Human Salmonellosis and Rickettsial Zoonoses PDF

# HUMAN SALMONELLOSIS ## Incubation period - 6 to 72 hours (usually). ## Clinical features - The disease arises from the ingestion of the living organisms. - Recent studies indicate that Salmonella spp. possess both invasive and cholera-like enterotoxic properties (6). - Clinically, the disease...

# HUMAN SALMONELLOSIS ## Incubation period - 6 to 72 hours (usually). ## Clinical features - The disease arises from the ingestion of the living organisms. - Recent studies indicate that Salmonella spp. possess both invasive and cholera-like enterotoxic properties (6). - Clinically, the disease may be manifest by one of three syndromes: - **Enteric fever**: - S. typhi, S. paratyphi A and C are human pathogens, and are not considered zoonotic agents (2). - S. paratyphi B, while predominantly found in man has also been isolated from turkeys, chickens, cattle, sheep, swine, mice and monkeys. - This syndrome (enteric fever) is dealt with separately (see page 234). - **Salmonella enterocolitis (gastroenteritis)**: - This is the most common manifestation of Salmonella infection. - 6 to 48 hours after ingestion of Salmonellae there is nausea, headache, vomiting and diarrhoea. - Low grade fever is common. - Most infections are mild with diarrhoea as the only symptom. - In severe cases there may be dehydration requiring replacement of fluids and electrolytes. - The episode usually resolves in 2 to 3 days, but the stools often remain loose for several weeks. - The excretion of salmonella may be prolonged by antimicrobial therapy. - Blood cultures are usually negative but stool cultures are positive for salmonella and may remain positive for several weeks after clinical recovery. - Death is rare and occurs primarily in neonates, infants and elderly. - **Septicaemia with focal lesions**: - Non-typhoid salmonellae (e.g., S. cholera-suis) may occasionally invade the blood stream leading to generalized or localized infection presenting itself as pyrexia of unknown origin. - Focal infection may result in osteomyelitis, pyelonephritis, arthritis, meningitis, cholecystitis and endocarditis. - Stool cultures are negative but blood cultures are positive. ## Prevention and control - Since salmonellosis is zoonotic in origin, preventive measures should begin at the farm and embrace all the elements of the food chain through live animals, animal products, processing, final food preparation to consumption. - Approaches indicated at the farm level are: - disease control, e.g., immunization of farm animals against salmonellosis. - the use of hygienic animal feed, and - ensuring a sanitary environment for the animals. - The aim is to raise "salmonella-free" animals. - The other approaches include: - hygienic slaughtering and milking, - pasteurization of milk and eggs; - proper disposal of liquid and solid wastes, - cold storage facilities, and - health education and training. - Since the health sector alone cannot solve the problem of salmonellosis, responsibility for prevention and control measures may fall to agriculture, veterinary and other ministries, outside the health sector (1, 7). ## References 1. WHO (1982). Economic aspects of communicable diseases, EURO 68. 2. WHO (1988). Salmonellosis control: the role of animals and product hygiene, TRS 774. 3. WHO (1988). WH Forum; 9 (1) 123. 4. WHO (2005). Fact Sheet No. 139, Internet, Drug-resistant Salmonella. 5. WHO (1976). TRS 598 (Microbiological aspects of food hygiene). 6. Velimirovic, B. et al (1984). Infectious diseases in Europe, A fresh look WHO, Copenhagen. 7. WHO (1984) TRS 705 (The role of food safety in health and devlop.). # HUMAN SALMONELLOSIS ## RICKETTSIAL ZOONOSES ### (Rickettsial diseases) - Rickettsial zoonoses are a group of specific communicable diseases caused by rickettsial organisms and transmitted to man by arthropod vectors, (Q fever excepted). - Increasingly, it is realized that rickettsial diseases are under-diagnosed and that they contribute substantially to the acute febrile burden and preventive illness in many populations (1). ## Classification - Rickettsial diseases may be grouped on the basis of clinical features and epidemiological aspects as follows (Table 1): | Diseases | Rickettsial agent | Insect vectors | Mammalian reservoirs | |---|---|---|---| | **1. Typhus group** | | | | | - Epidemic typhus | R. prowazekii | Louse | Humans | | - Murine typhus | R. typhi | Flea | Rodents | | - Scrub typhus | R. tsutsugamushi | Mite* | Rodents | | **2. Spotted fever group** | | | | | - Indian