Category Archives: Infectious Diseases Tropical Medicine and Sexually Transmitted Diseases

Sexually transmitted diseases

Sexually transmitted diseases (STDs) remain epidemic in all societies and the range of pathogens that are known to be spread by sex continues to increase. In 1990 over 578000 new cases were seen in genitourinary medicine (GUM) clinics in the UK. In the last 50 years there has been an increase in viral conditions, particularly Herpes simplex virus (HSV) and human papillomavirus, but a decrease in cases of syphilis and gonorrhoea. The recognition of AIDS and human immunodeficiency virus (HIV) has heightened awareness of STDs. In GUM clinics up to 25% of patients attend for advice and checks on their sexual health.

HISTORY

Three of the commonest presenting symptoms are vaginal discharge, urethral discharge and genital ulceration. In addition to a full general medical history the following should be obtained:
SEXUAL HISTORY: number and types of sexual contact (e.g. orogenital), partner’s sex, use of condoms and other forms of contraception, previous history of STDs including dates and treatment received, HIV testing and results and hepatitis B vaccination

Causes of vaginal discharge.

Causes of vaginal discharge.

Causes of urethral discharge.

Causes of urethral discharge.

Causes of genital ulceration.

Causes of genital ulceration.

TRAVEL ABROAD to areas where antibiotic resistance is known or where particular pathogens are endemic

DRUG MISUSEIN WOMEN, menstrual and obstetric history

EXAMINATION

General examination must include a review of the mouth, throat, skin and lymph nodes in all patients. Signs of HIV infection are covered.The inguinal, genital and perianal areas should be examined with a good light source. The groins should be palpated for lymphadenopathy and hernias. The pubic hair must be examined for nits and lice. The external genitalia must be examined for signs of erythema, fissures, ulcers, chancres, pigmented or hypopigmented areas and condylomata. Signs of trauma may be seen. In men, the penile skin should be examined and the foreskin retracted to look for balanitis, ulceration, condylomata or tumours. The urethral meatus is located and the presence of discharge noted. Scrotal contents are palpated and the consistency of the testes and epididymis noted. A rectal examination/proctoscopy should be performed in patients with rectal symptoms, those who practise anoreceptive intercourse and patients with prostatic symptoms. A search for rectal condylomata is indicated in patients with perianal lesions. In women, Bartholin’s glands must be identified and examined. The cervix should be inspected for ulceration, discharge, bleeding and ectopy and the walls of the vagina for condylomata. A bimanual pelvic examination is performed to elicit adnexal tenderness or masses, cervical tenderness and to assess the position, size and mobility of the uterus. Rectal examination and proctoscopy are performed if the patient has symptoms or practises anoreceptive intercourse.

INVESTIGATIONS

Although history and examination will guide investigation it must be remembered that multiple infections may coexist, some being asymptomatic.

1 In men:

(a) Urethral smears for Gram staining
(b) Urethral swabs for gonococcal culture and Chlamydia testing
(c) Two glass urine test and urinalysis
(d) Rectal swabs for Gram staining and culture
(e) Throat swab for culture
(f) Blood for syphilis serology

2 In women:

(a) Smears from the lateral vaginal wall for Gram staining
(b) Vaginal swab for culture of Candida and Trichomonas
(c) A wet preparation is made from the posterior fornix for Trichomonas and for the potassium hydroxide test for bacterial vaginosis
(d) The pH of vaginal secretions using narrow range indicator paper
(e) Endocervical smears and swabs for Gram staining, gonococcal  culture and Chlamydia tests
(f) Urethral smears and swabs for Gram staining and gonococcal culture
(g) Rectal and throat swabs, if indicated
h) Urinalysis
i) Cervical cytology
j) Blood syphilis serology

3 Additional investigations when appropriate include:

a) Blood for hepatitis Band C serology, HIV antibody testing (with full counselling)
b) Swabs for HSV and Haemophilus ducreyi from clinically suspicious lesions in special media
(c) Smears and swabs from subpreputial area in men with balanoposthitis (inflammation of glans penis and prepuce)
d) Scrapings from lesions suspicious of early syphilis for immediate dark-ground microscopy
e) Pregnancy testing
(f) Stools for Giardia, Shigella or Salmonella from homosexual men

TREATMENT, PREVENTION AND CONTROL

The treatment of specific conditions is considered in the appropriate section. Many GUM clinics keep basic stocks of medication and dispense directly to the patient. Tracing the sexual partners of patients is crucial in controlling spread of SIDs. The aims are to prevent the spread of infection within the community and to ensure that people with asymptomatic infection are properly treated. Interviewing people about their sexual partners requires considerable tact and sensitivity and specialist health advisors are available in GUM clinics. Prevention starts with education and information. People begin sexual activity at ever younger ages and education programmes need to include school pupils as well as young adults. Education of health professionals is also crucial. Appropriate and accessible services must be well advertised. The risks of acquiring an SID may be reduced by avoiding multiple partners, correct and consistent use of condoms and avoiding sex with people who have symptoms of infection. For those who change their sexual partners frequently regular check-ups (approximately 3- monthly) are advisable. Once people develop symptoms they should be encouraged to seek medical advice as soon as possible to reduce complications and spread to others.

Helminthic (cestode) infections

Tapeworms belong to the subclass Cestoda. These are flat worms measuring a few millimetres (Echinococcus granulosus) to several metres (Taenia saginata) in length. Structurally they consist of a head that is adorned with suckers and hooks (Taenia solium) or suckers alone (T. saginata). The head is attached via a short slender neck to several segments or proglottids that form a chain-like structure or strobila. The terminal proglottide is the most mature. The entire worm is covered with a continuous elastic cuticle. Tapeworms are devoid of a gastrointestinal tract or vascular system; nutrients are absorbed directly through the cuticle. They are hermaphrodites and crossfertilization between proglottids is frequent. Adults live in the intestinal tract of vertebrates, whereas the larvae (oncospheres) exist in the tissues of vertebrates and invertebrates. Infection is transmitted to humans by ingestion of meats infected with larval forms. Four tapeworms commonly infect humans: T. saginata, T. solium, Diphyllobothrium latum and Hymenolepsis nana.

Taenia saginata (beef tapeworm)infection

T. saginata measures up to 10 m in length, inhabits the upper jejunum, and is prevalent in humans in all beefeating countries. The majority of patients are asymptomatic. Symptoms are mild, with vague epigastric and abdominal pain, and occasional diarrhoea and vomiting. Weight loss is unusual. Rarely, appendicitis and pancreatitis due to obstruction of the appendix and pancreatic ducts, respectively, by the adult worms may occur. The commonest symptom is the presence of proglottids in the faeces, bed or underclothing.

DIAGNOSIS

The presence of proglottids, which are visible macroscopically, or the eggs, which are seen microscopically, in the faeces or perianal region is diagnostic. A higher positive yield is obtained by examining perianal clear adhesive tape swabs for ova, in which case the scolex (the head) or proglottids are required to establish the species.

TREATMENT

Niclosamide 2 g as a single chewed dose is effective. Praziquantel 10 mg kg'” as a single dose is effective but is not available on the UK market.

PREVENTION

Prevention is easily effected by careful inspection of beef for cysticerci (encysted larval forms). Refrigeration of beef at O°C for S days or cooking it at S7°C for a few minutes destroys the cysticerci.

Taenia solium-schematic lifecycle.

Taenia solium-schematic lifecycle.

Taenia solium infection and cysticercosis

T. solium (the pork tapeworm) measures up to 6 m in length. It has a worldwide distribution but is seen most frequently in Eastern Europe, South East Asia and Africa. In the adult form it lives in the human upper jejunum. The clinical features are similar to those caused by T. saginata. Treatment is similar to that for T. saginata. However, because release of ova can occur during treatment and, theoretically, could be carried back into the stomach, releasing the intermediate larval stage, treatment for T. solium should be followed by a saline purge.

