REVIEW ARTICLE

Cryptosporidium infections in man, animals, birds and fish P . J . O’DONOGHUE

Central Veterinary Laboratories, Department of Agriculture, Adelaide, South Australia 5000

SUMMARY: The protozoan parasite Cryptosporidium has gained better recognition over the last decade as an enteropathogen in a wide variety of host animals. Prior to 1975, infections were thought to occur infrequently and to be largely asymptomatic in nature. However, recent studies have revealed the organism to be more prevalent and pathogenic than previously thought. Infections producing clinical disease have been recorded in numerous host species including man, and the organism is now regarded as a newly- emergent zoonosis. This paper collates information currently available on the host range and specificity, life cycle and pathogenicity of the parasite and summarises the various techniques used to diagnose infections. Aust. vet. J. 62: 253-258

Host Range

Cryptosporidium was first described in mice at the begin- ning of this century (Tyzzer 1907) and infections have since been reported in a broad range of vertebrate hosts (cf. reviews by Angus 1983; Tzipori 1983). The current range of known hosts includes 7 orders of mammals, 4 orders of birds, 1 order of reptiles and 2 orders of fish (summarised in Table 1). Most infections have been detected in close association with the epithelial cells in the small and large intestines, but some organisms have been found in the stomach, bile ducts, pancreatic ducts, gall bladder and tonsils of various mammals; in the respiratory tract, conjunctival sacs, bursa and cloaca of several bird species and in the stomach walls of reptiles.

Host Specificity

Cryptosporidia were originally thought to be host-specific, therefore new species of the parasite were described for each new host species. Some 19 species have been named (Levine 1984). More recently, however, cross-transmission studies have shown that cryptosporidia are transmissible between a wide range of host species (Tzipori et a l 1980; Heine and Boch 1981; Moon and Bemrick 1981; Reese et a! 1982). Various isolates from mammals and birds have been suc- cessfully transmitted to both homologous and heterologous host species as summarised in Table 2 .

Several authors have suggested that the cryptosporidia be classified within a monotypic (or single-species) genus due to this apparent lack of host specificity (Tzipori et al 1980). Differences observed between the infectivities of the various isolates were therefore thought to result from parasite strain differences or from variations in host susceptibility (that is, due to age-related or immune-mediated resistance). However, most transmission studies were performed with Cryptospor- idium isolates from mammals and it has not yet been established whether isolates from other vertebrate classes exhibit a similar lack of host specificity. Our studies have shown that isolates from quail and pheasant are only transmissible to other avian hosts and not to mammalian hosts (P. J . O’Donoghue and V . L. Tham, unpublished data). Converseley, isolates from man were found to be infective only to other mammals and not to birds. Further comprehensive studies on parasite variations are required before different species or strains can be identified and characterised. Nevertheless, because the parasite can cross host species barriers, infections in domestic animals and pets may be regarded as reservoirs of infection for susceptible humans.

Morphology Recent ultrastructural studies performed on experimentally

and naturally infected animals have succeeded in determining the unique morphological characteristics of the parasite (Vetterling el af 1971; Pohlenz et al 1978; Iseki 1979; Boch et a1 1982).

Endogenous developmental stages of the parasite range in size from 2 to 6 pm and are located within the brush border or microvillous layer of the host epithelial cells. When examined by light microscopy or scanning electron micros- copy, the organisms appear to be situated on the surface of the epithelial cells within the lumina of the infected organs (Figures 1 , 2). However, transmission electron microscopic studies have revealed that the organisms are intracellular (but extracytoplasmic) within parasitophorous vacuoles formed by a continuous covering of microvillous membranes (Figure 3).

The exogenous infective stage of the organism consists of an oocyst containing 4 sporozoites and a crystalline residual body (Figure 4). The oocysts are excreted in the faeces of the host and they appear spherical in shape and range in size from 4 to 5 pm (Figures 5 , 6). Contrary to most other enteric coccidia, sporocysts are not formed within the oocysts.

Special morphological features unique to the endogenous stages of the parasite include a thickened adhesion zone at the base of the parasitophorous vacuole (formed by fusion of the outer microvillous membrane and the epithelial plasma membrane) and a comb-like metabolic lamella adjacent to the adhesion zone (formed by repeated folding of the parasite pellicle) (Figure 7). These specialised structures are thought to facilitate the intake of nutrients by the parasite from the host cell.