tick typhus | R. conorii | Tick* | Rodents, dogs | | - Rocky mountain spotted fever | R. rickettsii | Tick* | Rodents, dogs | | - Rickettsial pox | R. akari | Mite* | Mice | | **3. Others** | | | | | - Q fever | C. burnetii | Nil | Cattle, sheep, goats | | - Trench fever | Rochalimaea quintana | Louse | Humans | * Also serve as arthropod reservoir, by maintaining the rickettsiae through ovarian transmission. ## Source: (2) ## Causal agents - Rickettsiae are small bacteria that are obligate intracellular parasites. - They are pleomorphic, appearing either as short rods, or as cocci and they occur singly, in pairs, in short chains, or in filaments. - With Giemsa's stain they stain blue and are readily visible under microscope. - They grow readily in the yolk sac of the embryonated egg. - Rickettsial growth is enhanced by the presence of sulfonamides. ## Clinical features - Excepting for Q fever, in which there is no skin lesion, rickettsial infections are characterized by fever, headache, malaise, prostration, skin rash and enlargement of the spleen and liver. - Tetracycline is the drug of choice for specific treatment of all rickettsial diseases. - Long-acting antibiotics (doxycycline, minocycline) now make single dose treatment possible (3). ## Diagnostic procedures - These include: - isolation of rickettsiae. - established serological tests such as indirect fluorescent antibody (IFA) test, the complement fixation test, and the Weil Felix reaction. - The newer techniques include ELISA and the fluorescent antibody staining of frozen tissue sections from rickettsial lesions. # EPIDEMIOLOGY OF COMMUNICABLE DISEASES - Among the major groups of rickettioses, the commonly reported diseases in India are scrub typhus, murine flea-born typhus, Indian tick typhus and Q fever. These are considered in more detail: ## Distribution ### SCRUB TYPHUS - Of the diseases caused by rickettsiae in man, the most widespread is scrub typhus. - It exists as a zoonoses in nature between certain species of trombiculid mites and their small mammals (e.g., field mice, rats, shrews. - Scrub typhus is endemic in Northern Japan, South East Asia, the Western Pacific Islands, Eastern Australia, China, Maritime areas and several parts of South-Central Russia, India and Sri Lanka. - More than 1 million cases occur annually. - Most travel-acquired cases of scrub typhus occur during visits to rural areas in endemic countries for activities such as camping, hiking or rafting, but urban cases have also been described (4). ## Epidemiological determinants ### Agent factors - **(a) AGENT**: The causative agent of scrub typhus is Rickettsia tsutsugamushi. There are several serologically distinct strains. - **(b) RESERVOIR**: The true reservoir of infection is the trombiculid mite (Leptotrombidium delinese and L.akamushi). - The infection is maintained in nature transovarially from one generation of mite to the next. - The nymphal and adult stages of the mite are free-living in the soil; they do not feed on vertebrate hosts. - It is the larva (chigger) that feed on vertebrate hosts and picks up the rickettsiae. - The larval stage serves both as a reservoir, through ovarian transmission, and as a vector for infecting humans and rodents. ## Mode of transmission - By the bite of infected larval mites. - The transmission cycle may be depicted as below: - Mite → Rats and mice → Mite → Rats and mice → Man - The disease is not directly transmitted from person to person. ## Incubation period - Usually 10 to 12 days; varies from 6 to 21 days. ## Clinical features - Scrub typhus resembles epidemic typhus clinically. - The onset is acute with chills and fever (104°-105°F), headache, malaise, prostration and a macular rash appearing around the 5th day of illness. - Generalized lymphadenopathy and lymphocytosis are common. - One typical feature is the punched-out ulcer covered with a blackened scab (eschar) which indicates the location of the mite bite. - The pyrexia falls by lysis in the 3rd week in untreated cases. - The Weil Felix reaction is strongly positive with the Proteus strain OXK. ## Control measures - **(a) TREATMENT**: Tetracycline is the drug of choice. With proper therapy the mortality is nil. - **(b) VECTOR CONTROL**: - Clearing the vegetation where rats and mice live; application of insecticides such as lindane or chlordane to ground and vegetation. - **PERSONAL PROPHYLAXIS**: Impregnating clothes and blankets with miticial chemicals (benzyl benzoate) and application of mite repellents (diethyltoluamide) to exposed