Genital herpes is one of the most common STIs world-wide. Between 1997 and 2002 there has been a 17% increase in diagnoses of genital herpes in the UK. The peak incidence is in 16- to 24-year-olds of both sexes. Infection may be either primary or recurrent. Transmission occurs during close contact with a person who is shedding virus. Most genital herpes is due to type 2. Genital contact with oral lesions caused by HSV-1 can also produce genital infection.

Susceptible mucous membranes include the genital tract, rectum, mouth and oropharynx. The virus has the ability to establish latency in the dorsal root ganglia by ascending peripheral sensory nerves from the area of inoculation. It is this ability which allows for recurrent attacks.

Clinical features

Asymptomatic infection has been reported but is rare. Primary genital herpes is usually accompanied by systemic symptoms of varying severity including fever, myalgia and headache. Multiple painful shallow ulcers develop which may coalesce. Atypical lesions are common. Tender inguinal lymphadenopathy is usual. Over a period of 10-14 days the lesions develop crusts and dry. In women with vulval lesions the cervix is almost always involved. Rectal infection may lead to a florid proctitis. Neurological complications can include aseptic encephalitis and/or involvement of the sacral autonomic plexus leading to retention of urine.

Recurrent attacks occur in a significant proportion of people following the initial episode. Precipitating factors vary, as does the frequency of recurrence. A symptom prodrome is present in some people prior to the appearance of lesions. Systemic symptoms are rare in recurrent attacks.

The clinical manifestations in immunosuppressed patients (including those with HIV) may be more severe, asymptomatic shedding increased, and recurrences occur with greater frequency. Systemic spread has been documented.

Diagnosis

Although the history and examination can be highly suggestive of HSV infection, a firm diagnosis can be made only on the basis of isolation of virus from lesions. Swabs should be taken from the base of lesions and placed in viral transport medium. Virus is most easily isolated from new lesions. Type-specific immune responses can be found 8-12 weeks following primary infection and may form the basis for newer serological assays, although these are not yet available in routine clinical practice.

Management

Primary

Saltwater bathing or sitting in a warm bath is soothing and may allow the patient to pass urine with some degree of comfort. Aciclovir 200 mg five times daily, famciclovir 250 mg three times daily or valaciclovir 500 mg twice daily, all for 5 days, are useful if patients are seen whilst new lesions are still forming. If lesions are already crusting, antiviral therapy will do little to change the clinical course. Secondary bacterial infection occasionally occurs and should be treated. Rest, analgesia and antipyretics should be advised. In rare instances patients may need to be admitted to hospital and aciclovir given intravenously, particularly if HSV encephalitis is suspected.

Recurrence

Recurrent attacks tend to be less severe and can be managed with simple measures such as saltwater bathing. Psychological morbidity is associated with recurrent genital herpes and frequent recurrences impose strains on relationships; patients need considerable support. Long-term suppressive therapy is given in patients with frequent recurrences. An initial course of aciclovir 400 mg twice daily or valaciclovir 250 mg twice daily for 6-12 months significantly reduces the frequency of attacks, although there may still be some breakthrough. Therapy should be discontinued after 12 months and the frequency of recurrent attacks reassessed.

HSV in pregnancy

The potential risk of infection to the neonate needs to be considered in addition to the health of the mother. Infection occurs either transplacentally or via the birth canal. If HSV is acquired for the first time during pregnancy, transplacental infection of the fetus may, rarely, occur. Management of primary HSV in the first or second trimester will depend on the woman’s clinical condition and aciclovir can be prescribed in standard doses. Aciclovir therapy during the last 4 weeks of pregnancy may prevent recurrence at term.

Primary acquisition in the third trimester or at term with high levels of viral shedding usually leads to delivery by caesarean section.
For women with previous infection, concern focuses on the baby acquiring HSV from the birth canal. The risk is very low in recurrent attacks. For women with recurrent episodes, only those with genital lesions at the onset of labour are delivered by caesarean section. Sequential cultures during the last weeks of pregnancy to predict viral shedding at term are no longer indicated.

Prevention and control

Patients must be advised that they are infectious when lesions are present; sexual intercourse should be avoided during this time or during prodromal stages. Condoms may not be effective as lesions may occur outside the areas covered. Sexual partners should be examined and may need information on avoiding infection.

Syphilis is a chronic systemic disease, which is acquired or congenital. In its early stages diagnosis and treatment are straightforward but untreated it can cause complex sequelae in many organs and eventually lead to death.