Life Cycle

The life cycle of Cryptosporidiurn is generally similar to that of other enteric coccidia (Pohlenz e ta! 1978; lseki 1979; Bird and Smith 1980; Boch et al 1982). A diagrammatical representation of the life cycle is given in Figure 8. Viable oocysts that are ingested by a susceptible host excyst in the gastro-intestinal tract thereby releasing the infective sporo- zoites. The sporozoites then undergo asexual proliferation (termed merogony or schizogony) and form first-generation meronts each containing 8 merozoites. Each merozoite con- tains 28 subpellicular microtubules and an apical complex. Second-generation meronts are then formed each containing 4 merozoites. Sexual reproduction (termed gamogony) then occurs whereby macrogametocytes containing large lipid granules and microgametocytes containing 16 microgametes

253 Australian Veterinary Journal, Vol. 62, No. 8, August , 19x5

TABLE 1 Known hos t s of CrVDtOSDOridia

Mammals Primates: Artiodactyla:

Perissodactyia: Carnivora: Lagomorpha: Rodentia:

Marsupialia:

m a n , r h e s u s monkeys, macaques cattle, s h e e p , goats , red deer , m u l e dee r , gazelle, pigs horses dogs, cats , raccoons rabbits laboratory mice, field mice, red- backed mice, laboratory r a t s , brown r a t s , g u i n e a p i g s , ham- sters, gray squirrels brown a ntec h in u s

Birds Galliformes: chickens, t u r k e y s , quail, pheas-

Anseriformes: g e e s e , ducks Psittaciformes: parrots, budgerigars Passeriformes: canaries

ant, peafowl, peacocks

Rep tiles Squamata: rattlesnakes, rat snakes, boas,

black snakes , corn snakes f ish

Perciformes: surgeon f i sh Cypriniformes: carp

T A B L E 2 Homologous and heterologous cross-transmission

of Cryptosporidia between hosts

Isolates Recipients

human

calf

lamb guinea pig chicken quail mouse deer Pig cat

.-b

+

h u m a n , calf , lamb, pig, mouse, r a t , chicken, guinea pig, cat , dog, goat calf, human, lamb, goat, pig, foal, deer , mouse, rat, guinea pig, hamster, chicken, rabbit, cat lamb, mouse, rat guinea pig chicken chicken mouse mouse Pig cat

TABLE 3 Taxonomic classification of CrvDtosDoridia

Classification Main characters

Phylum: Apicomplexa apical complex present; mi- cropores present; no cilia; no flagella (except in micro- gametes of some groups); all parasitic

Class: Sporozoea

Subclass: Coccidia

o o c y s t s o r “ s p o r e s ” fo rmed ; h o m o x e n o u s or h e t e r o x e n o u s fife cyc le ; conoid complete intracellular “coccidians”; mainly in vertebrates; ma- ture gamonts small

Order: Eucoccidiida merogony (or schizogony)

Suborder: Eimeriina non-motile zygote; no s y - ZYgY

Family: Cryptosporidiidae oocyst with 4 naked sporo- zoites and residual body; no sporocysts formed

present

254

are formed. After fertilisation, the zygote undergoes further asexual development (termed sporogony) resulting in the formation of an oocyst. The mature oocysts are passed in the faeces of the host and infections in other animals become established following oocyst ingestion. It is also thought that oocysts can excyst within the same host animal resulting in a new cycle of development and a relapse or continuance of infection (Iseki 1979).

The time interval between infection and oocyst excretion (termed the prepatent period) ranges from 2 to 9 days in the various host species whereas the duration of oocyst excretion (termed the patent period) may be quite variable ranging from several days to several weeks.

Classification

The genus Cryptosporidiurn has been classified together with the enteric coccidia which mainly parasitise the intestinal tracts of vertebrates (cf. Levine et a / 1980). The main taxonomic characters used to classify Cryptosporidiurn are given in Table 3. Better known genera of the suborder Eimeriina include the intestinal coccidians Eirneria and fsospora and the tissue cyst-forming coccidians Toxoplasrna and Sarcocystis.

Pathogenicity

Some early reports tentatively associated Cryptosporidiurn with clinical disease but most reported the organism as an incidental finding and not as the causative agent. It was not until the mid 1970s that infections were directly associated with clinical disease in scouring calves (Meuten et al 1975; Shmitz and Smith 1975). Since then, numerous reports have been made on naturally-occurring and experimentally-induced cryptosporidiosis in a variety of mammals and birds (cf. reviews by Anderson 1982; Tzipori 1983). Neonates in particular appear to be highly susceptible to infection. However, not all infections have been linked with acute disease. Asymptomatic infections are commonly reported in rodent species (Tyzzer 1907; Hampton and Rosario 1966; Vetterling et a / 1971) and recent studies have detected subclinical infections in mammals (Heine and Boch 1981) and birds (Fletcher ef af 1975).