Human cysticercosis

Cysticercosis occurs after autoinfection or heteroinfection by eggs of T. solium and invasion of tissues by the intermediate larval form-cysticercus cellulosae. Cysticercosis is most commonly seen in parts of Asia, Africa and South America. Cysticerci may develop in any tissue in the body. Most commonly, however, three clinical forms are recognized:
1 Cerebral cysticercosis may present as various forms of epilepsy, as a space-occupying lesion or as focal neurological deficits including hemiplegia and behavioural changes.
2 Ocular cysticercosis may present as retinitis, uveitis, conjunctivitis or choroidal atrophy. Blindness may ensue.
3 Subcutaneous cysticercosis presents as small, pea-sized, hard nodules in the subcutaneous tissue. The diagnosis is established by biopsy of a subcutaneous ule and demonstrating the characteristic translucent embrane. Radiography may demonstrate calcified enerating cysticerci. CT brain scan should be pered when subcutaneous cysticercosis has been diag- Indirect haem agglutination tests are useful.

Treatment involves surgical excision of the cysticerci if possible. Praziquantel is the drug of choice for cyscosis; steroids are given during therapy to avoid reaction. Antiepileptic drugs are usually necessary for cerebral cercysticercosis.

Diphyllobothrium latum infection

DiphyIlobothriasis is particularly prevalent in Scandinavountries, the Baltic region, Japan and the lake region – itzerland. Infection in humans, the definitive host, from ingestion of fish that contain the infected ercoid form. The adult tapeworm measures several in length. The proglottids differ from those of tacnia in that they are more wide than long. The adult usually attaches itself to the jejunum.

clinical features are usually mild and consist of abdominal discomfort, anorexia, nausea and vomiting. Megaloblastic anaemia, due to competitive utilization of ingested vitamin B12 by the parasite, may occur small percentage of patients. Rarely, intestinal obstruction occurs.
Trearment is similar to that described for T. saginata.

Hydatid disease

Hydatid disease occurs when humans ingest the hexacanth embryos of the dog tapeworm Echinococcus granulosus or of E. multilocularis. Human infection with E. granulosus frequently occurs in early childhood by direct contact with infected dogs, or by eating uncooked, improperly washed vegetables contaminated with infected canine faeces. In the duodenum the hexacanth embryos hatch, penetrate the intestinal wall, enter the portal system and are then carried to the liver. Further dissemination of embryos to the lung and to almost every organ in the body may occur, where they form hydatid cysts. The disease is seen in all parts of the world particularly in those countries where sheep and cattle-raising constitutes an important means of livelihood. It is rare in the UK but is seen in the Middle East, North and East Africa, Australia and Argentina. These animals perpetuate the life-cycle of the parasite. Symptoms largely depend upon the site of the unilocular hydatid cyst. The liver is the commonest site for cyst formation (60%), followed by the lung (20%), kidneys (3%) and brain (l %). In the liver the majority of cysts are situated in the right lobe. The symptoms are those of a slowly growing benign tumour. Pressure on the bile ducts may cause jaundice. Rupture into the abdominal cavity, pleural cavity or biliary tree may occur. In the latter instance, intermittent jaundice, abdominal pain and fever associated with eosinophilia result. A cyst rupturing into a bronchus may result in its expectoration and spontaneous cure, but if secondary infection supervenes a chronic pulmonary abscess will form. Haemoptysis, dyspnoea and chest pain may lead to a mistaken diagnosis of malignancy. Focal seizures may occur if cysts are present in the brain. Renal involvement produces lumbar pain and haematuria. Calcification of the cyst occurs in about 40% of cases.

Echinococcus granulosus-schematic life-cycle.

Echinococcus granulosus-schematic life-cycle.

The alveolar hydatid cyst caused by E. multilocularis results from its larval stage. E. multilocularis is seen in parts of Canada, the former USSR and Alaska. Foxes and small rodents constitute the intermediate hosts; humans are accidental hosts. The majority of the lesions are in the liver and metastasis may occur. The diagnosis and treatment of hydatid disease.

LIVER AND BILIARY TRACT INFECTIONS

Fascioliasis

Fasciola hepatica infects sheep, goats and cattle, in which it produces liver disease, and is only accidentally transmitted to humans via consumption of wild watercress grown on the grazing land of infected animals. The disease is found worldwide, including the UK. Animals excrete eggs in their faeces, from which ciliated miracidia emerge. These enter the freshwater snail (the intermediate host) in which larval development takes place. Eventually cercaria are released and these encyst on aquatic or surface vegetation.
After ingestion by a mammalian host, the parasites excyst, migrate through the intestinal wall and penetrate the liver capsule after traversing the peritoneal cavity. Immature flukes reach the bile duct by passing through liver parenchyma and after maturation begin to produce eggs. Adult flukes remain within the biliary tract for many years.

CLINICAL FEATURES

Early symptoms of intermittent fever, malaise, weight loss, right upper quadrant pain and urticaria relate to migration of flukes through the liver and generally occur 2-3 months after infection. A second phase of the illness relates to the presence of ukes in the biliary tract, where they can cause obstrucn with jaundice and cholangitis, although infection y remain asymptomatic. Flukes have been found in y ectopic sites, including lung, brain and skin.

DIAGNOSIS

Eosinophilia is common in the early phase of the illness d is often associated with liver biochemical abnormalies and a positive complement fixation test. Ova are notd in the stool until the second phase of the illness en the mature flukes are established in the biliary tract.  Ho “ever, in up to 30% of cases, stools remain negative; e diagnosis can then be confirmed either by identifying “3 in duodenal aspirate or by serological tests. Treatt is with bithionol 30-50 mg kg'” for 10-15 doses either daily or on alternate days.

 Clonorchiasis

Cnorchis sinensis is a common fluke of the dog, cat and pig that affects millions of animals in the Far East, pararly Indo-China, Japan, Korea, Hong Kong and Vietnam. A related fluke, Opisthorchis felineus, also affects  foxes and is found predominantly in India, the Philipines Korea and Japan. The life-cycles of both these flukes are similar to that of F. hepatica, except that freshwater fish become infected by the cercaria and thereby function as a second intermediate host. Human infection occurs by ingestion of infected raw fish.

CLINICAL FEATURES

Infected individuals may remain symptom-free, although prolonged exposure with heavy infection results in recurrent cholestatic jaundice, suppurative cholangitis, liver abscess and cholangiocarcinoma.

DIAGNOSIS

The diagnosis is made on microscopic examination of faeces or duodenal aspirate.

TREATMENT

Praziquantel 25 mg kg” as a single dose is the treatment of choice.

INTESTINAL INFECTIONS

Fasciolopsiasis

Fasciolopsis buski causes intestinal infection in humans and pigs. There are two intermediate hosts-freshwater snails and water plants. Human infection is initiated by oral contact with contaminated water plants. These large flukes, which are several centimetres in length, are common in China, Vietnam, Thailand and Taiwan. Mucosal ulceration and inflammation are apparent at the site of attachment in the intestine; abscess formation, haemorrhage and occasionally bowel obstruction may result. The symptoms are usually non-specific. Heavy infection in children may simulate or precipitate proteinenergy malnutrition. Anaemia and eosinophilia are common.

DIAGNOSIS

The diagnosis may be simple if the patient is vomiting or passing flukes per rectum, but may be confirmed by identifying ova in the stools.

TREATMENT

Treatment is with tetrachloroethylene 0.12 ml kg:’ as a single dose (maximum dose of 5 ml) or dichlorophen 100 mg kg-l as a single dose (which may be repeated 1 week later).

Trematode (fluke) infections

BLOOD INFECTIONS

Schistosomiasis (bilharzia)

Three major species of schistosomes produce human disease. These have marked differences in geographical distribution. Prevalence is dependent on the presence of a susceptible intermediate snail host and faecal contamination of water supplies. The size of snail populations varies with the season and availability of freshwater breeding grounds. An increase in the world prevalence of schistosomiasis is partly due to dam construction and irrigation programmes.

Trematode (fluke) infection.

Trematode (fluke) infection.

