patient (see text for each virus). Wash hands after leaving room.

predominantly

by the

Cleaning & terminal disinfection Clean surfaces with 1000 ppm (0.1%) hypochlorite. No special terminal disinfection.

et al. (1982)

1985). The relatively low prevalence of immunity amongst young children in the United Kingdom (Morgan-Capner et al., 1988) may result in admission to hospital of the occasional child (or visiting sibling) in the incubation period of measles. Whilst not common, nosocomial infection may occur if adequate precautions to prevent spread are not taken (Sue McQueen, personal communication). For those children diagnosed in hospital, immediate isolation from the immunosuppressed, babies (including those breastfeeding), non-immune staff and patients, is mandatory. Wherever possible, children with measles should be sent home. Infected children remaining in hospital must be nursed in conditions of source isolation by immune staff, either in cohorts or individual rooms, during the period of infectivity (from 4 days preceding to 2 days following the appearance of the rash) (Lowbury et al., 1982) (Table II). As the incubation period of vaccine measles is 7 days (range 4-10) compared with 10 days (range 7-14) for clinical measles (Gershon, 1987), all immunocompetent, non-immune staff and children in contact with the index case should be vaccinated immediately or if possible within 72 h of exposure, unless a valid contraindication exists (Department of Health, 1988). Work from Japan suggests that vaccination of leukaemic children in remission with live attenuated vaccine may produce a protective antibody response (Torigoe Hirai & Oitani, 1981), without the risk of vaccine-related measles as previously reported (Mitus et al., 1962); these results remain to be verified. At present only human normal immunoglobulin is available for the prophylaxis of exposed immunosuppressed patients and even the efficacy of this is not proven (Kernahon, McQuillan & Craft, 1987). Two doses of 750 mg human normal immunoglobulin should be given, 48 h apart, to any immunosuppressed patient over 3 years old regardless of previous vaccination or history of infection, as the evidence suggests that immunity acquired previously may not be protective (Gray et al., 1987). For children under one year old the dose of human normal immunoglobulin

Control

of nosocomial

viruses

195

is 2 doses of 250 mg, 48 h apart (for age l-3 years the dose is 500 mg in 2 doses, 48 h apart). The use of high titre measles immunoglobulin produced by the Scottish National Blood Transfusion Service is at present under evaluation (Kernahon, McQuillan & Craft, 1987). Non-immune, healthy staff and patients, for whom vaccination is too late to subvert the disease and who have been in contact with the index case during the period of infectivity (from 4 days preceding the rash to 2 days following its appearance), must be regarded as potentially infectious from the seventh day of first contact to the fourteenth day of last contact. During this time they should be kept away from susceptible individuals. It is invaluable if a record of staff immunity to childhood illnesses is kept either by the sister in charge or by the Occupational Health Department although, in practice, 97% of adults are immune to measles (Morgan-Capner et al., 1988). Compiling comprehensive records may involve staff checking the medical history of children with their parents. Failing a definite history, laboratory confirmation may be useful and is more easily obtained outside the pressure of an outbreak. Many virology laboratories are not equipped for routine determination of measles immunity as standard complement fixation tests (CFT) are only of use in the acute situation and are a poor indicator of protective immunity. This may now change; with the advent of the Measles, Mumps, Rubella (MMR) vaccine details of antibody status to measles may be requested prior to vaccination in the same way as with rubella at present. The new enzyme-linked immunosorbent assays (EIAs) for measles IgG correlate very well with neutralizing (protective) antibody (Weigle, Murphy & Brunell, 1984). EIAs are more convenient to use than the standard haemagglutination-inhibition test which employs monkey red blood cells, and are easier to store, rendering them more amenable to use by laboratories performing few tests for measles (Weigle, Murphy & Brunell, 1984).

Varicella

zoster

Chickenpox, like measles, is primarily an infection of childhood. Infection is mainly by droplet spread (Trlifajova, Bryndova & Rye, 1984) although the virus may survive on hands or fomites. Isolation measures must apply, with particular attention to handwashing and the wearing of gloves and gowns to ensure that infection is not carried to the next patient. Nursing should be carried out by immune staff only. A register of staff immunity is important in view of the susceptibility of 510% of the adult population (Gershon et al., 1976; Evans et al., 1980). Indeed, amongst adults from developing countries susceptibility rates may be as high as 16% (Gershon et al., 1976). Th is is reflected in a number of outbreaks of nosocomial chickenpox involving, in particular, nurses and patients from Africa, Asia and South America (Gershon et al., 1976; Hastie, 1980; Venkitaramen & John, 1982). Adult chickenpox, even in previously healthy individuals, may

196

J. Breuer

and D. J. Jeffries

be more severe than childhood chickenpox, and can even be fatal (Treibwasser et al., 1967; Barss, 1983). Individuals with chickenpox are infectious from 4 days prior to appearance of the rash until the lesions have formed crusts, approximately 5 days later (Gold, 1966) (Table I). Those susceptible to the infection may develop chickenpox from 10 days following first contact with the index case to 21 days after the last day of contact and should have no contact with immunosuppressed or, if possible, other susceptible individuals during this period. On wards with predominantly immunosuppressed patients this may necessitate sending staff home. Infection can be confirmed by detection of specific IgM by EIA or radioimmune assay (RIA) or by a rise in titre of complement-fixing antibodies. The virus may also be visualized by electron microscopy of vesicle fluid although it is of course indistinguishable from herpes simplex virus which may produce disease similar to varicella infection in the immunosuppressed. Newer tests using monoclonal antibodies to detect varicella antigen are under development (P. Grint, personal communication). Complement fixation tests carried out at 15°C rather than 4°C may be used to determine natural immunity as may EIAs, but overall, radioimmune assay (RIA) is most sensitive (Ndumbe, Craddock-Watson & Levinski, 1988). Chickenpox in the immunosuppressed carries a mortality of 7% or higher (Feldman, Hughes Sz Daniel, 1977). Zoster immunoglobulin (ZIG), 0.1 ml kg-‘), which is prepared from people who have recently had chickenpox or herpes zoster (shingles), should be given to susceptible leukaemic and transplant patients and to non-immune patients receiving immunosuppressive drugs within 72 h of contact with varicella zoster (Brunell et al., 1972). Acyclovir may also be given following exposure (H. Kangro, personal communication). A regimen of oral acyclovir 800 mg four times per day (or half this dose in children under two) for 3 weeks following exposure to varicella zoster is at present under evaluation in a multi-centre trial (P. Fiddian, personal communication). Immunosuppressed patients who develop chickenpox or herpes zoster should be treated with high dose acyclovir; adult dose 10-l 5 mg kg-’ iv thrice daily for 7 days (Prober, Kirk & Keeney, 1982; Balfour et al., 1983; Balfour, 1984). Elective prophylactic acyclovir, 5-l 0 mg kg -’ tds given intravenously for 3 weeks followed by 800 mg tds orally for up to 6 months, has been tried in leukaemic patients following bone marrow transplant (Parren et al., 1988). This regimen is effective in preventing episodes of herpes zoster during the period of most severe immunosuppression. ZIG is not indicated for susceptible immunocompetent contacts even though it has been shown to attenuate or prevent the development of chickenpox (Brunell et al., 1969). The situation is less clear cut where the contact is pregnant, as congenital defects do occur, albeit rarely, following maternal chickenpox in the first half of pregnancy (Seigle, 1973). ZIG may