Clinical signs of disease commonly observed in domestic animals are an intermittent watery diarrhoea, dehydration and anorexia (Meuten et a / 1975; Tzipori ef a / 1980; Heine and Boch 1981). Progressive wasting and loss of bodyweight may also be evident. The disease usually appears to be self- limiting with high morbidity although mortality rates may vary considerably. Birds with tracheal infections exhibited respiratory signs such as convulsive coughing, sneezing and mucoid discharges (Hoerr et a l 1978; Tham et af 1982).

TABLE 4

Techniques used to diagnose Cryptosporidia infections

lndirecf demonstration of infections Symptomatology: - relatively nonspecific clinical

signs (watery diarrhoea, de- hydration, etc)

(parasite infectivity and host susceptibility may vary)

(antibody responses not yet characterised)

Animal inoculation: - passage to laboratory animal

Immunoserology: - specific antibody tes ts

Direct demonstration of organisms Histology: - microscopy of biopsy material

( e n d o g e n o u s s t a g e s d e - tected in stained t issue sec- tions)

(exogenous s tages detected in faecal smear s or concen- trates)

Coprology: - microscopy of faecal material

Ausrralian Veterinary Journal, Vol. 62, N o . 8, August, 1985

Infections in snakes have been reported in conjunction with severe chronic hypertrophic gastritis (Brownstein et a1 1977). Clinical signs commonly observed were persistent postprandial regurgitation and firm rnidbody swellings. In- fections in fish have only recently been reported in the literature and one report described a progressive illness characterised by intermittent anorexia, regurgitation of food and the passage of faeces containing apparently undigested food (Hoover et al 1981).

Clinical infections in man have involved persistent diar- rhoea accompanied by malabsorption, abdominal pain, fever and vomiting (Jokipii et al 1983). Many acute and sometimes lethal infections in man have been detected in immunocom- promised hosts; that is, in individuals with congenital im- munodeficiencies (Lasser et al 1979; Sloper et af 1982), acquired immunodeficiencies (Payne et a1 1983; Ma and Soave 1983) or in those undergoing immunosuppressive chemotherapy (Meisel el a1 1976; Miller et a1 1983). Recent

Figure 1. Light micrograph of endogenous developmental stages of Cryptosporidium in calf small intestine. Haematoxylin and eosin x 450.

Figure 2. Scanning electron micrograph of endogenous stages of Cryptosporidium in quail trachea. x 3400.

Figure 3. Transmission electron micrograph of Crypfosporidium meront (left) and macrogametocyte (right) in chicken bursa. x 7000.

Figure 4. Transmission electron micrograph of Cryptosporidium oocyst containing sporozoites in mouse small intestine. x 6000.

Figure 5. Light micrograph of mature Crypfosporidium oocysts in human faecal smear. Modified Ziehl-Neelsen stain x 1600.

Figure 6. Light micrograph of Cryptosporidium oocysts recovered from human faeces by potassium iodide flotation. Phase-contrast microscopy x 1100.

Australian Veterinary Journal, Vol. 6 2 , No. 8 , August, 1985 255

ENDOGENOUS STAGES

MEROGONY GAMOGONY FERTILIZATION formation of formation of formation of merozoites gametes zygote

EXOGENOUS STAGES

SPOROGONY formation of sporozoi tes

1'. pellicle( ' ' parasitophorous I 1 . " - _: . . ..: '' soorozoites

. . membranes

endogenous development in host epithel ial cel ls

~~

oocysts excreted in faeces of host

- located intracellular

(but extracytoplasmic)

- sporogony (formation of sporozoites)

occurs endogenously

- parasitophorous vacuole formed by - sporocysts no t present w i th in oocyst

(unique amongst enteric coccidia) covering of microvillous membranes

- adhesion zone formed by fusion of - oocysts contain 4 naked sporozoites

microvillous and plasma membranes and a crystal l ine residual body

- comb-like metabolic lamella formed by

repeated folding of parasite pel l icle - oocyst envelope consists

o f 5 membranes

Figure 7. Special morphological features of Cryptosporidiurn.

INGESTION

0OCyst

@- 5 membranos

v

1s t . Sen. meront - 2nd. gen.

oocyst

4 Sporozoites residual body (no sporocysts

8 merozoites 4 merozoites

(28 subpellicular microtubules

EXCRETION

inter- host f infection

-~

Figure 8. Diagrammatical life cycle of Cryptosporidiurn.