LIFE-CYCLE AND PATHOGENESIS

Human infection occurs after penetration of the skin ormucous membranes by cercariae, the infective form of the parasite that is liberated into fresh water by the specific intermediate snail host. Cercariae penetrate unbroken skin and migrate as schistosomules through the venous circulation to the liver, where the adult worms mature. Eventually pairs of male and female worms migrate upstream along the portal vein to the mesenteric venules, until the calibre of the vessels halts their progress. They remain in this location for many years copulating continuously and producing enormous numbers of eggs. To complete the life-cycle, eggs must leave the body, either by penetrating the intestinal wall (Schistosoma mansoni and S. japonicum) or the bladder wall (5. haematobium) and returning to the environment via faeces or urine, respectively. The larvae (miracidia) develop inside the eggs but do not hatch until they arrive in fresh water, when they search actively for the specific snail host to invade. Once inside the snail, multiplication occurs-a single miracidium produces up to 100 000 cercariae, released at the rate of 5000 per day. Eggs retained in host tissues, particularly the liver, urinary bladder and intestine, are responsible for the clinical manifestations of schistosomiasis. Egg antigens initiate both immediate and delayed-type hypersensitivity reactions with granuloma formation. Humoral substances such as lymphokines, macrophage migration inhibitory factor and fibroblast stimulating factors are found at the site of these granulomas and presumably support the cellular inflammatory response. Healing eventually occurs by fibrosis.

CLINICAL FEATURES

The first clinical sign of an acute infection is a local inflammatory response at the site of the invading cercariae known as ‘swimmer’s itch’. Within a week or more there is a generalized allergic response characterized by fever, urticaria, eosinophilia, myalgia and malaise. Nausea, vomiting and profuse diarrhoea are common, as are respiratory symptoms, particularly cough. Clinical findings at this time include generalized lymphadenopathy, hepatosplenomegaly and signs of patchy pneumonia. In ia the acute disease is called Katayama fever. It is most pronounced in infection with S. japonicum and S. manSOnt.

Chronic schistosomiasis varies in its clinical presentation depending on the type of schistosome involved.

Schistosomiasis-geographical distribution.

Schistosomiasis-geographical distribution.

Chronic schistosomiasis varies in its clinical presentation depending on the type of schistosome involved. Schistosoma mansoni and Schistosoma japonicum S. mansoni is found predominantly in Africa, South America and the West Indies, whereas S. japonicum is common in China and other specific sites in South East Asia. S. mansoni predominantly affects the colon, where the presence of ova produces macroscopic lesions such as mucosal granularity, erythema and superficial ulceration. However, a particularly severe form of colonic disease is seen in Egyptians, with gross ulceration and polyp formation, particularly in the rectosigmoid; extensive polyposis results in significant blood and protein loss from the colon. Progressive fibrosis in the intestinal wall leads to rigidity and stricture formation, although intestinal obstruction is rare. A localized granulomatous reaction in the intestine (pseudotumour or bilharzioma) may be mistaken for a colonic cancer. The development of granulomatous hepatitis, followed by progressive periportal fibrosis and portal hypertension, is signified by marked hepatosplenomegaly, often associated with osophageal varices. In advanced cases death is due to the complications of portal hypertension, as hepatocellular function remains remarkably good. S. japonicum affects the small intestine and proximal colon in addition to causing fibrotic liver disease. S. japonicum produces larger numbers of eggs than S. mansoni, which accounts for the more extensive pattern of disease and the frequency of ectopic deposition of ova, particularly in the lungs, spinal cord and brain. The latter may result in fits or hemiplegia. Epithelial dysplasia in the colon has been reported in patients with chronic S. japonicum colitis, and it is nowclear that this condition has premalignant potential in  endemic areas.

Schistosoma haematobium

This is mainly a urinary tract schistosome found predominantly in Egypt, East Africa and the Middle East. Chronic inflammation is found in the bladder, ureters and urethra, causing urinary frequency, dysuria and haematuria. Chronic infection leads to obstructive uropathy, chronic pyelonephritis and renal failure, and contraction of the bladder. Epidemiological studies confirm an association between bladder carcinoma and this infection. The internal genitalia may be involved and rectal inflammation and ulceration may be found in up to 70% of patients.

DIAGNOSIS

In endemic areas a confident diagnosis can often be obtained on clinical grounds. Confirmation is achieved by detecting the characteristic eggs in the stools, the urine or in a rectal biopsy. Different species of Schistosoma can be distinguished not only by the clinical pattern but also by egg morphology.

Schistosoma-5chematic life-cycle.

Schistosoma-5chematic life-cycle.

A plain abdominal radiograph may reveal intramural calcification in the wall of the bladder or the colon. Barium contrast studies of the colon show spiculating mucosal ulceration, polyposis, strictures, and possibly a mass lesion that could either be a bilharzioma or, in the case of S. japonicum infection, a carcinoma. Intravenous urography may confirm an obstructive uropathy and demonstrate bladder contraction. Immunodiagnostic tests are available, the most sensitive of which detect antibodies against a gut-associated polysaccharide antigen by either ELISA or indirect immunofluorescence.

TREATMENT

The two major objectives of treatment of schistosorruasis are:
1 Reduction in egg production
2 Prevention or reduction of tissue damage by eggs already in situ

In endemic and hyperendemic areas, curative therapy is usually inappropriate, since reinfection occurs rapidly, whereas infected individuals who are no longer exposed to the parasite can be effectively treated. Suppressive noncurative chemotherapeutic approaches have been used in mass treatment programmes in Egypt with good clinical improvement following a reduction in the ‘worm burden’. All antischistosomal drugs have the same effect: they cause worms to leave the mesenteric and vesical veins and to enter the liver and lungs where they are eventually destroyed by host tissue responses. Praziquantel is active against all species of schistosome and is probably the drug of choice as it is well tolerated and relatively free from serious side-effects. A single dose (40 mg kg”) cures more than 90% of patients with S. haematobium, with slightly lower rates against S. mansoni. S. japonicum is best treated with a total dose of 60 mg kg'” given in divided doses over 1 or 2 days. Oxamniquine is active against S. mansoni and rnetriphonate against S. haematobium.

Colonscopic polypectomy can control the number of colonic polyps, but surgery may be required to relieve obstructive uropathy and for inflammatory masses in the eNS.

PREVENTION

Personal protection is to avoid infected water. General control is difficult but depends on the provision of good sanitation, which is largely an economic problem

Trichuris trichiura (whipworm) infection

T. trichiura is a common parasite and is found worldwide. Prevalence varies from 1% to 90%, being highest in poor communities with inadequate sanitation. Adult worms are most commonly found in the distal ileum and caecum, although in heavy infection no part of the colon is spared. The adult worm embeds its cephalic region into the intestinal mucosa, leaving the distal tail free within the lumen. Such invasion damages the intestinal mucosa and in heavy infection overt colonic and rectal ulceration may result, leading to significant blood and protein loss.

CLINICAL FEATURES

Most infections are asymptomatic and haematological or biochemical deficits do not occur provided nutritional intke is adequate. Heavy infection is associated with diarrhoea with blood and mucus, often associated with abdominal discomfort, tenesmus, anorexia and weight loss. Involvement of the appendix can cause appendicitis, and rectal prolapse has been reported in children.

DIAGNOSIS

Stool examination confirms the presence of typical barrelshaped eggs. Proctosigmoidoscopy may reveal adult worms firmly attached to the rectal mucosa.

TREATMENT

Mebendazole 100 mg twice daily for 3 days or a single dose of pyrantel pamoate 10 mg kg-l are effective therapies.

Enterobius vermicularis (threadworm) infection

This parasite occurs worldwide but is more prevalent in temperate and cold climates. Children are most commonly infected, but it may affect whole families, inhabitants of residential institutions, and any group of people living in overcrowded circumstances. Adult worms reside largely in the colon, the female migrating to the anus to deposit embryonated eggs on the perianal and perineal areas. Superficial damage to the colonic mucosa occurs during heavy infection and secondary bacterial infection of these lesions may rarely result in submucosal abscesses.