Control

of nosocomial

viruses

197

reduce the severity of infection in susceptible pregnant contacts (Miller et al., 1986) but whether this diminishes the risk to the fetus is not known. Given the short supply of ZIG, its use is not indicated in this group at the present time (Miller et al., 1986). However, the development of chickenpox in the pregnant woman six days prior to delivery or up to 7 days postnatally, is an indication for ZIG (250 mg) to be given to the neonate as chickenpox can be a serious disease in babies with a mortality of up to 30% (Gershon, 1975). Onset of infection 7 or more days before delivery should obviate this requirement as maternal antibody will have developed and passed to the baby by the time it is born (Miller et al., 1986). Infants born more than 2 months prematurely will also not have acquired maternal immunity and may need ZIG if contact with chickenpox occurs before they leave hospital (American Academy of Pediatrics, 1986). The use of acyclovir in neonates at risk for chickenpox has not yet been properly evaluated. In view of the fact that babies treated with ZIG still develop chickenpox, some severely (Miller et al., 1986), it would seem reasonable to give babies-at-risk prophylactic acyclovir 1O-l 5 mg kg- ’ tds intravenously for 5 days, restarting the treatment together with additional ZIG if clinical chickenpox occurs (Sills et al., 1987). Vaccination of health-care workers against varicella has not been widespread mainly because of doubts about the duration of immunity (Ndumbe et al., 1985). H owever, trials have shown that the OKA vaccine strain of live attenuated virus (obtainable from Smith Kline & Beecham) may be used safely in patients with cancer or leukaemia not receiving immunosuppressive therapy (Takahashi et al., 1974; Brunell et al., 1982) and may be protective when given as late as 3 days after exposure (Takahashi et al., 1974). Again, the duration of immunity, is variable (Ndumbe, Craddock-Watson & Levinsky, 1988). Patients with shingles are infectious for about 5 to 7 days from the onset of their rash, although immunosuppressed patients may shed virus for longer. Nosocomial outbreaks of chickenpox resulting from contact with a case of shingles have been described (Hunter & Skovgaard, 1988). For this reason such patients are best nursed as for chickenpox. In addition to its antiviral action, there is also some evidence that oral acyclovir accelerates healing and significantly reduces post-herpetic neuralgia if given within 48 h to immunocompetent patients with shingles (Morton & Thomson, 1989). The cost of treatment is such, however, that it would seem sensible to restrict its use to patients aged over 50 years who are most likely to suffer more severe disease and sequelae (W-atson & Evans, 1986).

Mumps Mumps is not generally a serious illness in children, although it is the commonest cause of viral meningitis under 15 years of age (Noah & Urcquart, 1980). Ten per cent of the adult population are non-immune

J. Breuer

198

and D. J. Jeffries

(Morgan-Capner et al., 1988) and they may suffer the additional complications of orchitis or oophoritis, which can occur in about 20% of adults leading, rarely, to sterility (Werner, 1950). Standard isolation for the duration of infectivity (from 2 days before to 4 days after the first appearance of the parotitis, Table II) is necessary and only immune personnel should be involved in the care of the patient (Henle et al., 1948). Diagnosis may be confirmed by demonstrating mumps S and V antibodies by complement fixation test (CFT) on two serum samples taken 10-14 days apart. S antibodies are present at the time of the parotitis, falling over the next 2 weeks, whilst V antibodies rise towards the end of the first week and may persist for years. Another simple serological test for diagnostic purposes is radial haemolysis (RH) on paired sera; a 2 mm change in diameter of the zone of haemolysis indicates acute infection. EIAs for mumps IgM antibodies are also being used in the routine virus laboratory (Leinikki et al., 1979) and can be more convenient (and more expensive) for confirming acute infection, than older serological methods. The virus may also be grown in tissue culture from saliva, CSF and urine. When an assessment of the immune status is required, EIAs or RH are most accurate. The former, in particular, are easily performed by the ordinary diagnostic virology laboratory if the need arises (Leinikki et al., 1979). With the advent in Britain of the MMR vaccine from 1988 (DHSS, 1988) the incidence of mumps should decline as in the USA (CDC, 1987a). The possibility of an acute outbreak occurring in hospital should therefore decrease.

Respiratory

syncytial

virus

In the majority of healthy individuals respiratory syncytial virus (RSV) causes mild upper respiratory tract infections. More severe and sometimes life-threatening respiratory tract infections may occur in the very young (bronchiolitis) and in the elderly or debilitated (pneumonia or exacerbation of chronic bronchitis). A number of hospital outbreaks of RSV infection have been described in infants (Breese Hall et al., 1978), the immunosuppressed (Hall et al., 1981) and the elderly (Mintz et al., 1979). The message from these is three-fold. First, affected patients identified clinically as having RSV must be isolated immediately, or cohort nursed, for the duration of virus shedding which corresponds to the duration of symptoms and lasts up to 6 or 7 days in otherwise healthy children (Breese Hall et al., 1978) but can be much longer in immunosuppressed, leukaemic children and adults (Brugman & Hutter, 1980; Hall et al., 1981) (Table II). As the virus is mainly spread by close contact and survives for up to 20 min on skin and up to 6 h on fomites (Breese Hall, Doughlas & Gelman, 1980), careful attention must be paid to handwashing, and the wearing of disposable gowns and gloves. Secondly, effective control of the outbreak requires rapid identification of the virus.

Control

of nosocomial

viruses

199

Direct immunofluorescence of infected epithelial cells obtained from a nasopharyngeal aspirate is both rapid and sensitive (Mintz et al., 1979). Finally, it is wise to restrict entry to the room in which the patient is being nursed to the same few designated staff who do not, in so far as is possible, care for other patients. This is in order to prevent staff becoming infected and transmitting the virus during the asymptomatic 3-day incubation period (Breese Hall et al., 1978). Ribavirin is thought to have specific antiviral activity against RSV but the drug is expensive and benefits are most clearly seen in children with pre-existing cardiopulmonary disease or in children who are ill enough to require ventilation (Milner, 1988). Immunosuppressed patients benefit from treatment with ribavirin but will relapse unless and until their immune system recovers (McKintosh et al., 1984). Ribavirin does not affect virus excretion and therefore is of limited use in the management of outbreaks (Milner, 1988).