The causative organism, Treponema pallidum (TP), is a motile spirochaete that is acquired either by close sexual contact or can be transmitted transplacentally. The organism enters the new host through breaches in squamous or columnar epithelium. Primary infection of non-genital sites may occasionally occur but is rare.

Both acquired and congenital syphilis have early and late stages, each of which has classic clinical features (Table 2.49).

Primary

Between 10-90 days (mean 21 days) after exposure to the pathogen a papule develops at the site of inoculation. This ulcerates to become a painless, firm chancre. There is usually painless regional lymphadenopathy in association. The primary lesion may go unnoticed, especially if it is on the cervix or within the rectum. Healing occurs spontaneously within 2-3 weeks.

Table 2-49. Classification and clinical features of syphilis

	Clinical features
Acquired
Early stages
Primary	Hard chancre Painless, regional lymphadenopathy
Secondary	General: Fever, malaise, arthralgia, sore throat and generalized lymphadenopathy Skin: Red/brown maculopapular non-itchy, sometimes scaly rash; condylomata lata Mucous membranes: Mucous patches, ’snail-track’ ulcers in oropharynx and on genitalia
Late stages
Tertiary	Late benign: Gummas (bone and viscera) Cardiovascular: Aortitis and aortic regurgitation Neurosyphilis: Meningovascular involvement, general paralysis of the insane (GPI) and tabes dorsalis
Congenital	Stillbirth or failure to thrive
Early stages	‘Snuffles’ (nasal infection with discharge) Skin and mucous membrane lesions as in secondary syphilis
Late stages	‘Stigmata‘: Hutchinson’s teeth, ’sabre’ tibia and abnormalities of long bones Keratitis, uveitis, facial gummas and CNS disease

Secondary

Between 4-10 weeks after the appearance of the primary lesion constitutional symptoms with fever, sore throat, malaise and arthralgia appear. Any organ may be affected – leading, for example, to hepatitis, nephritis, arthritis and meningitis. In a minority of cases the primary chancre may still be present and should be sought.

Signs include:

• Generalized lymphadenopathy (50%)
• Generalized skin rashes involving the whole body including the palms and soles but excluding the face (75%) – the rash, which rarely itches, may take many different forms, ranging from pink macules, through coppery papules, to frank pustules
• Condylomata lata – warty, plaque-like lesions found in the perianal area and other moist body sites
• Superficial confluent ulceration of mucosal surfaces – found in the mouth and on the genitalia, described as ’snail track ulcers’
• Acute neurological signs in less than 10% of cases (e.g. aseptic meningitis).

Untreated early syphilis in pregnant women leads to fetal infection in at least 70% of cases and may result in stillbirth in up to 30%.

Latent

Without treatment, symptoms and signs abate over 3-12 weeks, but in up to 20% of individuals may recur during a period known as early latency, a 2-year period in the UK (1 year in USA). Late latency is based on reactive syphilis serology with no clinical manifestations for at least 2 years. This can continue for many years before the late stages of syphilis become apparent.

Tertiary

Late benign syphilis, so called because of its response to therapy rather than its clinical manifestations, generally involves the skin and the bones. The characteristic lesion, the gumma (granulomatous, sometimes ulcerating, lesions), can occur anywhere in the skin, frequently at sites of trauma. Gummas are commonly found in the skull, tibia, fibula and clavicle, although any bone may be involved. Visceral gummas occur mainly in the liver (hepar lobatum) and the testes.

Table 2-5. Notifiable diseases in England & Wales under the Public Health (Infectious Diseases) Regulations 1988

Acute encephalitis

Acute poliomyelitis

Anthrax

Cholera

Diphtheria

Dysentery (amoebic or bacillary)

Food poisoning

Leprosy

Leptospirosis

Malaria

Measles

Meningitis

Meningococcal septicaemia (without meningitis)

Mumps

Ophthalmia neonatorum

Paratyphoid fever

Plague

Rabies

Relapsing fever

Rubella

Scarlet fever

Smallpox

Tetanus

Tuberculosis

Typhoid fever

Typhus

Viral haemorrhagic fever

Viral hepatitis

Whooping cough

Yellow fever

Man constantly interacts with the world of microorganisms from birth to death. The majority cause no harm and some play a role in the normal functioning of the mouth, vagina and lower intestinal tract. However, many microorganisms have the potential to produce disease. This may result from inoculation of damaged tissues, tissue invasion, a variety of virulence factors or toxin production.