CLINICAL FEATURES

Intense pruritus ani is usually the only symptom of threadworm infection. This is usually nocturnal and related to egg-laying in the perianal region by the female worms. Scratching results in dissemination of eggs and autoinfection. Infection has little significance while the parasite remains within the intestinal lumen, although on occasions migration occurs to the peritoneum and the viscera may be involved.

DIAGNOSIS

Diagnosis is best achieved by applying a piece of clear adhesive tape to the perianal region; this tape may then be examined microscopically for the presence of adherent eggs. Adult worms may be observed leaving the anus bythe child’s parents.

TREATMENT 

A single dose of mebendazole 100 mg followed by a second dose 2 weeks later is usually effective. Alternatives include pyrantel pamoate or piperazine. Family members should also be treated.

INTESTINAL NEMATODE INFECTION

Some adult nematodes live within the intestinal lumen. The disease is spread to humans:
PASSIVELY by ingesting infective eggs, as occurs with Ascaris lumbricoides (’roundworm’), Trichuris trichiura (whipworm) and Enterobius vermicularis (threadworm) ACTIVELY by percutaneous spread of filariform larvae that penetrate the skin (hookworm and Strongyloides) Ascaris deviates from the simplified life-cycle shown in that it invades the duodenum and enters the venous system, via which it reaches the lungs. The worm is eventually expectorated and swallowed, entering the intestine where it completes its maturation. Strongyloides  is the only nematode that is able to complete its life-cycle in humans; its rhabditiform larvae, which hatch in the intestine, are able to reinfect the host by penetrating the intestinal wall and entering the venous system.

Intestinal nernatodes=schernatlc life-cycle.

Intestinal nernatodes=schernatlc life-cycle.

Strongyloidiasis

Strongyloides stercoralis is found worldwide but is particularly common in warm, wet regions such as parts of Central America and South-East Asia. Infection can persist for decades and is still being discovered in war veterans, particularly prisoners of war who worked on the Burma- Thailand railway and veterans from Vietnam. Adult worms inhabit the crypts of the small intestine, causing little damage, but in heavy infection worms are embedded in the mucosa, and cause an inflammatory response with mucosal injury. The worms are passed in the stools and autoinfection is common.

CLINICAL FEATURES

After penetration of the skin by the filariform larvae, a local reaction occurs characterized by itching, erythema, oedema and urticaria. This subsides within 2 days. A week later, migration of the adolescent worms causes irritation of the upper airways, producing cough and occasionallymore severe respiratory symptoms. After about 3 weeks,  intestinal colonization occurs, often leading to abdominal discomfort, intermittent diarrhoea and constipation. These symptoms can be mild and may pass unnoticed. However, in some individuals, heavy infection may lead to persistent diarrhoea, nausea, anorexia and evidence of intestinal malabsorption, notably steatorrhoea. Hypoalbuminaemia and weight loss also occur. Disseminated strongyloidiasis is a very serious and often fatal condition and has been described in patients receiving cortico-steroid or other immunosuppressive therapy or in those who are irnmunocompromised for other reasons.

DIAGNOSIS

Motile rhabditiform larvae can be detected in fresh stool or in duodenal aspirate. Eosinophilia is common. In heavy infection, anaemia and biochemical evidence of malabsorption are found.

TREATMENT

Treatment consists of thiabendazole 1.5 g twice daily for 2 days. Therapy should be given for at least 5 days (often longer) in the hyperinfected patient with disseminated disease. Albendazole 400 mg kg” for 3 days is also effective. Repeated therapy may be required. The mortality is high in the hyperinfected group owing to an accompanying Gram-negative septicaemia and treatment should include i.v. broad-spectrum antibiotics. Hookworm infection Hookworm is seen worldwide and affects approximately 25% of the world’s population. Ancylostoma duodenale is found in Europe, the Middle East and North Africa, whereas Necator american us is found in the Western Hemisphere, sub-Saharan Africa, South-East Asia and the Far East.
Adult worms inhabit the small intestine and attach firmly to the intestinal mucosa by the teeth or cutting plates in their large buccal capsule. Blood loss is approximately 0.2 ml daily in A. duodenale infection (five- to tenfold less with N. americanus); in heavy infection it has been estimated that up to 100 ml of blood is lost daily.

Ancylostoma braziliensis (dog hookworm) causes this characteristic cutaneous lesion.

Ancylostoma braziliensis (dog hookworm) causes
this characteristic cutaneous lesion.

CLINICAL FEATURES

Local irritation at the site of larval entry in the skin is known as ‘ground itch’, but this rapidly disappears to be followed some 2 weeks later by mild and transitory pulmonary symptoms. Most patients are asymptomatic once the larvae have reached the small intestine. Some patients experience ulcer-like symptoms and those with heavy chronic infection eventually develop symptoms and signs of anaemia. Hookworm infection is the commonest cause of iron deficiency anaemia worldwide. A. braziliensis (dog hookworm) causes characteristic patterns of subcutaneous infection in children.

DIAGNOSIS

Hookworm ova appear in the stool, the number of eggs present giving a guide to the severity of the infection. Early in the infection, eosinophilia may be found in the peripheral blood. This is followed later by the appearance of iron deficiency anaemia.

TREATMENT

Mebendazole 100 mg twice daily for 3 days is effective in ooth types of hookworm, although the infection may not be cleared with a single course of treatment.

Ascaris lumbricoides (’roundworm’)
infection

A lumbricoides is a large worm that is found orldwide but is particularly common in poor rural communities where there is heavy faecal contamination of the immediate environment. Infection may be entirely asymptomatic, although heavy infections are associated with nausea, vomiting, abdominal discomfort and anorexia. Worms may obstruct the small intestine, the commonest site being at the ileocaecal valve. Worms occasionally invade the appendix, causing acute appendicitis, or the bile duct, resulting in biliary obstruction and suppurative cholangitis. Larvae in the lung may produce pulmonary eosinophila. The nutritional impact of Ascaris infection in children is controversial, although it is very likely that heavy infection in malnourished children compounds the situation, largely by competition for host nutrients.

Ascaris lumbricoides, approximately 20 em long.

Ascaris lumbricoides, approximately 20 em long.

DIAGNOSIS

Ascaris eggs may be identified in the stool and occasionally adult worms emerge from the mouth or the anus.

TREATMENT

Mebendazole 100 mg twice daily for 3 days or a single dose of piperazine 100 mg kg-lor pyrantel pamoate 10 mg kg-l are effective. Surgical or endoscopic intervention may be required for intestinal or biliary obstruction.

Onchocerciasis

Onchocerciasis (river blindness) is produced by the filarial bworm Onchocerca volvulus. The gravid female has a life-expectancy of 15 years. The micro filariae are found in the skin and subcutaneous tissue. Humans are the only known definitive host and the day-biting female blackfly of the genus Simulium is the vector. The flies breed in rapidly flowing water both in the rain forest and savannah. The species involved are S. damnosum and S. neavei in Africa and S. metallicum in Venezuela. The disease is confined to West, Central and East Africa, Central and South America, and southern parts of Saudi Arabia.

CLINICAL FEATURES

The incubation period averages 1 year. Initially a papular, reddish, itchy rash develops. With repeated infections, characteristic subcutaneous nodules of various sizes appear. Usually they number fewer than 10 and are unevenly distributed over the body. In chronic disease, lichenification, xeroderma, pseudo ichthyosis and atrophy of the skin occur. The nodules may be associated with the development of genital elephantiasis, hydrocele and the so-called ‘hanging groin’, in which large folds of wrinkled and thickened skin develop in the groin. Ocular lesions represent the most serious manifestation of this disease and in some communities 40% of people are blind by 50 years of age. Eye disease is commoner in the savannah. Initially the patient complains of lacrimation, photophobia and a foreign-body sensation in the eye. Conjunctivitis, iridocyclitis, chorioretinitis, secondary glaucoma and optic atrophy may occur. The eye lesions have been attributed to toxin production by the microfilariae and adult worms, mechanical irritation and hypersensitivity.