Influenza

and parainjhenza

Influenza can cause cross-infection problems in hospital, which may result in pneumonia and death, especially in elderly and institutionalized patients and the very young (Meibalane et al., 1977; Mathur, Bently & Hall, 1980). Outbreaks of parainfluenza causing croup in young children, may also occur (Gardiner et al., 1973). In both, infection is spread by small droplets and therefore standard isolation measures or cohort nursing for the duration of viral shedding (5 days after onset of symptoms in adults (Stuart-Harris & Schild, 1970) and 7 days in children (Hall & Doughlas, 1975) apply (Tables I, II). Diagnosis is quickly achieved by immunofluorescence of infected cells in respiratory secretions or by isolation in tissue culture (McQuillan, Madeley & Kendal, 1985). Vaccination with inactivated or subunit vaccine of the current epidemic strains of influenza may prevent outbreaks amongst those groups at particular risk: the elderly, the mentally ill and those with chronic cardiac or respiratory illnesses (Arden, Patriarca & Kendal, 1986). Influenza A may be prevented in 70% of individuals if amantadine 100 mg bd for 7-10 days is given to contacts of a case as soon as the diagnosis is made (O’Donaghue et al., 1973).

Rubella Rubella is generally an innocuous infection except when it affects the foetus. Up to 80% of foetuses may develop severe congenital defects if primary rubella infection occurs during the first 8 weeks of pregnancy (Miller, Craddock-Watson & Pollock, 1982). In an effort to reduce the incidence of congenital rubella in Britain, girls between the ages of 11 and 14 yrs (DHSS, 1970) and susceptible post-natal women (DHSS, 1972a) have been offered vaccination with a live attenuated vaccine. While these measures have succeeded, to some extent, in reducing the incidence of rubella in pregnancy (PHLS, 1988a), there remains both a

200

J. Breuer

and D. J. Jeffries

high prevalence of natural infection in the community and a residuum of susceptible pregnant women (Miller, Craddock-Watson & Pollock, 1982; PHLS, 1988a). Rubella outbreaks occurring in hospital wards or outpatients, affecting susceptible pregnant women are therefore still a possibility and should be anticipated when drawing up guidelines for infection control. This situation should change in line with the North American experience (CDC, 1989a) now that rubella vaccination, as part of the MMR vaccine, is being offered to all children over the age of 15 months (Department of Health, 1988). Spread is by the respiratory route and cases are infectious from about 1 week prior to the appearance of the rash to 10 days after its onset. Affected patients should be sent home or isolated from pregnant women during the infectious period with all care being carried out by immune staff only (Tables I, II). Susceptible staff who may be infectious should not work with pregnant women for the same period of time. Babies with congenital rubella may excrete large amounts of virus for many months and should, again, be nursed in standard isolation by immune staff (Horstman et al., 1965). In the event of a cross-infection problem, records of the rubella status of staff should be obtained from the Occupational Health Department and those of pregnant women from antenatal clinic notes. Where no record exists staff and patients should be tested for pre-existing rubella IgG antibodies by single radial haemolysis (SRH) or EIA. A four-fold or more rise in rubella antibody titre in a second serum tested by haemagglutination inhibition (HI) or demonstration of seroconversion by EIA, at least 5 to 7 days later, is evidence of acute rubella infection (Pattison, 1981). Susceptible pregnant women should also be tested weekly for rubella-specific IgM by RIA or EIA for up to 4 weeks following contact (Pattison, 1981). In cases where rubella infection is thought to have occurred some weeks prior to testing or is thought to be a reinfection in a previously immune person, the avidity of rubella specific IgG and/or IgM antibody may be suggests tested (Hedman & Rousseau, 1989). High avidity antibody primary infection more than four months previously whilst low avidity antibody indicates seroconversion within the previous two months (Hedman & Rousseau, 1989). Non-immune staff and patients should not have contact with pregnant women during the period of infectivity (1 week after first contact to 2 weeks after last contact). Those who do not seroconvert and who are not pregnant should be vaccinated with the attenuated rubella vaccine. Pregnant women contracting rubella in the first trimester may decide to terminate the pregnancy. However recent evidence suggests that rubella infection up to 11 days after the last menstrual period (LMP) constitutes a less than 3% risk of congenital infection. Infection more than 11 days following the LMP increases the risk of congenital infection sharply (Enders et al., 1988). These findings should be taken into account when

Control

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viruses

201

counselling a woman for abortion. Those who wish to continue with the pregnancy whatever the outcome should be given 750mg normal immunoglobulin as soon as possible after contact and again 4-6 days later as it may attenuate the viraemia (Hanshaw, Dudgeon & Marshall, 1985) although the evidence for this is conflicting (Christie, 1987). Parvovirus Parvovirus B19 is firmly established as the cause of the benign childhood illness erythema infectiosum (fifth disease) (Anderson et al., 1983). In susceptible individuals such as those with sickle cell anaemia (Pattison et al., 1981) and other chronic haemolytic anaemias (Serjeant & Goldstein, 1988), leukaemias (Kurtzman et al., 1988) and immunosuppressive disorders (Kurtzman et al., 1987) the red cell hypoplasia whch normally occurs in parvovirus B19 infection may result in a severe aplastic anaemia. In addition, infection in pregnancy may lead to intrauterine infection in around 25% of cases and foetal loss, with or without hydrops fetalis (Anand et al., 1987; Anderson et al., 1988) in approximately 10% of cases (PHLS 1987). No congenital abnormalities have been reported in live-born children following maternal infection (PHLS, 1987). Over 60% of adults are immune (Cohen, Mortimer & Pereira, 1983). Spread is thought to be by the respiratory route (Anderson et al., 1985a; Chorba et al., 1986) and the secondary attack rate for close contacts is about 50% (Plummer et al., 1985; Chorba et al., 1986; Bell et al., 1989). By the time the rash of erythema infectiosum has appeared an index case is no longer infectious (Anderson et al., 1985a). However, susceptible individuals in contact with such a case in the previous 10 days may contract the infection and will themselves be infectious from around days 6-8 (Kurtzman et al., 1988) (Table II). Patients with aplastic anaemia due to parvovirus are, however, infectious and nosocomial spread from such patients has been described (Bell et al., 1989). Infectious patients should be isolated and contact prevented with other individuals at risk of aplastic anaemia and pregnant women, until the anaemia improves (CDC, 1989b). Staff caring for the patient should be restricted to a minimum until such time as the diagnosis is confirmed and if possible their immunity has been checked. The latter, whilst desirable, may not be feasible and should be discussed with the local reference laboratory. There is some evidence that intravenous human normal immunoglobulin (400 mgkg-‘) given periodically until viral DNA cannot be detected, may cure or speed recovery from aplastic anaemia caused by parvovirus (Kurtzman et al., 1989). Theoretically, normal immunoglobulin could also be protective post-exposure to parvovirus B19, although this has not been tested. Before the the use of immunoglobulin is proposed in either situation, discussion should take place with the local reference laboratory in order that proper virological monitoring can be carried out. Confirmation of the diagnosis of parvovirus in erythema infectiosum is by