256 Australian Veterinary Journal, Vol. 6 2 , N o 8 , August, 1985

studies, however, have shown that the organism may cause mild transient disease in immunologically normal individuals (Fletcher et a1 1982; Jokipii et a/ 1983).

The diagnosis of cryptosporidosis is frequently complicated by the presence of other enteropathogenic agents (cf. Tzipori 1981). Concomitant infections with other protozoan parasites, viruses and bacteria have been reported but cases where Cryptosporidium is the sole pathogen isolated are being reported with increasing frequency. In all clinical cases of cryptosporidiosis, the excretion of oocysts in the faeces of the host coincided well with the duration of the clinical signs of disease.

Diagnosis

The various techniques previously used to diagnose Cryp- tosporidium infections are outlined in Table 4. The diagnosis of infections by indirect methods, such as comparative symptomatology or animal inoculation, has proven difficult for a variety of reasons. The clinical signs of disease vary considerably between the different classes of vertebrates but nonetheless, they are relatively nonspecific and therefore not suited for diagnostic use (Angus 1983; Tzipori 1983). The inoculation of infected host material into laboratory animals has been used to confirm infections in mammals (Reese et al 1982) but variations in parasite infectivity and host susceptibility may severely interfere with the outcome of such studies. Specific antibodies against Cryptosporidium have been demonstrated in the sera of several host species by indirect immunofluorescence tests using frozen section antigens (Tzipori and Campbell 1981). However, the kinetics and dynamics of the various host antibody responses to infection have yet to be characterised before such tests can be used to differentially diagnose acute clinical infections.

Recourse is therefore made to direct demonstration of the organisms by microsopic examination of biopsy or autopsy material for endogenous developmental stages (Lasser et a/ 1979; Sloper et a1 1982) or of faecal material for exogenous stages (Heine and Boch 1981; Garcia et a / 1983). Microscopic examinations must be performed at high magnifications due

TABLE 5 Methods of detection of Cryptosporidia oocysts

Oocyst concentration Sedimentation: - in water

(oocysts retain some buoy- ancy and are quite adherent to faecal debris)

- in formollether solution (good for carnivorous host species)

(oocysts become sticky and distort)

(oocysts float well in heavy- metal salt solutions such a s saturated potassium iodide solutions)

- in saturated sugar solutions

- in saturated salt solutions

Flotation:

Oocyst appearance Stained: - Giemsa

(oocysts pale blue with red granules; s o m e confusion with yeasts)

- carbol fuchsin (modified Ziehl-

(oocysts deep red with blue granules; yeasts do not stain)

(oocysts semi-translucent and non-refractile)

- phase-contrast microscopy (oocysts dull blue with highly refractile crystalline residual

Neelsen technique)

- bright-field microscopy

body)

Unstained:

~~ ~ ~ ~~

Australian Veterinary Journal, Vol. 62, No. 8, August, 1985

to the small size of the organisms. Endogenous stages detected in tissue sections appear as small basophilic bodies on the surface of the host epithelial cells thereby giving the brush border a spotty appearance. However, biopsy and autopsy materials must be fixed as quickly as possible to reduce the rapid autolysis or sloughing of the epithelial tissues resulting in the detachment of the parasitic stages from the host cells.

Oocysts in faecal material, on the other hand, appear to be quite resistant to many laboratory preparative techniques used to demonstrate their presence (Table 5 ) . Oocysts may be detected in fixed smears of faecal material by direct staining with Giemsa (Heine and Boch 1981; Willson and Acres 1982) or carbol-fuchsin (modified Ziehl-Neelsen tech- nique) (Henriksen and Pohlenz 1981; Garcia et a1 1983) or by negative staining with periodic acid-Schiff (Horen 1983) or nigrosin (Pohjola 1984). However, because oocysts may be present only in low numbers, it is advisable to use various sedimentation or flotation techniques to concentrate them from the bulk of the faecal material (Heine and Boch 1981; Willson and Acres 1982). Our studies have shown that oocysts are best concentrated from faeces by centrifugal flotation in high specific-gravity salt solutions (for example, saturated potassium iodide solutions). The oocysts are rela- tively non-refractile and difficult to detect by normal bright- field microscopy and some confusion may also be experienced with yeast organisms. However, oocysts are readily detected by phase-contrast microscopy due to the presence of the highly refractile crystalline residual body (Figure 6 ) . The demonstration of oocysts concentrated from faecal samples therefore appears to be the most efficient means of diagnosing not only clinical but also subclinical infections.