DIAGNOSIS

This is established by demonstrating micro filariae in snips of bloodless tissue obtained from the nodules and kept in saline for 30 min to 1 hour before microscopic examination. The organism may also be identified in the anterior chamber of the eye by slit-lamp examination. Serological tests are not helpful in the indigenous population as the positivity rate is high. Eosinophilia occurs.

TREATMENT

Ivermectin, a broad-spectrum antiparasitic drug, is effective in filariasis and is now the drug of choice. A single dose of 150 J-Lgkg-t orally produces a prolonged reduction in microfilarial levels. Six- to twelve-monthly therapy must be given in endemic areas as ivermectin is not curative and re-infection occurs. DEe is still sometimes used when ivermectin is unavailable but reactions (pruritus and a rash) occur and were used for diagnosis (Mazzotti’s test).

PREVENTION AND CONTROL

Prevention and control depends partly on personal protection to avoid bites and attempts at destroying the vector. Eradication of blackfly is expensive and mass treatment with ivermectin (provided free by the pharmaceutical industry) once a year is being used in endemic areas with good success.

DRACUNCULIASIS

Dracunculiasis (Guinea worm infection) results from infection with Dracunculus medinensis. It is found sporadically throughout the tropics but is common in certain parts of India, Central, East and West Africa, Pakistan, the Middle East, parts of South America and the eastern regions of the former USSR. Humans are the definitive host and are infected by ingestion of water containing infected Cyclops. The larvae are liberated in the human stomach by the action of acid. These penetrate the intestinal wall, where the male dies after fertilizing the female. The gravid female then wanders in connective tissue for several months before emerging through the skin. On reaching the skin, the parasite elicits an allergic reaction with blister formation and later protrusion of the worm associated with the discharge of motile larvae. The larvae are then taken up by Cyclops, which once again are infective to humans.

CLINICAL FEATURES

A generalized reaction can occur that is associated with nausea, vomiting, generalized urticaria and diarrhoea. These symptoms abate with rupture of the blister. Secondary bacterial infection, especially with streptococci, is common and results in cellulitis and abscess formation. In Nigeria, tetanus is a frequent complication. If attempts at extraction of the worm result in damage to it, intense cellulitis may occur. Arthritis, synovitis, ankylosis of joints and epididymitis are rare sequelae.

DIAGNOSIS

Keeping the appropriate part of the body immersed in water may induce the worm to wriggle out. Fluorescent antibody tests are useful. Radiography may reveal the presence of the worm.

TREATMENT

Gradual physical extraction of the worm by winding it carefully around a stick is the treatment of choice. It may take several days before the entire worm is extruded. Niridazole and thiabendazole are of questionable value in facilitating worm extrusion.

PREVENTION AND CONTROL

Prevention of this parasitosis is easily effected by chemically treating infected sources of water.

ANIMAL NEMATODES

Toxocariasis

Toxocariasis (visceral larva migrans) occurs worldwide and is caused by Toxocara canis or T. cati. The adult worm is found in the intestine of dogs and cats. The infective ova are passed in animal faeces and may be accidentally ingested by humans. The liberated larvae penetrate the intestinal wall and reach the liver and lung via the circulation. Epidemiologically, puppies are the most important natural hosts and the infection is most commonly seen in children between 1 and 4 years of age. Several viscera may be involved and the clinical manifestations are dependent on the organ involved and the intensity of infection. Eosinophilia is common. Urticaria and dermatitis may occur. With pulmonary involvement the presentation is that of bronchial asthma. Chest radiographs may reveal transient pulmonary infiltrates. Splenomegaly and hepatomegaly may occur: Rarely involvement of the myocardium and eNS may result in death. Eye involvement (ocular larva migrans) produces a retinoblastoma-like picture; other organs are usually spared.

DIAGNOSIS

The presence of marked eosinophilia, hepatomegaly, and elevated plasma IgG, IgM and IgE is suggestive, as is the identification of foreign-body eosinophilic granulomas in histological sections. Recently detection of specific antibodies by ELISA has been found to be useful.

TREATMENT

Treatment is difficult to evaluate in view of the mild nature of the illness and the tendency for spontaneous cure. DEe 2-6 mg kg-t daily in divided doses for 3 weeks or thiabendazole 25 mg kg-t twice daily for 5 days is probably effective. Cutaneous larva migrans Cutaneous larva migrans (creeping eruption) is a disease of the hot, humid areas of tropical and subtropical countries. It is caused by the dog and cat hookworms Ancylostoma braziliense and A. caninum and, occasionally, the human parasites A. duodenale, Necator americanus and Strongyloides stercoralis. The adult forms of these worms are found in the intestine of the host. The filariform larva emerges from the ova passed in the faeces and penetrates intact human skin. An itchy papule develops at the site of larval entry. Two to three days later a markedly itchy, erythematous, serpiginous skin lesion develops. This is due to the larva, which migrates at approximately 1 ern per day. The skin over the lesion may vesiculate. Healing occurs by crusting. Although the lesions are more frequent on the lower limbs, any part of the body may be affected. Secondary bacterial infection may result in a mistaken diagnosis of pyoderma. The only systemic manifestations are transient pulmonary infiltrates and occasional breathlessness. Eosinophilia is seen.

TREATMENT

Thiabendazole applied locally as a 10% solution or given -stemically (25 mg kg” for 5 days) is effective.

Anisakiasis

Anisakiasis (herring worm disease) is caused by the larval stage of several species of Anisakis, and possibly of the related nematode Phocanema, which are found in abuncance in herring, and dolphins, whales and other large sea mammals. The disease is prevalent in Japan and northern Europe, where raw herring and other raw fish are conered a delicacy. In Japan the illness is characterized by acute gastric syndrome that presents as epigastric pain, usea and vomiting. Upper gastrointestinal endoscopy 11 reveal the presence of larvae in the gastric mucosa. In – ntrast, in Europe the small intestine is predominantly ‘oIved and the patient presents with colicky, generalized abdominal pain and fever. Eosinophilia is usual.

Trichinosis

is caused by the intestinal nematode Trichinella spirid The larval form is found in rats, hares, pigs, dogs d cats. Although cases of trichinosis have been reported – m all parts of the world, it is found predominantly in the USA and Europe. It is uncommon in India. Transmission to humans occurs when improperly cooked eats, contaminated with infective larvae, are eaten.

CLINICAL FEATURES

“Vomiting, diarrhoea, abdominal pain and headache occur24-72 hours after ingestion of contaminated meat. The erity of the clinical manifestations depends on the aamber of infecting larvae. The larvae mature into the adult form in the intestine, ere they reproduce and discharge larvae into the circuion. When these larvae migrate into the bloodstream and striated muscles (a stage that lasts 10-21 days), periorbital oedema, conjunctivitis, photophobia, fever withchills, and muscle pain and spasm occur. An urticarial rash, diarrhoea, dyspnoea and pleurisy may also occur. Myocardial and CNS involvement is unusual and, if it occurs, may result in death. In the next stage of development, larvae encyst in striated muscle. During encystment symptoms gradually subside, although weakness, muscle pain and cramps may persist for several months.

Intestinal nematode (roundworm) infections.

Intestinal nematode (roundworm) infections.

DIAGNOSIS

A firm diagnosis can be made on the clinical presentation, marked eosinophilia, and positive serology using ELISA. If necessary the diagnosis can be established by a biopsy of the deltoid or gastrocnemius muscle 3 weeks after the onset of illness and demonstrating the presence of the larvae.

TREATMENT

Analgesics, sedatives and bed rest are the mainstays of treatment. Steroids are indicated only in the presence of myocarditis, CNS involvement or marked allergic phenomena. Thiabendazole 25 mg kg-l body weight twice daily for 7 days is effective against intestinal worms and larvae.