202

J. Breuer

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detection of specific IgM by counter current electrophoresis, radioimmune assay (RIA) or enzyme immunoassay (EIA), at present only performed in certain reference centres (Cohen, Mortimer & Pereira, 1983; Anderson et al., 1986). In patients with anaemia the virus itself must be detected by EIA of the patient’s serum against anti-parvovirus antibody (Anderson et al., 1986), electron microscopy of serum or bone marrow (Anand et al., 1987), dot-blot or in-situ hybridization techniques (Anderson, Jones & Minson, 1985); all are available at reference centres. Viruses

spread

by the faecal-oral

route

(see Tables

I, III)

Viruses causing diarrhoea Viral diarrhoea, both community and hospital-acquired, necessitates standard ‘faecal-oral’ isolation and gloves and gowns should be worn when in contact with the patient (Lowbury et al., 1982). Most admissions from the community for viral diarrhoea, other than in a food-related outbreak, occur in winter and are children under 3 years of age. This reflects the epidemic pattern of rotavirus which is responsible for over 50% of episodes of acute viral diarrhoea in children (Kapikian et al., 1976). Rotaviruses, together with astrovirus and fastidious adenoviruses, also exist endemically in the community and all are therefore capable of causing outbreaks in semi-closed environments amongst children (Chrystie, Totterdell & Banatvala, 1978) and adults, especially the elderly (Cubitt & Holzell, 1980). In infants and children shedding of rotavirus, adenovirus and astrovirus continues for many days following resolution of the symptoms and they should therefore continue to be isolated for 5 days (Table I) after the symptoms have cleared (Vesikari, Sarkkinen & Maki, 1981). Adults shed less rotavirus once the acute episode has passed and need only to be isolated until their symptoms clear (von Vonasoedd et al., 1978). Cohort nursing where several patients are affected is acceptable as long as no patients are admitted to the cohort unless infection is proven, and staff care only for the infected or uninfected group and not both (Bagshawe, Blowers & Lidwell, 1978). Eradication of rotavirus from a long-stay geriatric ward or

Table

III.

Isolation

Virus Rotavirus Other viral diarrhoeas Viral food poisoning Enteroviruses Hepatitis A

and disinfection precautions for viruses faecal-oral route Isolation

precautions

Single room enteric precautions

transmitted

Cleaning

predominantly

& terminal

by the

disinfection

In general, 1000 ppm (0.1%) hypochlorite for surfaces. Rotavirus: 70 or 95% alcohol hand rubs. SRSVs: 20 000 ppm (2%) hypochlorite for surfaces and contaminated areas

Control

of nosocomial

viruses

203

neonatal unit may be impossible partly as a result of recolonization of the ward by chronic carriers such that even closure and cleaning are ineffective (Chrystie, Totterdell & Banatavala, 1978). Some reports, however, suggest that rinsing of the hands with alcohol after washing may reduce viral contamination (Kurtz, Lee & Parsons, 1980). Screening of asymptomatic staff and patients for virus should not be performed routinely as it has been shown that in the case of rotavirus alone, up to 12% of people may be shedding virus (Bolivar et al., 1978) and their stools will clear over a period of 10 days (Vesikari, Sarkkinen & Maki, 1981). Electron microscopy has been the mainstay of diagnosis because these viruses do not grow easily in tissue culture. However, this technique requires skill and is slow when large numbers of specimens need to be processed. Newer antigen detection techniques such as latex agglutination and EIA are less sensitive and specific but are useful for screening large numbers of samples in an outbreak (Madeley, 1989). Polyacrylamide gel electrophoresis of stool samples is proving to be a sensitive and specific tool in the detection of viruses causing diarrhoea and has the advantages of being cheap and easy to perform once the technique is established. So far it has been developed for rotavirus and adenovirus (Madeley, 1989) but it is not yet being widely used. Certain of the viruses causing gastroenteritis, including both caliciviruses and small round structured viruses (e.g. Norwalk virus), are more likely to be associated with contaminated food, including shellfish (Gill et al., 1983) and fresh fruit (PHLS, 1988b). Spread by infected food handlers also occurs (Reid et al., 1988) and secondary spread within hospitals has been described (Riorden & Wills, 1986). In general, specimens should be sent in a sterile plastic container within 24-48 h of the onset of symptoms. This is because electron microscopy which is the principal diagnostic tool, requires 106-10’ particles per ml, a number only seen early on in the diarrhoeal illness (PHLS, 1988b). Affected patients should be isolated for up to 2 days after the last symptoms have cleared (Reid et al., 1988; PHLS, 1988b) whilst staff members with symptoms, however mild, should not work until 48 h after their symptoms have ceased, as these viruses are highly infectious and easily transmitted (PHLS, 1988b). In the event of an outbreak, cleaning of the ward with hypochlorite solution 2% (20 000 parts per million available chlorine) (PHLS, 1988b), coupled with stringent handwashing and the minimization of staff and patient transfers to other wards, are probably the most practical measures (Riorden & Wills, 1986). Where possible, the source of the outbreak should be investigated, especially if an infected food handler is involved. Enteroviruses Non-polio enteroviruses (NPEV). Echovirus and coxsackie outbreaks causing meningitis, systemic collapse and death

B virus amongst

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neonates are well described (Cramblett et al., 1973; Nagington et al., 1978). The survival of these viruses on hands and fomites coupled with the long duration of faecal carriage (up to 60 days in some cases) (Nagington et al., 1978) and the length of time for isolation in tissue culture (3-14 days) may make control of such an outbreak very difficult. Past experience suggested that isolation of infected babies with rigorous handwashing and closure of the nursery to new admissions until the last case was free of virus was the only means of halting such an outbreak (Cramblett et al., 1973; Nagington et al., 1978). However, this view has recently been challenged. An outbreak of echovirus 11 in the special care baby unit in Oxford, was controlled by the combination of rigorous handwashing by staff together with virological surveillance of babies to monitor quickly any cross infection. The unit was thus able to keep precious neonatal cots available for other patients (Isaacs et al., 1989). The use of prophylactic human normal immunoglobulin 250 mg im has also been suggested as a measure for controlling cross-infection (Nagington et al., 1978). Older children and adults suffering from infections caused by coxsackie viruses A and B or echoviruses may require admission to hospital. Barrier nursing with enteric precautions is advised for children and incontinent patients suffering from enteroviral infections (Dowsett, 1988). Otherwise, attention to handwashing, cleaning of surfaces with hypochlorite 0.1% (1000 ppm available chlorine) and heat or steam sterilization of bedpans and instruments etc. should suffice. Staff and patients affected should avoid contact with neonates (Dowsett, 1988). Pregnant women who become infected risk the possibility of transmitting the virus to the baby during labour and should also therefore avoid contact with infected staff (Dowsett, 1988). There is very little evidence that enteroviruses cause intrauterine infection (Hanshaw, Dudgeon & Marshall, 1985). Immunosuppressed patients are also at risk from enteroviral infections. Persistent meningoencephalitis in children with congenital agammaglobulinaemia caused by echoviruses (Wilfert, et al., 1977) and coxsackie B viruses (Cooper et al., 1983) may occur and has been successfully treated with intravenous immunoglobulin (Mease, Ochs & Wedgwood, 1981). Chronic diarrhoea caused by coxsackie Al in bone marrow transplant patients has also been reported (Townsend et al., 1982) as has myocarditis caused by coxsackie B virus infection in a heart-lung transplant patient (Wreghitt et al., 1986). Poliovirus. Widespread use of the Sabin live oral polio vaccine in Britain has resulted in virtual elimination of paralytic poliomyelitis (Begg, Roebuck & Chamberlain, 1988). Cases do still occur, caused by wild type strains acquired abroad (Kubli, Steffen & Schar, 1987) or, at a rate of 1 in 5.1 to 8.1 million doses of vaccine, by the vaccine strain itself (WHO, 1976). At greatest risk of paralytic polio are immunocompromised children less than four years of age receiving the vaccine (Moore et al., 1982) and young