Skin manifestations of tuberculosis

• Lupus vulgaris usually arises as a post-primary infection. It usually presents on the head or neck with red-brown nodules which look like apple jelly when pressed with a glass slide. They heal with scarring, and new lesions slowly spread out to form a chronic solitary erythematous plaque. Chronic lesions are at high risk of developing squamous cell carcinoma.
• Tuberculosis verrucosa cutis arises in people who are partially immune to tuberculosis but who suffer a further direct inoculation in the skin. It presents as warty lesions on a ‘cold’ erythematous base.
• Scrofuloderma arises when an infected lymph node spreads to the skin causing ulceration, scarring and discharge.
• The tuberculides are a group of rashes caused by an immune manifestation of tuberculosis rather than direct infection. Erythema nodosum is the commonest. Erythema induratum (’Bazin’s disease’) produces similar deep red nodules but these are usually found on the calves rather than the shins and they often ulcerate.

The endogenous skin and bowel commensals can cause disease in the host, either because they have been transferred to an inappropriate site (e.g. bowel coliforms causing urinary tract infection), or because host immunity has been attenuated (e.g. candidiasis in an immunocompromised host). Many infections are acquired from other people, who may be symptomatic themselves or be asymptomatic carriers. Some bacteria, like the meningococcus, are common transient commensals, but cause invasive disease in a small minority of those colonized. Infection with other organisms, such as the hepatitis B virus, can be followed in some cases by an asymptomatic but potentially infectious carrier state.

Zoonoses are infections that can be transmitted from wild or domestic animals to man. Infection can be acquired in a number of ways: direct contact with the animal, ingestion of meat or animal products, contact with animal urine or faeces, aerosol inhalation, via an arthropod vector, or by inoculation of saliva in a bite wound. Many zoonoses can also be transmitted from person to person. Some zoonoses are listed in Table 2.2.

Table 2-2. Zoonotic infections

Disease	Pathogen	Animal reservoir	Mode of transmission
Prions
vCJD	Prion protein	Cattle	Ingestion (CNS tissue)
Viral
Lassa fever	Arenavirus	Multimammate rat	Direct contact
Japanese encephalitis	Flavivirus	Pigs	Mosquito bite
Rabies	Rhabdovirus	Dog and other mammals	Saliva, faeces (bats)
Yellow fever	Flavivirus	Primates	Mosquito bite
Monkey pox	Orthopox virus	Rodents, small mammals	Uncertain
SARS	Coronavirus	Civet cats and small mammals	Droplet
Bacterial
Gastroenteritis	Escherichia coli 0157	Cattle, chickens	Ingestion (meat)
	Salmonella enteritidis and others	Chickens, cattle	Ingestion (meat, eggs)
	Campylobacter jejuni	Various, e.g. chicken	Ingestion (meat, milk, water)
Leptospirosis	Leptospira interrogans	Rodents	Ingestion (urine)
Brucellosis	Brucella abortus Brucella melitensis	Cattle Sheep, goats	Contact; ingestion of milk/cheese
Anthrax	Bacillus anthracis	Cattle, sheep	Contact; ingestion
Lyme disease	Borrelia burgdorferi	Deer	Tick bite
Cat scratch fever	Bartonella henselae	Cats	Flea bite
Plague	Yersinia pestis	Rodents	Flea bite
Typhus	Various Rickettsia spp.	Various	Arthropod bite
Psittacosis (ornithosis)	Chlamydia psittaci	Psittacine and other birds	Aerosol
Others
Toxoplasmosis	Toxoplasma gondii	Cats and other mammals	Ingestion (meat, faeces)
Cryptosporidiosis	Cryptosporidium parvum	Cattle	Ingestion (faeces)
Hydatid disease	Echinococcus granulosus	Dogs	Ingestion (faeces)
Trichinosis	Trichinella spiralis	Pigs, beans	Ingestion (meat)
Toxocariasis	Toxocara canis	Dogs	Ingestion
Cutaneous larva migrans	Ancylostoma caninum	Dogs	Penetration of skin by larvae
Leishmaniasis	Leishmania spp.	Dogs	Ingestion

vCJD, variant Creutzfeldt-Jakob disease; SARS, severe acute respiratory syndrome

Most microorganisms do not have a vertebrate or arthropod host but are free-living in the environment. The vast majority of these environmental organisms are non-pathogenic, but a few can cause human disease (Table 2.3). Person-to-person transmission of these infections is rare. Some parasites may have a stage of their life cycle which is environmental (for example the free-living larval stage of Strongyloides stercoralis and the hookworms) even though the adult worm requires a vertebrate host. Other pathogens can survive for periods in water or soil and may be transmitted from host to host via this route (see below): these should not be confused with true environmental organisms.