Helminthic infections

Nematode (roundworm) infections

FILARIASIS

Several nematodes belonging to the superfamily Filarioidea are responsible for filariasis. The adult worms are thread-like. Females are larger than males. The viviparous females give birth to larvae known as microfilariae. The microfilariae of various species can be easily differentiated from each other by the presence or absence of a sheath and the pattern of nuclear distribution in the tail. These nematodes require two hosts to complete their life-cycle. Bancroftian and Malayan (lymphatic) filariasis Wuchereria bancrofti is found mainly in the tropics and subtropics-in northern Australia, the Pacific Islands, West and Central Africa, South America and India. Brugia malayi infection is less widespread than Bancroftian filariasis and is found in India, southern China, Malaysia, Indonesia and Borneo. Humans are the definitive hosts and mosquitoes of various types are the intermediate hosts. Humans are the only known reservoirs of Bancroftian filariasis, whereas, in addition to humans, animals such as cats are reservoirs of Malayan filariasis. Culex fatigans, which bites at night, is the main vector of Bancroftian filariasis. Aedes and Anopheles spp. have also been implicated. The major vector for Malayan filariasis is Mansonia annulifera. Following the bite of an infected mosquito, the larvae penetrate the skin, enter the lymphatics and are carried to the regional lymph nodes. Here they grow and mature for up to 18 months. After fertilization the microfilariae produced are carried from the lymphatics into the blood; they do not produce any symptoms or signs. Adult worms produce lymphangitis, which is believed to be a hypersensitivity reaction. The lymphangitis is followed by fibrosis, a granulomatous reaction and later irreversible lymphatic blockade. Secondary bacterial infection may add considerably to the inflammatory response and resultant fibrosis.

Habitat, vectors and major clinical manifestations of some nematodes of the superfamily Filarioidea.

Habitat, vectors and major clinical manifestations of some nematodes of the superfamily Filarioidea.

Filariasis-geographical distribution.

Filariasis-geographical distribution.

CLINICAL FEATURES

Following an incubation period that averages 10-12 months, the patient presents with fever ranging from 39 to 41°C accompanied by lymphangitis, both of whichusually subside in 3-5 days. Lymphangitis typically involves the lymphatics of the lower or upper limbs or  of the abdomen. Involvement of the lymphatics of the epididymis, testis and spermatic cord occurs almost exclusively in Bancroftian filariasis. The involved superficial lymphatics appear as red streaks on the skin, and are tender and cord-like. The inflammation may subside either with treatment or spontaneously but there is a tendency for recurrences. The inflammatory phase is usually followed by the obstructive phase, which is characterized by features of lymphatic blockade. Many sites may be affected, but lower limb and scrotal oedema occur frequently. Long-standing obstruction produces thick, rough skin, which occasionally ulcerates. Less frequently chyluria, chylous ascites and pleural effusions occur. The obstructive phase may be punctuated by episodes of acute lymphangitis.

DIAGNOSIS

The clinical presentation is characteristic. Eosinophilia and the presence of microfilariae in thin or thick peripheral blood smears is diagnostic. Since W. bancrofti and B. malayi are released into the peripheral circulation at night coinciding with the time of the mosquito bite, blood for examination should be taken between 9 p.m. and 1 a.m. If, despite repeated examination, microfilariae cannot be demonstrated in thick or thin blood smears, diethylcarbamazine 100 mg given as a single dose followed by blood removal 30 min later for examination may give a positive yield. Various parasite-concentration techniques such as Knott’s concentration or membrane filtration techniques have resulted in a higher positive yield. Serological tests are available but not highly specific.

TREATMENT

Diethylcarbamazine (DEe) 3-9 mg kg-I daily in three divided doses for 2-3 weeks is recommended. A second course after 6 weeks increases the cure rate. The WHO Expert Committee has recommended that a total of 72 mg kg-I be given for eradication of Bancroftian filariasis and 30-40 mg kg-I for Malayan filariasis. DEe is filaricidal. Following initiation of therapy, marked allergic reactions can occur and require concomitant administration of antihistamines or steroids. Associated bacterial infections should be appropriately treated. Reconstructive surgery plays an important role in removing unsightly tissue.

PREVENTION AND CONTROL

Mass chemotherapy with DEe (often added to table salt) has been effective in decreasing the microfilariae rate (the ~centage of individuals who have micro filariae in a unit lume of their blood in a given population) and the icrofilariae density (the number of micro filariae per unit lume of blood in individual patients). Primary prophylaxis  should be aimed at vector control and protection – humans from mosquitoes, particularly at night with regnated nets and repellant creams and sprays.

Tropical eosinophilia

Tropical eosinophilia has been attributed to micro filariae as Dirofilaria and more recently to W. bancrofti and -B.malayi. Two forms are recognized, one characterized mphadenopathy and splenomegaly, and the other by gh, bronchospasm and an asthma-like picture.

Loiasis

loiasis is caused by Loa loa. As in Bancroftian and _Wayan filariasis, the micro filariae of L. loa do not produce any symptoms. Unlike Bancroftian filariasis, the ofilariae are found in the peripheral circulation mainly during the day. The disease is confined to the hot,
id, swampy areas of West and Central Africa, in environment the deerfly vectors Chrysops silacea Chrysops dimidiata thrive. Following the bite of a female Chrysops, the microfilariae are introduced into the of the human host and tend to migrate in the subcueous tissues. They have a predilection for subconctival and periorbital tissues.

CLINICAl FEATURES

The main feature of loiasis is Calabar swellings, which are  painless, localized, transient, hot, soft-tissue swellings, “often near joints. They persist for periods varying from a hours to several weeks. They occur more commonly during the hotter months and may be preceded by numband tingling. They are produced by toxin released from the adult worm.
Urticaria, pruritus, lymphoedema, arthritis and chorioretinitis may occur.
A picture resembling meningo-encephalitis that occurs nly during treatment is thought to be an allergic reacn,

DIAGNOSIS

The worm can be seen in subcutaneous tissues or crossing the conjunctivae.
The characteristic micro filariae may be demonstrable in peripheral blood smears. Eosinophilia is present. Seroical tests such as the complement-fixation test are also useful.

TREATMENT

DEC 2-6 mg kg-l in gradually increasing dosage is effective against both adult worms and micro filariae although multiple courses may be necessary. Treatment should be continued for 2-3 weeks. Side-effects of treatment (caused by death of parasites) are fever, headache, urticaria and encephalitis; steroids may be necessary for these effects.

PREVENTION AND CONTROL

Prevention is best effected by adequate personal protection. In addition, houses should be sprayed with dieldrin. Mass treatment of all the inhabitants of villages with DEC 2 mg kg-l daily for 3 days has reduced the incidence of this disease.

Intestinal and genital infections

Amoebiasis

The most important human disease due to amoebae is amoebiasis, which is caused by Entamoeba histolytica. This intestinal pathogen can be differentiated from other enteric amoebae such as  ntamoeba hartmani, Entamoeba coli and Endolimax nana, since E. histolytica is the only amoeba found in the intestine that phagocytoses RBCs. It occurs worldwide, although much higher incidence rates are found  n the tropics and subtropics. It can be found in active male homosexuals who carry the pathogen (usually strains of low virulence) and between whom it is spread by sexual contact.

LIFE-CYCLE AND PATHOGENESIS

The organism exists both as a motile trophozoite and as a cyst that can survive outside the body. Cysts are transmitted chiefly by ingestion of contaminated food or water or spread directly by person-to-person contact. Trophozoites emerge from the cyst in the small intestine and then pass on to the colon, where they multiply.  Many individuals can carry the pathogen without obvious evidence of clinical disease (asymptomatic cyst passers). However, under certain conditions, E. histolytica trophozoites invade the colonic epithelium, probably with the aid of their own cytotoxins and proteolytic enzymes. The parasites continue to multiply and finally frank ulceration  of the mucosa occurs. If penetration continues trophozoites may enter the portal vein, via which they reach the liver and cause hepatitis and intrahepatic abscesses. This invasive form of the disease is particularly serious and unless treated promptly is often fatal.

CLINICAL FEATURES

The incubation period is highly variable and may be as short as a few days or as long as several months or even a year. The presentation of amoebic colitis may be:

RADUAL ONSET with mild intermittent diarrhoea and abdominal discomfort, usually progressing to bloody diarrhoea with mucus. Systemic manifestations such as headache, nausea and anorexia are often present.