Control

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viruses

205

adults, not previously immunized, in contact with vaccinees (Schonberger, McGowan & Gregg, 1976). Poliovirus may be isolated from stools, throat swabs and CSF and can be identified and typed by virus neutralization. In most cases such an isolate is an incidental finding in the stool of a child who has recently received the oral vaccine. Provided the child is well, no action other than preventing contact with immunosuppressed patients, need be taken. If a case of poliomyelitis is diagnosed all normally immune contacts should receive a dose of live vaccine (DHSS, 1972b) and the original isolate must be further investigated at a reference centre to determine whether the virus is vaccine derived or wild type. Th ose for whom live vaccination is contraindicated (the immunosuppressed and pregnant women) may be given the killed Salk vaccine (Grist, 1983). In the event of an epidemic, widespread use of the attenuated live oral polio vaccine has proved effective in limiting spread (Hovi, Cantell & Huovikunen, 1986). Hepatitis A virus. Hepatitis A, a picornavirus, is also spread by the faecal-oral route. Outbreaks tend to occur where there is close contact or overcrowding for example amongst nursery school children or military recruits (Hooper et al., 1977; Hadler et al., 1980), in conditions of poor hygiene (Dienstag et al., 1978) or in relation to contaminated food (PHLS, 1988b). Most cases recover uneventfully. About 0.01% of cases develop fulminant hepatic failure (Gust, 1984). The incubation period is between 2 and 6 weeks and the patient is infectious for up to 3 weeks before the jaundice develops until about 1 week after (Dienstag et al., 1975). The diagnosis is confirmed by the detection of specific IgM by RIA or ELISA (CDC, 1979). Outbreaks in hospital must be controlled by implementing strict hygiene. Affected patients should be sent home or isolated for a week following the onset of jaundice, although by this time, the patient is no longer excreting much virus (Dienstag et al., 1975). Outbreaks must be investigated to determine the source. Contaminated shellfish have been implicated as an increasingly common cause of outbreaks of hepatitis A (PHLS, 1988b). Prophylactic human normal immunoglobulin (250 mg for children under 10, 500 mg im for all others), if given to all contacts within 14 days, including family members, will abort or attenuate the illness (ACIP, 198.5). Viruses

spread

by direct

inoculation

(see Tables

I, IV)

Herpes simplex Occasional cross-infection outbreaks of herpes simplex infection in neonates have been described with confirmation by DNA fingerprinting (Linneman et al., 1978; Adams et al., 1981). It is therefore prudent to nurse a mother with either genital or buccal herpes simplex and her infant separately from other inpatients, and for gowns and gloves to be worn by

206

J. Breuer

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Table IV. Isolation and disinfection precautions for viruses transmittedpredominantly inoculation

by direct

Virus

Isolation

Cleaning

Herpes simplex

Standard isolation for adenovirus & in certain circumstances for herpes simplex (see text). Gloves & gowns, handwashing

1000 ppm (0.1%) hypochlorite surfaces No special terminal cleaning

Adenovirus

& disinfection for

staff in attendance (Adams et al., 1981). There is little evidence to implicate close contact between mother and child postpartum as a cause of neonatal herpes (Light, 1979). Nonetheless, the mother should be encouraged to wash her hands beore handling the infant, to wear a protective gown and in addition, if she has oral herpes, a mask (Kibrick, 1980). Herpes simplex may also be spread either from staff with oral or whitlow lesions to patients, or from patient to patient on the hands of staff (Light, 1979). Several general rules applied routinely should prevent outbreaks. Staff should cover their lesions and not care for patients at risk of serious infection, i.e. the young, and those who are debilitated, immunosuppressed or suffer from eczema, until the crusts have separated from the lesions (Adams et al., 1981). Patients with lesions should be nursed separately from the groups mentioned above. Oral acyclovir 200 mg five times daily for 5 days shortens the time to crust separation from about 9 to 5 days (Raeborn et al., 1988) and should be offered to patients and staff with herpes whitlow or severe localized lesions. Patients at risk of developing severe herpes infection may need intravenous acyclovir (5 mgkg-’ tds for 1 week) or longer periods of oral treatment followed by prophylactic acyclovir if they are immunosuppressed. Airborn transmission does not seem to occur, so isolation of the patient is not necessary unless the lesions are widespread. Staff should always wear gloves when performing any procedure liable to bring their hands into contact with oral or genital secretions (Adams et al., 1981). Adenovirus Nosocomial outbreaks of adenovirus pneumonia and upper respiratory tract infections, particularly caused by types 3 and 7, have been described (Pingleton, Pingleton & Hill, 1978; Straube et al., 1983; Brummitt et al., 1988). Epidemic conjunctivitis in staff caring for a patient with adenovirus pneumonia, with virus being transferred on the hands to the eyes (Levandowski & Rubenis, 1981) has also been reported. In other outbreaks transfer of the virus on improperly sterilized equipment has caused cross-infection (Dawson & Darrel, 1973). Confirmation of the diagnosis is by isolation of the virus in tissue culture, immunofluorescence and typing of the isolate either by standard antisera or by restriction enzyme analysis (Wadell, 1984). Detection of antigen in the

Control

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207

specimen may also be carried out by indirect (August & Warford, 1987) or direct immunofluorescence (A. Freke, personal communication) using monoclonal antibodies for common antigens or by EIA of the specimen (August 8z Warford, 1987; Johansson et al., 1985). Restriction enzyme analysis or serotyping of isolates can be used to follow the epidemiology of outbreaks. (Wadell, 1984: Brummitt et al., 1988). Patients with eye infections should be discharged home as soon as possible. Staff with eye infections should not have contact with patients for the duration of viral shedding which lasts about 10 days (Levandowski & Rubenis, 1981). Patients with pneumonia or those required to remain in hospital for other reasons must be nursed in standard isolation. Staff should pay special attention to handwashing, the disposal of infected secretions and the sterilization of instruments used (Levandowski & Rubenis, 1981: Brummitt et al., 1988).

