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Infections Acquired Through the Gastrointestinal Tract


Many of the important pathogens that gain entry through the gastrointestinal tract are cosmopolitan in their distribution. They include viruses, bacteria, protozoa, helminths and endoparasitic arthropods. The first three of these can be directly infectious for humans when they are passed in the faeces but, in the case of helminths, the eggs may become infectious only after maturation in the soil (e.g. Ascaris lumbricoides ) or after passing through an intermediate host (e.g. Taenia saginata ). Helminthiases acquired from the soil and those requiring a snail intermediate host are considered in Chapter 2 . Some pathogens pass from the intestinal tract to cause systemic infection and may localize in other organs (e.g. poliomyelitis, acute viral hepatitis, trichinosis). Localized infection of the gastrointestinal tract itself with pathogenic viruses or bacteria accounts for a high proportion of deaths in infants and young children in low- and middle-income countries.

The most important pattern of transmission is the passage of infective material from human faeces into the mouth of a new host, which is known as ‘faeco–oral’ transmission. This occurs mostly through inapparent faecal contamination of food, water and hands—the three main points of contact with the mouth.

Viral Infections

Fig. 3.1, Poliomyelitis virus.

Fig. 3.2, The shrinking global map of polio.

Fig. 3.3, Administration of bivalent oral polio vaccine in Jalalabad, Afghanistan.

Fig. 3.4, Adminstration of inactivated polio vaccine (IPV).

Fig. 3.5, Flaccid paralysis due to polio.

Fig. 3.6, Enterovirus 71.

Fig. 3.7, Hepatitis A virus.

Fig. 3.8, Course of acute hepatitis A infection.

Fig. 3.9, Panlobular inflammation and lobular disarray due to hepatitis A.

Fig. 3.10, Brachial neuritis and unilateral scapula winging in hepatitis E.

Fig. 3.11, Rotavirus.

Fig. 3.12, Progressive multifocal leucoencephalopathy (PML).

Bacterial Infections

Fig. 3.13, Rose spots in enteric fever.

Fig. 3.14, Unsafe domestic water supply, the source of an outbreak of multidrug-resistant enteric fever in Kinshasa.

Fig. 3.15, Temperature chart in typhoid.

Fig. 3.16, Ulceration of Peyer’s patches.

Fig. 3.17, Salmonella osteomyelitis of both tibias and fibulas in sickle cell anaemia.

Fig. 3.18, Salmonella mycotic aneurysm.

Fig. 3.19, Bloody, mucoid diarrhoea from a patient with shigellosis.

Fig. 3.20, Toxic megacolon due to Shigella dysenteriae .

Fig. 3.21, Shigellosis affecting the sigmoid colon.

Fig. 3.22, Enterotoxigenic Escherichia coli adhering to the brush border of the (intact) human intestinal mucosa.

Fig. 3.23, The perils of formula milk feeding (or why ‘breast is best’).

Fig. 3.24, Cholera in the 21st century.

Fig. 3.25, An ancient epicentre of cholera.

Fig. 3.26, Cholera vibrios.

Fig. 3.27, Choleraic facies.

Fig. 3.28, ‘Rice-water’ stool of cholera.

Fig. 3.29, Cholera bed in a treatment ward.

Fig. 3.30, Access to clean water is fundamental in controlling a cholera outbreak.

Fig. 3.31, Seafood as a source of cholera infection.

Fig. 3.32, Helicobacter pylori.

Fig. 3.33, Enteritis necrotica (also known as clostridial necrotizing enteritis, CNE) seen at operation.

Fig. 3.34, Rose Bengal test for brucellosis.

Fig. 3.35, Temperature chart in brucellosis.

Fig. 3.36, Brucella spondylitis.

Fig. 3.37, Subcutaneous haemorrhage due to Streptococcus suis sepsis.

Protozoal Infections

Fig. 3.38, Trophozoites and cysts of intestinal protozoa (after Ackers).

Fig. 3.39, Live Entamoeba histolytica .

Fig. 3.40, Entamoeba histolytica proctocolitis.

Fig. 3.41, Amoebic perforation and surgical resection.

Fig. 3.42, Amoebic liver abscess.

Fig. 3.43, Right upper-quadrant tenderness in a patient with an amoebic liver abscess.

Fig. 3.44, Chest radiograph in a patient with an amoebic liver abscess.