skin surfaces (5). - No vaccine exists at present. ## Distribution ### MURINE TYPHUS ### (Endemic or flea-borne typhus) - Murine typhus (MT) is a zoonoses. - It is worldwide in distribution especially in areas of high rat infestation. - It appears to be more prevalent in South-East Asian and Western Pacific countries than previously recognized. - In USA, cases tend to be scattered. - Successful isolation of the causative agent from rats, fleas and bandicoots was made at many places in India. - Focal infections are often associated with docks and shipping places where rats abound. ## Agent factors - **(a) AGENT**: Rickettsia typhi (R. mooseri). - **(b) RESERVOIR OF INFECTION**: Rats are the reservoir (Rattus rattus and R.norvegicus). - Infection in rats is inapparent, long-lasting and non-fatal. ## Mode of transmission - The infection spreads from rat to rat (X. cheopis) and possibly by the rat louse (6). - The actual mode of transmission is not by the bite of the rat flea, but by: - inoculation into skin of faeces of infected fleas, and - possibly by inhalation of dried infective faeces. - There is no direct man to man transmission. - Once infected the flea remains so for life. - The flea cannot transmit the rickettsiae transovarially. - The transmission cycle may be shown as below: - Rat → Rat flea → Man → Rat → Rat flea → Rat ## Incubation period - 1 to 2 weeks, commonly 12 days. ## Clinical features - The clinical features resemble that of louse-borne typhus, but milder and rarely fatal. - The Weil Felix reaction with Proteus OX-19 becomes positive in the 2nd week. ## Control measures - **(a) TREATMENT**: Tetracycline is the only drug of choice. Since rickettsial growth is enhanced in the presence of sulfonamides, these drugs should not be given. - **(b) CONTROL OF FLEAS**: Residual insecticides (e.g., BHC, malathion) are effective against rat fleas. - Rodent control measures should be implemented in the affected areas. - No murine typhus vaccine is currently available. ## Distribution ### INDIAN TICK TYPHUS ## Epidemiological determinants ### Agent factors - **(a) AGENT**: The causative agent is Rickettsia conorii, a member of the spotted fever group of rickettsiae, the best known member of which is R. rickettsii the causative agent of Rocky Mountain spotted fever. - **(b) RESERVOIR OF INFECTION**: The tick is the reservoir of infection. It is infective at all stages of its life cycle and remains infective for life (commonly 18 months). - Various tick genera (e.g., Rhipicephalus, Ixodes, Boophilus, Haemaphysalis) have been incriminated as vectors. - Infection in nature is maintained by transovarian and trans-stadial passage. - The rickettsiae can be transmitted to dogs, various rodents and other animals, which assist in maintaining the disease cycle. ## Mode of transmission - Man is only an accidental host. - He acquires infection by the bite of an infected tick. - Contamination of skin with crushed tissues or faeces of an infected tick may also cause infection. - The cycle of transmission is as follows: - Tick → Tick → Tick → Tick → Dog → Man → Tick → Man ## Incubation period - Usually 3 to 7 days. ## Clinical features - The patient usually gives history of a recent tick-bite and a careful examination will reveal a lesion or eschar at the site of the bite. - After an interval of 3 to 7 days, there is an acute onset of fever, which may persist for 2 to 3 weeks, malaise and headache. - A maculopapular rash appears on the third day. - Unlike the rash in other rickettsial diseases, the rash appears first on the extremities (ankles and wrist), moves centripetally and involves the rest of the body. - The clinical syndrome may be confused with atypical measles. ## Control measures - **(a) TREATMENT**: Broad spectrum antibiotics have proved to be effective. - **(b) PERSONAL PROPHYLAXIS**: Known tick-infested areas should be avoided. - Daily inspection of the body for ticks is particularly important for those who are exposed to the risk of infection. - Disinfection of dogs will minimize the tick population. - Health education of the people in the mode of transmission by ticks, and the means of personal protection is equally important. ## Distribution ### Q FEVER - Q fever is a highly infectious zoonotic disease with worldwide distribution. - It occurs mainly in persons associated with sheep, goats, cattle or other domestic animals. ## Agent factors - **(a) AGENT**: The causative agent is Coxiella burnetii. It is found in ticks which act as vectors as well as reservoir. - **(b) ANIMAL