Cytomegalovirus

(CM V)

The changes in both the patient population to include more who are immunosuppressed, and the presence amongst the hospital staff caring for patients of more pregnant women has increased awareness of CMV as a potential agent of cross-infection. There is no evidence that CMV is acquired nosocomially (Pass, 1985; Peckham et al., 1986). Studies in hospital nurses caring for children excreting CMV have not shown any evidence of increased infection rates when compared with women of similar ages working in other occupations (Yeagar et al., 1975). Furthermore, in those cases where CMV has been isolated from a baby following occupational exposure of the mother to the virus, restriction enzyme analysis has shown the baby’s isolate to be unrelated to that of the patient but identical to that of the mother, ruling out the possibility of cross-infection (Peckham et al., 1986). Nevertheless, whilst there has been no documented case of nosocomial infection with CMV, it would seem prudent to minimize the risks of cross-infection by careful attention to infection control measures in any patient known to be excreting CMV. Gloves and aprons should be worn and careful handwashing implemented as the virus may survive on surfaces for many hours (Faix, 198.5). Viruses

Hepatitis

B, hepatitis

spread

by parenteral

D, hepatitis

route

(See

Tables

I, V)

C and human immunodejiciency

viruses

Much has been written about the control of infection with the human immunodeficiency virus (HIV) (HIS, 1985, 1990; DHSS, 1986a; Jeffries, 1987; CDC, 1987b; CDC, 1988 a) and hepatitis B virus (Lowbury et al., 1982; CDC, 1988a). For the most part, the same principles may be applied to hepatitis C (formerly parenteral non-A, non-B) (CDC, 1988a.) Isolation

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of HIV antibody- or hepatitis e-antigen-positive patients and patients with hepatitis C is not strictly necessary unless for other reasons such as coexistence of another pathogen, which would in itself merit isolation (Jeffries, 1987; HIS, 1990). However, all invasive procedures likely to involve contact with blood or body fluids, must be carried out wearing gloves and if necessary, gowns, goggles and masks (Lowbury et al., 1982; DHSS, 1986a; Jeffries, 1987; HIS, 1990). For convenience, and to underline the necessary infection control measures, nursing in single rooms or in infectious disease wards is often preferred. In general, two areas must be considered in effective control of these viruses in hospital. Firstly, adequate disposal of infected material and decontamination of instruments, subjects extensively reviewed elsewhere (DHSS, 1986a; CDC, 1987b; CDC, 1988a; British Medical Association, 1989) and secondly, prevention and treatment of parenteral or mucous membrane exposure to infected material. Prevention of HIV, hepatitis C and hepatitis B cross-infection requires clear policies covering all eventualities from inpatient care to operating procedures and emergency resuscitation. Guidelines on the formulation and content of such policies are readily available (Lowbury et al., 1982; DHSS, 1986a; Jeffries, 1987; CDC, 1987b; CDC, 1988a; HIS, 1990) and will not be covered here. However, a few points are worth emphasizing. Of utmost importance is the prevention of infection following accidental exposure of staff and patients to infectious material. The infectivity of HIV following inoculation accident has been estimated at 0.4% (CDC, 1988b), whilst that of hepatitis B may be more than 20% if the donor serum is e-antigen positive (Seeff et al., 1978; Werner & Grady, 1982). The incidence of post-transfusion non-A non-B hepatitis is about 1% in the UK (Collins et al., 1983) and the majority of these are thought to be due to hepatitis C (Kuo, Choo & Alter, 1989). The risk of transmission of hepatitis from needlestick injury or other exposure is not known. Most accidents are preventable if established guidelines are followed and in this context the importance of staff and patient education cannot be stressed too highly. In all cases of exposure, the blood or body fluid should be washed away and puncture sites should be encouraged to bleed (Jeffries, 1987). Any incident involving staff must be reported to the Occupational Health Department. The hepatitis B antigen status of the infected material should be ascertained where possible, by obtaining a blood sample from the patient for testing. If the patient is surface antigen (HBsAg) positive and the victim of the accident has been previously immunized successfully against hepatitis B (see Table VI), a booster of hepatitis B vaccine should be given unless an antibody level has been taken within the previous 12 months and shown to be at least lomiuml-’ (ACIP, 1987) ( see Table VI). Unvaccinated or partially vaccinated individuals with no antibodies to hepatitis B should receive hepatitis B immune globulin 500 iu and the first dose of vaccine (Table VI). Exposure to delta antigen positive blood or body fluid should be treated as for hepatitis B (ACIP, 1985).

Control Table

V. Isolation

and disinfection

of nosocomial

viruses

precautions

for

viruses spread predominantly

parenteral

route

Isolation

Virus Hepatitis HIV Hepatitis

B

Viral haemorrhagic fevers

by the

Cleaning 10 000 ppm (1%) hypochlorite for visibly contaminated surfaces & spillages. Otherwise, 1000 ppm (0.1%) hypochlorite for cleaning surfaces. No special terminal disinfection. Cleaning as above Terminal fumigation of rooms with formalin.

Not

C

209

necessary unless for other reasons. Gloves to be worn when in contact with secretions & excreta. Gowns, goggles & masks should be worn when performing procedures likely to cause 1 bleeding or splashes. \ Strict isolation. Restriction of staff entry to minimum. I Full protective clothing

It is now possible to test for anti-hepatitis C virus antibodies (Kuo et al., 1989) and this could be used to assess the infectivity status of patients following needlestick injury. However, the only EIA available may not pick up all infectious cases and the degree to which a positive result reflects infectivity of the serum is not yet clear. Furthermore, no confirmatory tests exist. In view of these uncertainties it is our practice to test for anti-HCV in those patients with abnormal liver function. Where possible, serum from the source or patient together with that from the recipient of the inoculation injury should be saved for a period of 1 year. If hepatitis then occurs, the stored sera together with a repeat serum from the recipient may be tested.

Table

VI.