Treatment and Control A large number of drugs have been used in attempts to

treat Cryptosporidium infections in man, calves and mice (Sloper et a f 1982; Moon et al 1982; Tzipori et a1 1982). These drugs have included broad-spectrum antibiotics, con- ventional anticoccidials, antimalarials and other anti-proto- zoal drugs as well as anthelmintics. None appear to have been effective against clinical infections. More recent attempts at chemoprophylaxis with several anticoccidial drugs have given promising results in the partial prevention of experi- mental infections in mice (Angus et a1 1984). However, preliminary studies on experimental infections in lambs treated similarly gave disappointing results. In many in- stances, infections seem to have been self-limiting in immu- nocompetent hosts and fluid replacement therapy is therefore important in alleviating the dehydration accompanying acute diarrhoea while awaiting spontaneous recovery. Other than supportive therapy for the side-effects of infections, no real treatment for cryptosporidiosis is known.

Several methods of controlling infections by preventitive measures have also been examined. Studies have been performed on the resistance of Cryptosporidium oocysts to a range of disinfectants and to various environmental con- ditions (Angus et a1 1982; Campbell et a1 1982; Pavlasek and Mares 1983). Mature oocysts were found to be strongly resistant to many disinfectants used in hospital and laboratory situations but their infectivity was destroyed by exposure to household ammonia and 10% formol saline (Campbell et a1 1982). Oocysts also proved to be quite resistant to temperature variations and infectivity was lost only after freezing or heating to 65°C for 30 min (Tzipori 1983). Infected faeces stored under different laboratory conditions also remained infective for up to 6 months (Moon and Bemrick 1981; Sherwood et a / 1982). Clearly, the ability of oocysts to withstand a range of climatic conditions means that the contamination of the environment by host faecal material serves as a source of infection for susceptible hosts for some time. Some measure of control may be possible in hospitals, households and even intensive farm situations through the isolation of infected individuals, strict hygiene and the chemical sterilisation of the immediate surroundings.

251

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(Accepted for publicat ion 29 J a n u a r y 1985)

ORlG INAL ARTICLES

The significance of leptospiral titres associated with bovine abortion

J . K . ELDER, P . M. PEPPER, M . W . M . HILL and W. H . WARD

Queensland Department of Primary Industries, Animal Research Institute, Yeerongpilly, Queensland 4105

SUMMARY: To investigate relationships between serological titres to 2 serovars, pomona (L. pomona) and hardjo (L. hardjo), of Leptospira interrogans and abortions, log linear and logit models were fitted to herd and individual cow data from cattle serologically negative for brucellosis.

Serological titres to both serovars were significantly related to abortions in individual cows, with L. pomona having a stronger relationship than L. hardjo. L. hardjo was not significant when herd data were analysed. Differences between dairy and beef cattle in the serological titres found to both L. pomona and L. hardjo were detected when data sets of all cattle or cattle with no history of abortion were analysed. The beef/dairy differences may be due to different management practices and/or to di f ferent geographical distributions of both serovars and populations of beef and dairy cattle.

If there are no cattle in a herd with a reciprocal titre of 3000 or greater for L. pomona, it is unlikely that L. pomona is associated with the abortion problem. There was no specific L. hardjo titre which separated high and low probabilities that the serum came from a cow or herd with an abortion history. Aust. vet. J. 62: 258-262

Introduction

Leptospirosis refers to a number of disease syndromes in animals and man associated with infection by many lepto- spiral serovars belonging to a single species, Leptospira interrogans. Only 2 serovars, L. pomona and L . hard jo , have been isolated from cattle in Australia (Sutherland ef a / 1949; Sullivan and Stallman 1969; Hoare and Claxton 1972; Adler and Faine 1980) and both have been implicated as causes of abortion in cattle (Te Punga and Bishop 1953; Suliivan 1974; Ellis and Michna 1976a; 1976b; 1977; Ellis et a1 1982; Hathaway and Little 1983). L . pomona is the only

member of the Pomona serogroup yet isolated in Australia. L. hardjo is one of 3 members of the Sejroe serogroup (Faine 1982) isolated in Australia, but the other 2 have only been isolated from bandicoots and possums (Adler and Faine 1980). However, one serovar of the Sejroe serogroup, L . balcanica, produced leptospiruria and agglutinating antibody in calves following experimental inoculation (Durfee and Presidente 1979a) and has been isolated from cattle in New Zealand (Mackintosh e t a/ 1980) and the United States of America (White e t at 1982). In Queensland cattle, serological evidence of the presence of serovars belonging to other

258 Auslralian Veterinary Journal, Vol. 62, No. 8, August, 1985