Fig. 3.45, Aspiration of amoebic liver abscess.

Fig. 3.46, Amoebiasis of the skin.

Fig. 3.47, Giardia intestinalis in jejunal biopsy.

Fig. 3.48, Giardia -mediated partial villous atrophy.

Fig. 3.49, Sarcocystis oocysts in intestinal epithelium.

Fig. 3.50, Section of sarcocyst in human muscle.

Fig. 3.51, HIV-associated Cystisospora belli in mucosal cell of the ileum.

Fig. 3.52, Oocysts of Cryptosporidium hominis and Cyclospora cayetanensis compared.

Fig. 3.53, Toxoplasma gondii life cycle.

Fig. 3.54, Hydrocephalus in congenital toxoplasmosis.

Fig. 3.55, Skull radiograph in congenital toxoplasmosis.

Fig. 3.56, Fundal changes in congenital toxoplasmosis.

Fig. 3.57, Cerebral toxoplasmosis in HIV infection.

Fig. 3.58, Balantidial ileitis.

Fungi

Fig. 3.59, Mature spores of Enterocytozoon bieneusi in human jejunal enterocyte.

Helminth Infections

Nematodes

Enterobiasis

Fig. 3.60, Enterobius vermicularis visible at colonoscopy.

Fig. 3.61, Ovum of Enterobius vermicularis .

Fig. 3.62, Adult pinworms in appendix.

Fig. 3.63, Sellotape test to demonstrate perianal eggs.

Fig. 3.64, Sellotape test to demonstrate perianal eggs.

Ascariasis

Fig. 3.65, Life cycle of Ascaris lumbricoides , the roundworm.

Fig. 3.66, Adult Ascaris lumbricoides.

Fig. 3.67, Head of adult.

Fig. 3.68, Unfertilized and fertilized egg of Ascaris lumbricoides.

Fig. 3.69, Ecology of infection with Ascaris and Trichuris.

Fig. 3.70, Second-stage larva of Ascaris lumbricoides hatching in gut.

Fig. 3.71, Transverse sections of Ascaris lumbricoides larvae in the pulmonary alveoli.

Fig. 3.72, Loeffler's syndrome.

Fig. 3.73, A bolus of Ascaris expelled from a child with heavy infection following anthelminthic treatment.

Fig. 3.74, Adult roundworms migrating in liver.

Trichuriasis

Fig. 3.75, Life cycle of Trichuris trichiura (whipworm).

Fig. 3.76, Adult morphology of Trichuris trichiura.

Fig. 3.77, Ova of Trichuris trichiura.

Fig. 3.78, Cross-section of Trichuris trichiura associated with caecal tissue.

Fig. 3.79, Rectal prolapse in a child with Trichuris trichiura.

Anisakiasis

Fig. 3.80, Third larval stage of Anisakis simplex in a hake fillet.

Fig. 3.81, Third-stage larva of Anisakis simplex.

Fig. 3.82, Colonic anisakiasis.

Fig. 3.83, Morphology of third-stage larva of Anisakis species.

Capillariasis

Fig. 3.84, Koi pla, raw fish salad eaten in Laos PDR and Thailand.

Fig. 3.85, Capillaria philippinensis invading the small intestine.

Fig. 3.86, Female Capillaria philippinensis from human faeces.

Fig. 3.87, Capillaria hepatica in a liver section.

Trichinellosis

Fig. 3.88, Life cycle of Trichinella spiralis.

Fig. 3.89, Wild reservoir of trichinellosis.

Fig. 3.90, Adult female Trichinella spiralis .

Fig. 3.91, Trichinella spiralis larvae in crush preparation.

Fig. 3.92, Larvae in muscle from a fatal human case.

Fig. 3.93, Patient with acute trichinellosis.

Fig. 3.94, Splinter haemorrhages.

Fig. 3.95, Polar bear, host of Trichinella nativa .

Toxocariasis

Fig. 3.96, Life cycle of Toxocara canis.

Fig. 3.97, Embryonated Toxocara ovum.

Fig. 3.98, Adult worm of Toxocara.

Fig. 3.99, Toxocara canis migrating through the lung.

Fig. 3.100, Visceral larva migrans.

Fig. 3.101, Urticarial skin lesions in a patient with toxocariasis.

Fig. 3.102, Ocular larva migrans.

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