Hepatitis vaccination Unvaccinated (antibody following

Partially

Guidelines for action to be taken following

B,

Antibody

accident exposure to hepatitis B virus

testing

Action

status or non-responder level < 10 miu ml-’ full course of vaccine)

vaccinated

Vaccinated & known to have produced adequate antibody levels (> 10 miuml-‘) (a) < 12 months previously (b) > 12 months previously

Not

necessary

< 10 miu > 10 miu

Not Not

ml-’ ml-’

necessary necessary

(1)

Save serum for at least 9 months (2) Give 500 iu hepatitis B immunoglobulin im within 48 hours (Seeff & Hoofnagle, 1979) (3) Give one dose of hepatitis B vaccine in opposite arm (CDC, 1985b) (4) Ensure course of vaccine is completed As above Ensure course of vaccine is completed

No action necessary Give booster dose of vaccine

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J. Breuer

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Normal immune globulin has been shown to prevent post-transfusion hepatitis (Sanchez-Quijano et al., 1988) although, overall, the evidence is conflicting (Seeff & Hoofnagle, 1979). No proven preventative treatment exists for HIV exposure. Some centres advise post-exposure zidovudine (3-azidothymidine, ‘Retrovir’) for laboratory workers exposed by inoculation or contamination of eye and/or mucous membranes to high titres of virus, and to recipients of either intravenous HIV-positive material or deep intramuscular needlestick injuries with HIV-positive material (Henderson & Gerberding, 1989). Where the status of the source material is not known but is strongly suspected to be high risk, the patient from whom it was derived must be counselled before serum is tested for HIV. Our practice is to follow the normal procedure following inoculation or splash injury, i.e. wash the contaminated area thoroughly and where possible encourage bleeding. If the nature of the exposure is severe enough to justify chemoprophylaxis (as outlined above) and, following counselling, the accident victim requests such intervention, then formal consent is obtained and treatment with oral zidovudine 250 mg qds is begun as soon as possible, preferably within 1 hour and continued for 4 weeks. Treatment is accompanied by close follow-up including counselling and regular blood checks. Pregnant women are excluded from receiving treatment. Serum taken from the recipient at the time of the incident should be stored and follow-up sera taken at 3-monthly intervals for at least 6 months and if possible longer to determine whether seroconversion has occurred.

Viral haemorrhagic

fevers ( VHFs)

The viruses causing nosocomial viral haemorrhagic fevers are transmitted by contact with blood, urine and body secretions. Aerosol spread is very rare and has only been described in one case of Lassa fever (DHSS, 1986b). Of the viruses known to cause haemorrhagic fever, significant outbreaks of person-to-person spread have occurred with four. They are Lassa virus, Ebola virus, Marburg virus and Congo-Crimean haemorrhagic fever virus (CCHF). Lassa fever is endemic in Nigeria, Sierra Leone and Liberia (Keenlyside et al., 1983; McCormick et al., 1987) while Ebola virus is endemic in Zai’re and Sudan (WHO, 1978a, b). Marburg virus was first described in an outbreak originating from a consignment of African green monkeys imported from Uganda into Marburg, Germany and in more recent outbreaks in Zimbabwe (Gear et al., 1975) and Kenya (Smith et al., 1982). Congo-Crimean haemorrhagic fever virus is endemic in the Soviet Union (Hoogstraal, 1979), Zai’re (Casals, 1969) and around the Mediterranean, north-west China, central Asia and India (CDC, 1988~). Once the possibility of a VHF is raised the patient should be moved into a closed side room until full assessment of the risk can be undertaken. There is now evidence that nosocomial spread of Lassa fever, and possibly the other viruses mentioned, is effectively prevented by barrier nursing

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211

together with precautions with excreta and secreta such as are taken with patients with hepatitis B and HIV (Helmick et al., 1986). The guidelines described here, however, are in line with the most recent recommendations from the Department of Health in the UK (DHSS, 1986b). Patients with fever having returned from the tropics, particularly rural sub-Saharan Africa, within the preceding 3 weeks must be considered to be at high risk. Also in this category are contacts of confirmed cases and laboratory workers having handled material known to contain these viruses (DHSS, 1986b). At moderate risk are persons having returned from small towns within an endemic zone. Patients returning from large cities within an endemic area are at minimal risk unless they have recently been in rural areas or are health-care workers. A far commoner cause of fever of unknown origin in patients returning from Africa is malaria and this should be looked for in blood films taken from the patient using precautions outlined by the DHSS working party on VHFs (DHSS 1986b). The finding of malarial parasites in such a patient usually reduces the index of suspicion for a VHF as a cause of the pyrexia unless additional factors are felt to be overriding. Once a case of VHF is suspected, the Control of Infection Officer should be informed immediately and should in turn contact the Consultant for Communicable Disease Control (CCDC). Strict barrier nursing with full protective clothing has been shown to prevent nosocomial spread (Fisher-Hoch et al., 1985; Helmick et al., 1986). High- and moderately high-risk patients should be transferred as soon as possible by specially designated ambulance to an infectious diseases unit (DHSS, 1986b). A sample of the patient’s urine and blood should be sent to the nearest reference laboratory for category 4 pathogens. Low-risk patients, usually so by virtue of the fact that they only visited urban areas or are positive for malaria, should be barrier nursed until results of their serology are known (DHSS, 1986b). Records of contacts must be obtained by the CCDC. Those in direct contact with the patient or accidentally in contact with his or her blood, urine, faeces or vomitus etc., must be placed under surveillance for 21 days from the last day of exposure. Any such contact who develops a temperature of 38°C for more than 24 h during the period of surveillance should be considered a possible case and the Communicable Disease Surveillance Centre informed (DHSS, 1986b). Other more casual contacts are at minimal risk of infection. Prophylactic ribavirin 500 mg 6-hourly for 7 days may be beneficial in high risk Lassa and Congo Crimean haemorrhagic fever virus contacts. Ribavirin has also been shown to result in increased survival of patients with Lassa fever in a controlled clinical trial (McCormick et al., 1986). Finally it should be remembered that patients with VHF may continue to excrete virus for up to 2 months after their illness (Martini & Seigert, 1971; Emond et al., 1977; Emond et al., 1982). Urine should be regularly cultured for virus during this time. Patients must be advised not to

J. Breuer and D. J. Jeffries

212 resume sexual activity virus (CDC, 1988~).

or at least should

The role of the Occupational

use condoms,

Health

until

they are clear of

Department

The Occupational Health Department is responsible for ensuring the health, safety and welfare of the staff and minimizing the risk to patients from staff-borne illness. New staff who are found to have no immunity to rubella should be vaccinated provided they are not pregnant. It is also useful to test for immunity to varicella zoster virus where the member of staff has no history of chickenpox, as time may be saved if an outbreak occurs. Male members of staff who have no history of mumps may be tested for antibodies and offered vaccination if they are at risk. Staff whose work brings them into daily contact with blood products and needles should be offered vaccination against hepatitis B (Zuckerman, 1986 ). In practice this includes all staff who work directly or indirectly with patients, including porters, domestics, laboratory technologists and paramedical staff. Only administrative staff may be excluded from a vaccination programme. The Occupational Health Department is also responsible, in conjunction with the Control of Infection Officer, for ensuring staff receive the appropriate prophylaxis and follow-up, following inoculation injury or occupational exposure to a virus. This may include post-exposure to hepatitis B, ensuring a member of staff on prophylaxis immunosuppressive therapy receives ZIG following exposure to varicella zoster virus, or even monitoring a member of staff exposed to Lassa fever. The member of staff involved, their immediate superior, as well as the Control of Infection Officer and the laboratory should all see it as their responsibility to inform Occupational Health of the potential hazard so that the necessary action may be accomplished promptly. Finally, the Occupational Health Department must ensure that staff are not exposed to unnecessary risk from patients and vice versa. Staff at risk from viral infections, for example pregnant women working on paediatric wards who are susceptible to rubella, should be offered alternative employment for the period of risk, in this case the duration of the pregnancy. Infected staff who pose a potential cross-infection risk should themselves be prevented from having patient contact until they are no longer infectious. Staff, particularly surgeons, obstetricians and dentists, who are hepatitis B e-antigen positive carriers may infect their patients (Welch et al., 1989). Where such transmission occurs it may necessitate the member of staff moving to non-surgical duties. Guidelines for dealing with such cases have been issued by the Department of Health (DHSS, 1981). This review has attempted to address some of the problems of virus

Control

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viruses

213

cross-infection in hospitals. Obviously policies must be tailored to suit the needs of the individual hospital and the laboratory facilities available. Nevertheless, viruses cause measurable morbidity and mortality and careful planning of policy and procedure may prove vital to the smooth running of the hospital in the event of an outbreak.