HOSTS**: Cattle, sheep, goats, ticks and some wild animals are natural reservoirs. - Infected animals shed the disease agent in the faeces and urine and heavily contaminate the soil. - The placenta of infected cows and sheep contains the infectious agent which may create infectious aerosols during parturition. - Camels, horses, dogs and many other domestic animals have been shown to be capable of acting as maintenance hosts (7). ## Mode of transmission - Q fever differs from other rickettsial infections in that there is no arthropod involved in its transmission to man. - Transmission results from: - **inhalation of infected dust from soil previously contaminated by urine or faeces of diseased animals.** The organism can also be transmitted through aerosols. - **the organism can also gain entry into the body through abrasions, conjunctivae or ingestion of contaminated foods such as meat, milk and milk products.** - In most countries, the respiratory route is regarded as most important. ## Incubation period - Usually 2 to 3 weeks. ## Clinical features - The disease has an acute onset with fever, chills, general malaise and headache. - The clinical picture is one of influenza or non-bacterial pneumonia rather than a typhus fever. - There is no rash or local lesion. - The infection can cause pneumonia, hepatitis, encephalitis and rarely endocarditis. - Inapparent infections also occur. ## Control measures - **(a) TREATMENT**: Chronic Q fever requires prolonged treatment for 18 months or longer. - Doxycycline is the drug of choice. - **(b) PREVENTIVE MEASURES**: - Pasteurization or boiling of milk to inactivate the causative agent; - providing sanitary cattle sheds; - adequate disinfection and disposal of products. - An inactivated Coxiella vaccine has also been prepared to protect occupationally exposed workers. - Several purified vaccines are under development (8). ## OTHER RICKETTSIAL INFECTIONS ### 1. Epidemic typhus - Epidemic or louse borne typhus was in the past the most formidable disease caused by rickettsiae. - It was the cause of devastating epidemics among military and refugee populations and in areas affected by famine. - The advent of modern insecticides has considerably reduced the prevalence of epidemic typhus today. - No cases of this disease have been reported from South East Asia since 1978 or from the Western Pacific since 1969 (1). - It is still endemic in Africa (notably Burundi, Rwanda and Ethiopia) and South America (notably Peru, Bolivia, and Ecuador). - All of them are known endemic areas of the disease. - The infection is transmitted from man to man by the infected louse (P. corporis and P. capitis). - The louse gets infected by feeding on an infectious patient during the febrile stage. - The organisms multiply in the cells lining the intestinal tract of the louse and begin to appear in 3 to 5 days in the louse faeces. - Man acquires the disease not by the bite of the louse, but: - by scratching and inoculating himself with the infected louse faeces, - by crushing an infected louse on his person, and - possibly by inhalation of infected louse faeces or dust. - The infected louse after 10-14 days of existence dies of the infection. - In humans, the organisms can persist for many years as latent infection without any symptoms, and the disease may appear later as Brill-Zinsser disease, and can be transmitted to other humans by the louse. ## Control measures - The control measures comprise anti-louse measures and improvements in personal hygiene and living conditions. - Under the International Health Regulations, louse-borne typhus is subject to international surveillance. ### 2. Rickettsialpox - Man gets the infection through the bite of certain infected mites, which are found on mice (Mus musculus). - Transovarial transmission occurs in the mite. - The mouse acts as true reservoir as well as vector. - Rickettsialpox may be confused with atypical cases of chickenpox. ### 3. Trench fever - This disease is limited to central Europe. - The vector is louse and the disease is transmitted by louse faeces. - Man is the only known reservoir. ## References 1. WHO (1983). Bull WHO 61: 443. 2. Jawetz E et al (1986). Reivew of Medical Microbiology 17th ed. Lange Med. Publ. California. 3. WHO (1975). The work of WHO, Geneva. 4. Current Medical Diagnosis and Treatment, by Maxine A Padakis etc., 2014 ed., A Lange Publication. 5. WHO (1982). Bull WHO, P.162. 6. Saah, J.J. and Hormick, R.B. (1979). In Principles and Practice of Infectious Diseases, G.L. Mandell et al (eds), John Wiley, New York. 7. Sehgal, S and R. Bhatia eds (1985). Manual on Zoonosis NICD, 29-Sham Nath Marg, Delhi-54. 