EVERE ACUTE (AMOEBIC) DYSENTERY, closely resembling that due to Shigella (bacillary dysentery).

FULMINATING COLITIS. Typically, patients with amoebic colitis appear less unwell than those with bacillary dysentery, fever is low-grade or absent, and dehydration is unusual.

COMPLICATIONS

Complications are unusual, but include:
PROGRESSION OF FULMINANT COLITIS to toxic dilatation of the colon with perforation and peritonitis.
CHRONIC INFECTION leading to stricture formation.

A schematic life-cycle of intestinal protozoa.

A schematic life-cycle of intestinal protozoa.

SEVERE HAEMORRHAGE.

AMOEBOMA, i.e. a mass of fibrotic granulation tissue, develops most commonly in the caecum or rectosigmoid region. Amoebomas occur in 10% of patients and may bleed, cause obstruction, intussuscept and are sometimes mistaken for a carcinoma.
AMOEBIC LIVER ABSCESS, which often develops in the absence of a recent episode of colitis. Tender hepatomegaly, a high swinging fever and profound malaise are characteristic, although early in the course of the disease both symptoms and signs may be minimal.

DIAGNOSIS

Serodiagnosis

The amoebic fluorescent antibody titre (FAT) is positive in at least 90% of patients with liver abscess and 75% with active colitis. Seropositivity is low in asymptomatic cyst passers.

Colonic disease

Direct examination of colonic exudate obtained at sigmoidoscopy or of freshly passed stool as a saline-wet mount is the most rapid and least expensive way of confirming amoebic infection. E. histolytica trophozoites must be distinguished from non-pathogenic amoebae and from polymorphonuclear leucocytes, with which they are sometimes confused. Cysts may also be present in the stool. Sigmoidoscopy and barium enema examination may show colonic ulceration but are rarely diagnostic.

Liver disease

Liver abscess should be suspected if the serum alkaline phosphatase is elevated, even when clinical signs are absent. Hepatic ultrasound scan should confirm the presence of an abscess, which may be either single or multiple. Pus from an amoebic abscess has a classic ‘anchovy sauce’ appearance and may contain trophozoites.

TREATMENT

Metronidazole 800 mg three times daily for 5 days is given in amoebic colitis and a more prolonged course for 10- 14 days in liver abscess or other extra-intestinal spread. An alternative drug is the other nitroimidazole derivative, tinidazole. Dehydroemetine is used when nitroimidazoles fail (rarely). Diloxanide furoate is a luminal amoebicide and may be a helpful adjunct in clearing cysts. Large, tense abscesses in the liver may require percutaneous drainage, using an ultrasound scan to localize accurately the abscess and to position the drainage neeclle.

CONTROL AND PREVENTION

This disease will be difficult to eradicate because of the substantial human reservoir of asymptomatic cases. There is no immediate hope of vaccine development, particularly as the same individual may experience several episodes of amoebic infection, indicating that only partial protective immunity develops after exposure to the pathogen. Improved standards of personal hygiene and water quality are important. Cysts are destroyed by boiling water for at least 10 min, but the effects of chlorination are variable.

Balantidiasis

Balantidium coli is the only ciliate that produces clinically significant infection in humans. It is found throughout the tropics, particularly in Central and South America, Iran, Papua New Guinea and the Philippines. It is usually carried by pigs and infection is most common in those communities that live in close association with swine. Its life-cycle is identical to that of E. histolytica. B. coli produces a dysenteric illness owing to invasion of the distal ileal and colonic mucosa. The colitis may be acute and fulminant and if untreated may be fatal. Trophozoites rather than cysts are found in the stool. Treatment is with tetracycline, ampicillin or metronidazole.

Giardiasis

Giardia lamblia is a flagellate that is found worldwide. It causes small-intestinal disease, with diarrhoea and malabsorption. Prevalence is high throughout the tropics. It is an important cause of traveller’s diarrhoea worldwide usually occurring on return from travel. In certain parts of Europe, the former USSR, and in some rural and mountainous areas of North America, large water-borne epidemics have been reported. Person-toperson spread is common in day nurseries and residential institutions and between male homosexuals. Like E. histolytica, the organism exists both as a trophozoite and a cyst, the latter being the form in which the protozoon is transmitted. The organism colonizes and multiplies within the small intestine and may remain there without causing detriment to the host. Severe malabsorption may occur and is thought to be related to morphological damage to the small intestine; changes in villous architecture vary from mild partial villous atrophy to rarely subtotal villous atrophy. The mechanism by which Giardia causes alteration in mucosal architecture and produces diarrhoea and intestinal malabsorption is unknown. There is evidence that the morphological damage may be immune mediated. Bacterial overgrowth has also been found in association with giardiasis and may contribute to fat malabsorption.

Giardia lamblia. Courtesy of Dr A. Phillips, Department of Electron Microscopy, Queen Elizabeth Hospital for Children, London.

Giardia lamblia. Courtesy of Dr A. Phillips,
Department of Electron Microscopy, Queen Elizabeth Hospital
for Children, London.

CLINICAL FEATURES

Many individuals excreting Giardia cysts have no symptoms and are therefore carriers. Others develop symptoms within 1 or 2 weeks of ingesting cysts. These include diarrhoea, often watery in the early stage of the illness, nausea, anorexia, abdominal discomfort and distension. Stools may then become paler, with the characteristic features of steatorrhoea. If the illness is prolonged, weight loss ensues, which, even in previously healthy adults, can be marked. Chronic giardiasis can result in growth retardation in children.

DIAGNOSIS

Both cysts and trophozoites can be found in the stool, but negative stool examination does not exclude the diagnosis since the parasite may be excreted at irregular intervals. The parasite can also be seen in duodenal aspirates and in histological sections of jejunal mucosa. Raised specific anti-Giardia IgG and, in acute infections, IgM antibodies are found.

TREATMENT

Metronidazole 2 g as a single dose on three successive days will cure the majority of infections, although sometimes a second or third course is necessary. Preventive measures are similar to those outlined for E. histolytica.Alternative drugs include mepacrine, furazolidone and  albendazole.

Cryptosporidium parvum

This organism is found worldwide, cattle being a major natural reservoir. It has also been demonstrated in drinking water supplies. It produces a devastating diarrhoeal illness in patients with immunodeficiency, particularly those with AIDS. It has recently become a recognized cause of gastroenteritis, particularly in children. The parasite is able to reproduce both sexually and asexually and has a life-cycle in the intestine very similar to that of Plasmodium. The disease is spread by oocysts excreted in the faeces.

CLINICAL FEATURES

In healthy individuals cryptosporidiosis is a self-limiting illness lasting for 7-10 days. Acute watery diarrhoea is associated with fever and general malaise, but otherwise the disease follows a benign course. In the immunocornpromised patient diarrhoea is followed by severe weight loss and general debility, contributing significantly to the downhill course of AIDS. Occasionally toxic dilatation of the colon can occur. A syndrome of right upper quadrant abdominal pain, raised alkaline phosphatase and the typical bile duct abnormalities of sclerosing cholangitis is seen in AIDS patients.

DIAGNOSIS

The parasite can be detected in intestinal biopsies but is now most commonly found in faeces (as oocysts) usingoncentration techniques and a modified Ziehl-Nielsen  stain.

TREATMENT

As yet there is no effective antimicrobial treatment for this infection. AZT can reduce diarrhoea temporarily in _ IDS as can paromomycin, although the agent does not affect the cryptospiridiosis itself. Good hygiene, especially hand washing, prevents spread of organism.

B/astocystis hominis

B. hominis is a strictly anaerobic protozoan pathogen that inhabits the colon. For decades, its pathogenicity for umans was questioned but there is increasing evidence at it may cause diarrhoea. It is sensitive to metronidazole.