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15, 163-172. Anderson, M. J., Khousoum, M. N., Maxwell, D. J., Gould, S. J., Happerfield, L. C. & Smith, W. J. (1988). Human parvovirus B19 and hydrops foetalis. Lancet 1, 535. Arden, N. H., Patriarca, P. A. & Kendal, A. P. (1986). Experiences in the use and efficacy of inactivated influenza vaccine in nursing homes. In Options for the Control of Influenza (Kendal, A. P., Patriarca P. A., Eds), pp. 155-168. New York: Alan R. Liss. August, M. J. & Warford, A. L. (1987). Evaluation of commercial monoclonal antibody for detection of adenovirus antigen. Journal of Clinical Microbiology 25, 2233-2235. Badenoch, J. (1988). Big bang for vaccination. British Medical Journal 297, 75&7Sl. Bagshawe, K. D., Blowers, R. & Lidwell, 0. M. (1978). Isolating patients in hospital to control infection. Part II. Who should be isolated where? British Medical Journal 2, 684-686. Balfour, H. H., Bean, B., Laskin, 0. L., Ambinder, R. F., Meyers, J. D., Wade, J. C., Zaia, J. A., Appeli, D., Kirk, L. E., Segreti, A. C. & Keeney, R. E. (1983). Acyclovir halts progression in herpes zoster in immunocompromised patients. New England Journal of Medicine 308, 1445-1453. Balfour, H. H. (1984). Intravenous therapy for varicella in immunocompromised children. Journal of Pediatrics 104, 134-l 36. Barss, P. (1983). Death from chickenpox in adults in Papua New Guinea. Lancet 1, 126.

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Begg, N., Chamberlain, R. Sz Robuck, M. (1987). Paralytic poliomyelitis in England and Wales 1970-l 984. Epidemiology and Infection 99, 97-106. Bell, L. M., Naides, S. N., Stoffman, P., Hodinka, R. L. & Plotkin, S. A. (1989). Human parvovirus B19 infection among hospital staff members after contact with infected patients. New EnglandJournal of Medicine 321, 486491. Bolivar, R., Conklin, R. H., Vollett, J. J., Pickering, L. K. (1978). Study of an adult student population in Mexico. Journal of Infectious Disease 137, 321-327. Breese Hall, C., Gelman, B. S., Doughlas Jr, R. G. & Meagher, R. M. (1978). Control of nosocomial respiratory syncytial viral infections. Pediatrics 62, 728-732. Breese Hall, C., Doughlas, R. G. & Gelman, J. M. (1980). Possible transmission by fomites of respiratory syncytial virus. Journal of Infectious Diseases 141, 98-102. British Medical Association (1989). A Code for Sterilisation of Instruments and Control of Cross-Infection (Morgan, D., Ed.). London: British Medical Association. Brugman, S. & Hutter, J. J. (1980). Respiratory syncytial virus (RSV) pneumonitis in acute leukaemia. American Journal of Haematology and Oncology 2, 371-373. Brummitt, C. F., Cherrington, J. M., Katzenstein, D. A., Juni, B. A., Van Drunen, N., Eldelman, C., Rhame, F. S. &Jordan, M. C. (1988). Nosocomial adenovirus infections: Molecular epidemiology of an outbreak due to adenovirus 3a. Journal of Infectious Diseases 158, 423-432. Brunell, P. A., Ross, A., Miller, L. H. & Kuo, B. (1969). Prevention of varicella by zoster immune globulin. New England Journal of Medicine 280, 1191-l 194. Brunell, P. A., Gershon, A. A., Hughes, W. T, Harris, D., Riley, M. D. & Smith, J. (1972). Prevention of varicella in high risk children: A collaborative study. Pediatrics 50, 718-722. Brunell, P. A., Geiser, C., Shehab, 2. & Waugh, J. E. (1982). Administration of live varicella vaccine to children with leukaemia. Lancet 2, 1069-1073. Casals, J. (1969). Antigenic similarity between the virus causing Crimean haemorrhagic fever and Congo virus. Proceedings of the Society of Experimental Biology and Medicine 131, 223-6. Centers for Disease Control (CDC) (1979). Morbidity trends for viral hepatitis - United States, 1977. Morbidity and Mortality Weekly Report 28, 106-107. Centers :‘or Disease Control (CDC) (1987a). Mumps - United States 198.5-l 986. Morbidity and Mortality Weekly Report 36, 151-155. Centers for Disease Control (CDC) (1987b). Recommendations for prevention of HIV transmission in health-care settings. Morbidity and Mortality Weekly Report 36, S2. Centers for Disease Control (CDC) (1988a). Update: Universal precautions for prevention of transmission of human immunodeficiency virus, hepatitis B and other bloodborne pathogens in health care settings. Morbidity and Mortality Weekly Report 37, 377-388. Centers for Disease Control (CDC) (1988b). Update: Acquired human immunodeficiency virus infection among health care workers. Morbidity and Mortality Weekly Report 37, 229-239. Centers for Disease Control (CDC) (1988~). Management of patients with suspected viral haemorrhagic fever. Morbidity and Mortality Weekly Report 37, S3. Centers for Disease Control (CDC) (1989a). Rubella and rubella syndrome. Morbidity and Mortality Weekly Report 38, 173-178. Centers for Disease Control (CDC) (1989b). Risks associated with parvovirus B19 infection. Morbidity and Mortality Weekly Report 38, 81-97. Chorba, T., Coccia, P., Holman, R. C., Tattersall, P., Anderson, L. J., Sudman, J., Young, N. S., Kurczynski, E., Saarinen, U. M., Moir, R., Lawrence, D. N., Jason, J. M. & Evatt, B. (1986). The role of parvovirus B19 in aplastic crisis and erythema infectiosum (fifth disease). Journal of Infectious Diseases 154, 383-393. Christie, A. B. (1987). Rubella. In Infectious Diseases, Vol. 1,4th edn, pp. 586-628. London: Churchill Livingstone. Chrystie, I. L., Totterdell, B. M. & Banatvala, J. (1978). Asymptomatic endemic rotavirus infections in the newborn. Lancet 1, 1176-l 178.

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