8. Kazar, J. et al (1982). Bull WHO, 60 (3) 389-394. # TAENIASIS - A group of cestode infections which are important zoonotic diseases. - Two parasites of importance in taeniasis are Taenia saginata and T. solium. - These are classified as "cyclo-zoonoses" because they require more than one vertebrate host species (but no invertebrate host) to complete their developmental cycles. ## Problem statement - **(a) T. SAGINATA**: This parasite is virtually global in distribution, wherever beef is eaten. - Highly endemic regions (prevalence rates exceeding 10 per cent) exist in some African countries south of the Sahara, in Eastern Mediterranean countries and in parts of USSR. - There is a moderate prevalence in Europe, in most of the Indian subcontinent, Southern Asia, and in Japan. - Australia, Canada and USA are generally regarded as low endemic areas, with prevalence rate below 0.1 per cent (1). - The larval stage of T. saginata (Cysticercus bovis) occurs almost all over the world. - In some East African countries rates 30 to 80 per cent have been noted. - In European countries, it is found in 0.3 to 4.0 per cent of slaughtered animals (1). - **(b) T. SOLIUM**: T. solium infection is endemic in many countries of Latin America, Africa and Asia as well as in some parts of Europe and the USSR (2). - It is endemic in India, and has been widely reported (3). - Human cysticercosis caused by T. solium is a far more important public health problem than human taeniasis (4). ## Hosts of infection - T. saginata and T. solium pass their life cycles in two hosts. - In man, the adult parasites live in the small intestine. - The adult T. saginata measures 5 to 12 metres in length, and may be up to 24 metres; T. solium measures 2 to 6 metres. | Parasite | Definitive | Intermediate host | |---|---|---| | **1.** T. saginata | Man | Cattle (C. bovis) | | **2.** T. solium | Man | Pig (C. cellulosae) | - The larval stage of T. saginata (C. bovis) mainly occurs in cattle. - The pig is the main host for the larval stage of T. solium (C. cellulosae) but man may also be infected. - This may lead to muscular, ocular and cerebral cysticercosis. - The adult stages of T. saginata and T. solium may persist for several years in infected humans. - Mixed infections of both the parasites can occur. - Although the life span of C. cellulosae in man is not known, it is suspected to be some years. ## Mode of transmission - These infections are acquired: - through the ingestion of infective cysticerci in undercooked beef (T. saginata) or pork (T. solium); - through ingestion of food, water or vegetables contaminated with eggs; and - reinfection by the transport of eggs from the bowel to the stomach by retroperistalsis is considered to be rare. ## Incubation period - For the adult tapeworm, from 8 to 14 weeks. ## Clinical illness - The impact of tapeworm infection in man is difficult to quantify because in the vast majority of cases, they do not lead to clinical illhealth, except occasional abdominal discomfort, anorexia and chronic indigestion. - Straying of proglottids may sporadically cause appendicitis or cholangitis. - The most serious risk of T. solium infection is cysticercosis. ## Human cysticercosis - Human infection is caused by the ingestion of eggs of T. solium in contaminated water or food (hetero-infection) or regurgitated eggs from the small intestine (auto-infection). - The eggs disintegrate and the infective stages leave the intestine via the hepatic portal system, and are dispersed throughout the body where they develop to form cysticerci. - Cysticerci that develop in the central nervous system (neuro-cysticercosis), represent a serious threat to the individual and even to the community, if this condition is prevalent. - As a result of mechanical pressure, obstruction or inflammation, a variety of pathological changes are produced, leading to epilepsy, intracranial hypertensive syndromes, hydrocephalus, psychiatric diseases or death (4). ## Control measures - The methods usually employed for control are: - treatment of infected persons, - meat inspection, - health education, and - adequate sewage treatment and disposal (1, 4). - Early detection and early treatment of T. solium cases is essential to prevent human cysticercosis. - Effective drugs (e.g., praziquantel and niclosamide) are available for the treatment of these infections. - Surgical removal of symptom-producing cysts is indicated although