Cyclospora cayatenensis

Recently cyanobacterium-like bodies were detected in the ools of travellers returning from Nepal with diarrhoea. This coccidian parasite, which has not been detected “ithin enterocytes, is thought to cause diarrhoea and has entatively been named Cyclospora cayatenensis.

Microsporidiosis

This is now a common cause of diarrhoea in patients with HIV infection. Spores can be detected with high accuracy in the stools. Albendazole is effective in eradication. Trichomon iasis Trichomonas vaginalis is a flagellate that causes vaginitis and urethritis

CLINICAL FEATURES

The incubation period varies, being:
• 10-14 days in P. vivax, P. ovale and P. falciparum
• 18 days to 6 weeks in P. malariae infection Although individual variations in clinical presentation are noted, febrile paroxysms, anaemia, splenomegaly and · epatomegaly are usually present. Malarial febrile paroxms typically have three stages:
1 The ‘cold stage’ is characterized by marked vasoconstriction and lasts from 30 min to 1 hour. The patient feels intensely cold and uncomfortable. There is marked shivering. The temperature rises rapidly, often to as high as 41°C.
2 The ‘hot stage’ abruptly follows and lasts for 2-6 hours. The patient feels intensely hot and uncomfortable. Delirium may be present.
3 The ‘sweating stage’ then occurs, during which the bedclothes are drenched. The patient feels fatigued and exhausted but otherwise well and often sleeps. The fever is due to schizont rupture and the release of pyrogens. Herpes labialis frequently occurs in established malaria. Anaemia is usually present and is largely a result of haemolysis. P. vivax and P. ovale The fever occurs every other day when established. These species of Plasmodium give rise to a clinically mild infection. The presence of an exoerythrocytic stage is responible for relapses and makes eradication of the organisms difficult. P. malariae This is usually a mild disease with a fever, but tends to run a more chronic course. The nephrotic syndrome can complicate this type of malaria and may be fatal between the ages of 4 and 5 years. Because of its chronicity, the patient develops a sallow complexion, marked muscle wasting, mild icterus and massive splenomegaly. Growth retardation may occur in children.

P. falciparum

This is the most severe form of malaria (pernicious malaria), with high levels of parasitaemia. Infected RBCs develop peculiar knob-like surface projections that facili-tate adhesion of these RBCs to the endothelium of bloodvessels via I CAM-l. The consequent vascular occlusion causes severe organ damage, chiefly in the kidneys, liver, brain and gastrointestinal tract. The prodrome tends to be severe. The fever follows no particular pattern. Splenomegaly tends to occur late and the characteristic cold, hot and sweating stages are not prominent. The following clinical forms of falciparum malaria are recognized and are likely to occur when more than 2% of RBCs are parasitized (Information box 1.4).
CEREBRAL MALARIA is characterized by a marked elevation in body temperature, a rapid deterioration in consciousness, convulsions, coma and death.
BLACKWATER FEVER, so called because of the production of dark brown-black urine owing to intravascular haemolysis, is seen only in falciparum malaria. It can be precipitated by very small amounts of quinine in quinine-sensitive cases. This is a rapidly progressive illness characterized by the abrupt onset of fever, marked haemolysis, haemoglobinuria, hyperbilirubinaemia, vomiting, circulatory collapse and acute renal failure. Malarial parasites cannot usually be detected in peripheral blood smears after the onset of intravascular haemolysis.

Tropical splenomegaly syndrome

Tropical splenomegaly syndrome is seen in areas where malaria is hyperendemic. It is uncommon before 10 years of age. Characteristic features are massive splenomegaly, marked elevation in serum IgM levels, and IgM aggregates (detected by immunofluorescence) in Kupffer cells in the liver. The splenomegaly responds to antimalarial therapy. However, malarial parasites are not detected in the spleen or peripheral blood smears.

Some features of severe falciparum malaria.

Some features of severe falciparum
malaria.

PREVALENCE

The following indices are used to measure the prevalence of malaria:
SPLEEN RATE, defined as the percentage of children between 2 and 10 years of age with splenomegaly, is used as a measure of the endemicity of malaria in a community.
INFANT PARASITE RATE, defined as the percentage of infants below 1 year of age in whom malarial parasites are demonstrable in peripheral blood smears, is regarded as the most sensitive index of transmission of malaria to a locality.

DIAGNOSIS

The parasite can be demonstrated in either thin or thick peripheral blood smears stained with Giemsa, Wright or Leishman stains. Two to three blood smears taken each day for 3 or 4 days and found to be negative are necessary before a patient is declared malaria-free. Serological methods are not widely used but include indirect immunofluorescence, indirect haem agglutination and gel diffusion techniques. ELISA for antigen detection and probes for parasite DNA are currently being evaluated.

TREATMENT

General

Analgesics and antipyretics such as aspirin and paracetamol are given as necessary. Intravenous fluids may be required to combat dehydration and shock. Treatment of an acute attack The 4-aminoquinolines are the drugs of choice. Chloroquine- sensitive malaria is treated with chloroquine 600 mg of the base followed by 300 mg in 6 hours and then 150 mg twice daily for 3 days, or amodiaquine hydrochloride 600 mg of the base followed by 400-600 mg daily for 2 days up to a total maximum dose of 2400 mg. Chloroquine-resistant malaria is treated with quinine sulphate 650 mg three times daily for 5 days given in combination with pyrimethamine 25 mg twice daily for 3 days and sulphadiazine 500 mg twice daily for 5 days. Mefloquine is a synthesized quinolone which is useful in chloroquine- and some quinine-resistant cases; again resistance to this is developing. Halofantrine, an amino alcohol, is another drug for resistant cases. Both these last two drugs are too expensive for widespread use.

DRUG SIDE-EFFECTS. These drugs are potentially toxic. With quinine, tinnitus, haemolytic anaemia and drug fever may occur. Chloroquine may cause vomiting, abdominal pain, agranulocytosis or convulsions.

Eradication

1 P. [alciparum. Chloroquine alone or in combination with either pyrimethamine 25 mg or primaquine 45 mg as a single dose effects a radical cure because there is no exoerythrocytic stage in falciparum malaria.
2 P. vivax, P. malariae and P. ovale. Primaquine, an 8- aminoquinoline, is essential for eliminating the exoer-ythrocytic cycle and effecting a radical cure. A course of one of the 4-aminoquinolines should be followed by primaquine 7.5 mg daily for 14 days. Alternatively, 300 mg chloroquine combined with 45 mg primaquine once a week for 8 weeks is also effective.

Treatment of severe malaria

Severe malaria (more than 1% of RBCs infected) or any of the pernicious forms of falciparum malaria constitutes a medical emergency. Quinine, given by a slow intravenous infusion, is the drug of choice: Quinine dihydrochloride 20 mg kg” intravenously over 4 hours followed by 100 mg kg-t infused over 4 hours at 8-hourly intervals until the patient is able to tolerate oral therapy.

PREVENTION AND CONTROL

Owing to changing patterns of resistance, advice about chemoprophylaxis should be sought prior to leaving for a malaria-endemic area. Chemoprophylaxis is essential for those visiting endemic areas-generally chloroquine 300 mg once a week in areas where there is no chloroquine resistance, but where there is resistance it should be combined with proguanil 200 mg daily or in South East Asia or Papua New Guinea dapsone/pyrimethamine (Maloprim) one tablet (100 mg and 125 mg respectively) each week as above. Mefloquine 250 mg weekly (adults) can be used where falciparum malaria is highly resistant to chloroquine (East and Central Africa) for periods up to 6 months. Doxycycline has also been used apparently successfully in South East Asia. Prophylaxis should be continued for 6 weeks after leaving a high-risk area. On the basis of the 1979 WHO Expert Committee report on malaria, the following preventive measures have been suggested. Measures to be applied to the community include prevention of man-vector contact, destruction of adult mosquitoes and mosquito larvae, and active elimination of human infection by presumptive treatment (i.e. treatment of all fevers in endemic areas with antimalarials) and radical treatment. Measures to be applied to individuals include use of mosquito repellents, impregnated bed nets, protective clothing, chemoprophylaxis and chemotherapy where indicated.